Search

Your search keyword '"Sara S. Strom"' showing total 209 results
Start Over Author "Sara S. Strom"
209 results on '"Sara S. Strom"'

1. Author Correction: Germline variation at 8q24 and prostate cancer risk in men of European ancestry

Author

Marco Matejcic, Edward J. Saunders, Tokhir Dadaev, Mark N. Brook, Kan Wang, Xin Sheng, Ali Amin Al Olama, Fredrick R. Schumacher, Sue A. Ingles, Koveela Govindasami, Sara Benlloch, Sonja I. Berndt, Demetrius Albanes, Stella Koutros, Kenneth Muir, Victoria L. Stevens, Susan M. Gapstur, Catherine M. Tangen, Jyotsna Batra, Judith Clements, Henrik Gronberg, Nora Pashayan, Johanna Schleutker, Alicja Wolk, Catharine West, Lorelei Mucci, Peter Kraft, Géraldine Cancel-Tassin, Karina D. Sorensen, Lovise Maehle, Eli M. Grindedal, Sara S. Strom, David E. Neal, Freddie C. Hamdy, Jenny L. Donovan, Ruth C. Travis, Robert J. Hamilton, Barry Rosenstein, Yong-Jie Lu, Graham G. Giles, Adam S. Kibel, Ana Vega, Jeanette T. Bensen, Manolis Kogevinas, Kathryn L. Penney, Jong Y. Park, Janet L. Stanford, Cezary Cybulski, Børge G. Nordestgaard, Hermann Brenner, Christiane Maier, Jeri Kim, Manuel R. Teixeira, Susan L. Neuhausen, Kim De Ruyck, Azad Razack, Lisa F. Newcomb, Davor Lessel, Radka Kaneva, Nawaid Usmani, Frank Claessens, Paul A. Townsend, Manuela Gago-Dominguez, Monique J. Roobol, Florence Menegaux, Kay-Tee Khaw, Lisa A. Cannon-Albright, Hardev Pandha, Stephen N. Thibodeau, Daniel J. Schaid, The PRACTICAL Consortium, Fredrik Wiklund, Stephen J. Chanock, Douglas F. Easton, Rosalind A. Eeles, Zsofia Kote-Jarai, David V. Conti, and Christopher A. Haiman

Subjects
Science
Abstract

The original version of this Article contained an error in the spelling of the author Manuela Gago-Dominguez, which was incorrectly given as Manuela G. Dominguez. This has now been corrected in both the PDF and HTML versions of the Article.

Published
2019
Full Text
View/download PDF

2. Germline variation at 8q24 and prostate cancer risk in men of European ancestry

Author

Marco Matejcic, Edward J. Saunders, Tokhir Dadaev, Mark N. Brook, Kan Wang, Xin Sheng, Ali Amin Al Olama, Fredrick R. Schumacher, Sue A. Ingles, Koveela Govindasami, Sara Benlloch, Sonja I. Berndt, Demetrius Albanes, Stella Koutros, Kenneth Muir, Victoria L. Stevens, Susan M. Gapstur, Catherine M. Tangen, Jyotsna Batra, Judith Clements, Henrik Gronberg, Nora Pashayan, Johanna Schleutker, Alicja Wolk, Catharine West, Lorelei Mucci, Peter Kraft, Géraldine Cancel-Tassin, Karina D. Sorensen, Lovise Maehle, Eli M. Grindedal, Sara S. Strom, David E. Neal, Freddie C. Hamdy, Jenny L. Donovan, Ruth C. Travis, Robert J. Hamilton, Barry Rosenstein, Yong-Jie Lu, Graham G. Giles, Adam S. Kibel, Ana Vega, Jeanette T. Bensen, Manolis Kogevinas, Kathryn L. Penney, Jong Y. Park, Janet L. Stanford, Cezary Cybulski, Børge G. Nordestgaard, Hermann Brenner, Christiane Maier, Jeri Kim, Manuel R. Teixeira, Susan L. Neuhausen, Kim De Ruyck, Azad Razack, Lisa F. Newcomb, Davor Lessel, Radka Kaneva, Nawaid Usmani, Frank Claessens, Paul A. Townsend, Manuela Gago-Dominguez, Monique J. Roobol, Florence Menegaux, Kay-Tee Khaw, Lisa A. Cannon-Albright, Hardev Pandha, Stephen N. Thibodeau, Daniel J. Schaid, The PRACTICAL (Prostate Cancer Association Group to Investigate Cancer-Associated Alterations in the Genome) Consortium, Fredrik Wiklund, Stephen J. Chanock, Douglas F. Easton, Rosalind A. Eeles, Zsofia Kote-Jarai, David V. Conti, and Christopher A. Haiman

Subjects
Science
Abstract

Chromosome 8q24 is known to be a major susceptibility region for prostate cancer risk. Here the authors analyze genetic data across the 8q24 region from 71,535 prostate cancer patients identifying 12 risk loci, three previously unreported, highlighting the contribution of germline variation at this locus.

Published
2018
Full Text
View/download PDF

3. Atlas of prostate cancer heritability in European and African-American men pinpoints tissue-specific regulation

Author

Alexander Gusev, Huwenbo Shi, Gleb Kichaev, Mark Pomerantz, Fugen Li, Henry W. Long, Sue A. Ingles, Rick A. Kittles, Sara S. Strom, Benjamin A. Rybicki, Barbara Nemesure, William B. Isaacs, Wei Zheng, Curtis A. Pettaway, Edward D. Yeboah, Yao Tettey, Richard B. Biritwum, Andrew A. Adjei, Evelyn Tay, Ann Truelove, Shelley Niwa, Anand P. Chokkalingam, Esther M. John, Adam B. Murphy, Lisa B. Signorello, John Carpten, M. Cristina Leske, Suh-Yuh Wu, Anslem J. M. Hennis, Christine Neslund-Dudas, Ann W. Hsing, Lisa Chu, Phyllis J. Goodman, Eric A. Klein, John S. Witte, Graham Casey, Sam Kaggwa, Michael B. Cook, Daniel O. Stram, William J. Blot, Rosalind A. Eeles, Douglas Easton, ZSofia Kote-Jarai, Ali Amin Al Olama, Sara Benlloch, Kenneth Muir, Graham G. Giles, Melissa C. Southey, Liesel M. Fitzgerald, Henrik Gronberg, Fredrik Wiklund, Markus Aly, Brian E. Henderson, Johanna Schleutker, Tiina Wahlfors, Teuvo L. J. Tammela, Børge G. Nordestgaard, Tim J. Key, Ruth C. Travis, David E. Neal, Jenny L. Donovan, Freddie C. Hamdy, Paul Pharoah, Nora Pashayan, Kay-Tee Khaw, Janet L. Stanford, Stephen N. Thibodeau, Shannon K. McDonnell, Daniel J. Schaid, Christiane Maier, Walther Vogel, Manuel Luedeke, Kathleen Herkommer, Adam S. Kibel, Cezary Cybulski, Dominika Wokolorczyk, Wojciech Kluzniak, Lisa Cannon-Albright, Craig Teerlink, Hermann Brenner, Aida K. Dieffenbach, Volker Arndt, Jong Y. Park, Thomas A. Sellers, Hui-Yi Lin, Chavdar Slavov, Radka Kaneva, Vanio Mitev, Jyotsna Batra, Amanda Spurdle, Judith A. Clements, Manuel R. Teixeira, Hardev Pandha, Agnieszka Michael, Paula Paulo, Sofia Maia, Andrzej Kierzek, The PRACTICAL consortium, David V. Conti, Demetrius Albanes, Christine Berg, Sonja I. Berndt, Daniele Campa, E. David Crawford, W. Ryan Diver, Susan M. Gapstur, J. Michael Gaziano, Edward Giovannucci, Robert Hoover, David J. Hunter, Mattias Johansson, Peter Kraft, Loic Le Marchand, Sara Lindström, Carmen Navarro, Kim Overvad, Elio Riboli, Afshan Siddiq, Victoria L. Stevens, Dimitrios Trichopoulos, Paolo Vineis, Meredith Yeager, Gosia Trynka, Soumya Raychaudhuri, Frederick R. Schumacher, Alkes L. Price, Matthew L. Freedman, Christopher A. Haiman, and Bogdan Pasaniuc

Subjects
Science
Abstract

Over one hundred loci have been identified to be associated with the familial risk of prostate cancer but the functional effects are poorly understood. Here the authors use single-nucleotide variant and epigentic data to show an underlying genetic architecture marked by histone modification.

Published
2016
Full Text
View/download PDF

4. Meta-analysis of genome-wide association studies discovers multiple loci for chronic lymphocytic leukemia

Author

Sonja I. Berndt, Nicola J. Camp, Christine F. Skibola, Joseph Vijai, Zhaoming Wang, Jian Gu, Alexandra Nieters, Rachel S. Kelly, Karin E. Smedby, Alain Monnereau, Wendy Cozen, Angela Cox, Sophia S. Wang, Qing Lan, Lauren R. Teras, Moara Machado, Meredith Yeager, Angela R. Brooks-Wilson, Patricia Hartge, Mark P. Purdue, Brenda M. Birmann, Claire M. Vajdic, Pierluigi Cocco, Yawei Zhang, Graham G. Giles, Anne Zeleniuch-Jacquotte, Charles Lawrence, Rebecca Montalvan, Laurie Burdett, Amy Hutchinson, Yuanqing Ye, Timothy G. Call, Tait D. Shanafelt, Anne J. Novak, Neil E. Kay, Mark Liebow, Julie M. Cunningham, Cristine Allmer, Henrik Hjalgrim, Hans-Olov Adami, Mads Melbye, Bengt Glimelius, Ellen T. Chang, Martha Glenn, Karen Curtin, Lisa A. Cannon-Albright, W Ryan Diver, Brian K. Link, George J. Weiner, Lucia Conde, Paige M. Bracci, Jacques Riby, Donna K. Arnett, Degui Zhi, Justin M. Leach, Elizabeth A. Holly, Rebecca D. Jackson, Lesley F. Tinker, Yolanda Benavente, Núria Sala, Delphine Casabonne, Nikolaus Becker, Paolo Boffetta, Paul Brennan, Lenka Foretova, Marc Maynadie, James McKay, Anthony Staines, Kari G. Chaffee, Sara J. Achenbach, Celine M. Vachon, Lynn R. Goldin, Sara S. Strom, Jose F. Leis, J. Brice Weinberg, Neil E. Caporaso, Aaron D. Norman, Anneclaire J. De Roos, Lindsay M. Morton, Richard K. Severson, Elio Riboli, Paolo Vineis, Rudolph Kaaks, Giovanna Masala, Elisabete Weiderpass, María- Dolores Chirlaque, Roel C. H. Vermeulen, Ruth C. Travis, Melissa C. Southey, Roger L. Milne, Demetrius Albanes, Jarmo Virtamo, Stephanie Weinstein, Jacqueline Clavel, Tongzhang Zheng, Theodore R. Holford, Danylo J. Villano, Ann Maria, John J. Spinelli, Randy D. Gascoyne, Joseph M. Connors, Kimberly A. Bertrand, Edward Giovannucci, Peter Kraft, Anne Kricker, Jenny Turner, Maria Grazia Ennas, Giovanni M. Ferri, Lucia Miligi, Liming Liang, Baoshan Ma, Jinyan Huang, Simon Crouch, Ju-Hyun Park, Nilanjan Chatterjee, Kari E. North, John A. Snowden, Josh Wright, Joseph F. Fraumeni, Kenneth Offit, Xifeng Wu, Silvia de Sanjose, James R. Cerhan, Stephen J. Chanock, Nathaniel Rothman, and Susan L. Slager

Subjects
Science
Abstract

Chronic lymphocytic leukemia is a highly inheritable cancer. Here the authors conduct a metaanalysis of four genome-wide association studies and identify three novel loci located near EOMES, SERPINB6 and LPPassociated with risk of this disease.

Published
2016
Full Text
View/download PDF

5. Assessing the Optimum Use of Androgen-Deprivation Therapy in High-Risk Prostate Cancer Patients Undergoing External Beam Radiation Therapy

Author

Michelle S. Ludwig MD, MPH, PhD, Deborah A. Kuban MD, Sara S. Strom PhD, Xianglin L. Du MD, PhD, David S. Lopez PhD, and Jose-Miguel Yamal PhD

Subjects
Medicine
Abstract

The optimum use of androgen deprivation therapy (ADT) in high-risk prostate cancer patients has not been defined in the setting of dose-escalated external beam radiation therapy. A retrospective analysis of 1,290 patients with high-risk prostate cancer from June 1987 through March 2010 treated with external beam radiation therapy was performed. Median follow-up was 7.2 years, and 797 patients received ADT, with 384 patients experiencing a biochemical failure and 145 with distant metastasis. ADT was associated with lower risk of biochemical failure and distant metastasis than no ADT after adjusting for age, prostate-specific antigen (PSA), Gleason score, year of diagnosis, tumor stage, and radiation dose. ADT was associated with a greater reduction in biochemical failure in the low-dose radiation group than in the high-dose group. Patients with >24 months of ADT had a lower risk of PSA failures than those with 24 months of ADT in all patients who received ADT.

Published
2017
Full Text
View/download PDF

6. Racial/Ethnic Differences in Treatment Discussed, Preferred, and Received for Prostate Cancer in a Tri-Ethnic Population

Author

G. M. Monawar Hosain MD, PhD, Maureen Sanderson PhD, Xianglin L. Du MD, PhD, Wenyaw Chan PhD, and Sara S. Strom PhD

Subjects
Medicine
Abstract

This study was conducted to explore whether racial/ethnic differences exist in treatment discussed, preferred, and ultimately received for localized prostate cancer (PCa) as epidemiological data are scant on this issue. The authors recruited 640 localized PCa patients from the Texas Medical Center, Houston, Texas, between 1996 and 2004. The authors used a structured questionnaire to collect data through personal interviews. Three main treatment modalities for localized PCa, consisting of surgery, radiation therapy, and watchful waiting, were considered for this study. It was found that health professionals were less likely to discuss surgery (odds ratio [OR] = 0.35, 95% confidence interval [CI] = 0.18-0.68) and watchful waiting (OR = 0.53, 95% CI = 0.34-0.83) with Hispanics than Whites. However, African Americans were less likely to receive watchful waiting (OR = 0.22, 95% CI = 0.05-0.93). They were more likely to prefer (OR = 1.23, 95% CI = 0.78-1.94) and receive (OR = 1.27, 95% CI = 0.87-1.86) radiation therapy, although they did not achieve statistical significance ( p < .05). Higher age was associated with lower likelihood of discussing, preferring, and receiving surgical treatment. Higher Gleason sum was associated with lower likelihood of discussing treatment. A comparison of concordances between treatment preferred by patients and what was actually received, in general, showed a higher agreement for surgery and radiation therapy. More exploration needs to be done in other settings to confirm these findings.

Published
2012
Full Text
View/download PDF

7. Correction: Identification, Replication, and Fine-Mapping of Loci Associated with Adult Height in Individuals of African Ancestry.

Author

Amidou N'Diaye, Gary K. Chen, Cameron D. Palmer, Bing Ge, Bamidele Tayo, Rasika A. Mathias, Jingzhong Ding, Michael A. Nalls, Adebowale Adeyemo, Véronique Adoue, Christine B. Ambrosone, Larry Atwood, Elisa V. Bandera, Lewis C. Becker, Sonja I. Berndt, Leslie Bernstein, William J. Blot, Eric Boerwinkle, Angela Britton, Graham Casey, Stephen J. Chanock, Ellen Demerath, Sandra L. Deming, W. Ryan Diver, Caroline Fox, Tamara B. Harris, Dena G. Hernandez, Jennifer J. Hu, Sue A. Ingles, Esther M. John, Craig Johnson, Brendan Keating, Rick A. Kittles, Laurence N. Kolonel, Stephen B. Kritchevsky, Loic Le Marchand, Kurt Lohman, Jiankang Liu, Robert C. Millikan, Adam Murphy, Solomon Musani, Christine Neslund-Dudas, Kari E. North, Sarah Nyante, Adesola Ogunniyi, Elaine A. Ostrander, George Papanicolaou, Sanjay Patel, Curtis A. Pettaway, Michael F. Press, Susan Redline, Jorge L. Rodriguez-Gil, Charles Rotimi, Benjamin A. Rybicki, Babatunde Salako, Pamela J. Schreiner, Lisa B. Signorello, Andrew B. Singleton, Janet L. Stanford, Alex H. Stram, Daniel O. Stram, Sara S. Strom, Bhoom Suktitipat, Michael J. Thun, John S. Witte, Lisa R. Yanek, Regina G. Ziegler, Wei Zheng, Xiaofeng Zhu, Joseph M. Zmuda, Alan B. Zonderman, Michele K. Evans, Yongmei Liu, Diane M. Becker, Richard S. Cooper, Tomi Pastinen, Brian E. Henderson, Joel N. Hirschhorn, Guillaume Lettre, and Christopher A. Haiman

Subjects
Genetics, QH426-470
Published
2011
Full Text
View/download PDF

8. Evidence of Novel Susceptibility Variants for Prostate Cancer and a Multiancestry Polygenic Risk Score Associated with Aggressive Disease in Men of African Ancestry

Author

Fei Chen, Ravi K. Madduri, Alex A. Rodriguez, Burcu F. Darst, Alisha Chou, Xin Sheng, Anqi Wang, Jiayi Shen, Edward J. Saunders, Suhn K. Rhie, Jeannette T. Bensen, Sue A. Ingles, Rick A. Kittles, Sara S. Strom, Benjamin A. Rybicki, Barbara Nemesure, William B. Isaacs, Janet L. Stanford, Wei Zheng, Maureen Sanderson, Esther M. John, Jong Y. Park, Jianfeng Xu, Ying Wang, Sonja I. Berndt, Chad D. Huff, Edward D. Yeboah, Yao Tettey, Joseph Lachance, Wei Tang, Christopher T. Rentsch, Kelly Cho, Benjamin H. Mcmahon, Richard B. Biritwum, Andrew A. Adjei, Evelyn Tay, Ann Truelove, Shelley Niwa, Thomas A. Sellers, Kosj Yamoah, Adam B. Murphy, Dana C. Crawford, Alpa V. Patel, William S. Bush, Melinda C. Aldrich, Olivier Cussenot, Gyorgy Petrovics, Jennifer Cullen, Christine M. Neslund-Dudas, Mariana C. Stern, Zsofia Kote-Jarai, Koveela Govindasami, Michael B. Cook, Anand P. Chokkalingam, Ann W. Hsing, Phyllis J. Goodman, Thomas J. Hoffmann, Bettina F. Drake, Jennifer J. Hu, Jacob M. Keaton, Jacklyn N. Hellwege, Peter E. Clark, Mohamed Jalloh, Serigne M. Gueye, Lamine Niang, Olufemi Ogunbiyi, Michael O. Idowu, Olufemi Popoola, Akindele O. Adebiyi, Oseremen I. Aisuodionoe-Shadrach, Hafees O. Ajibola, Mustapha A. Jamda, Olabode P. Oluwole, Maxwell Nwegbu, Ben Adusei, Sunny Mante, Afua Darkwa-Abrahams, James E. Mensah, Halimatou Diop, Stephen K. Van Den Eeden, Pascal Blanchet, Jay H. Fowke, Graham Casey, Anselm J. Hennis, Alexander Lubwama, Ian M. Thompson, Robin Leach, Douglas F. Easton, Michael H. Preuss, Ruth J. Loos, Susan M. Gundell, Peggy Wan, James L. Mohler, Elizabeth T. Fontham, Gary J. Smith, Jack A. Taylor, Shiv Srivastava, Rosaline A. Eeles, John D. Carpten, Adam S. Kibel, Luc Multigner, Marie-Élise Parent, Florence Menegaux, Geraldine Cancel-Tassin, Eric A. Klein, Caroline Andrews, Timothy R. Rebbeck, Laurent Brureau, Stefan Ambs, Todd L. Edwards, Stephen Watya, Stephen J. Chanock, John S. Witte, William J. Blot, J. Michael Gaziano, Amy C. Justice, David V. Conti, Christopher A. Haiman, University of Southern California (USC), Keck School of Medicine [Los Angeles], Centre de Recherche pour les Pathologies Prostatiques [Paris] (CeRePP), Sorbonne Université (SU), Institut de recherche en santé, environnement et travail (Irset), Université d'Angers (UA)-Université de Rennes (UR)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), CHU Pointe-à-Pitre/Abymes [Guadeloupe], Centre de recherche en épidémiologie et santé des populations (CESP), and Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay

Subjects
Prostate cancer, MESH: Humans, Urology, MESH: Genetic Predisposition to Disease, MESH: Black People, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.MHEP.UN]Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, MESH: Male, Polygenic risk score, African ancestry, MESH: Risk Factors, MESH: Prostatic Neoplasms, MESH: Genome-Wide Association Study, Susceptibility loci, Aggressive prostate cancer
Abstract

Background: Genetic factors play an important role in prostate cancer (PCa) susceptibility.Objective: To discover common genetic variants contributing to the risk of PCa in men of African ancestry.Design, setting, and participants: We conducted a meta-analysis of ten genome-wide association studies consisting of 19378 cases and 61620 controls of African ancestry.Outcome measurements and statistical analysis: Common genotyped and imputed variants were tested for their association with PCa risk. Novel susceptibility loci were identified and incorporated into a multiancestry polygenic risk score (PRS). The PRS was evaluated for associations with PCa risk and disease aggressiveness.Results and limitations: Nine novel susceptibility loci for PCa were identified, of which seven were only found or substantially more common in men of African ancestry, including an African-specific stop-gain variant in the prostate-specific gene anoctamin 7 (ANO7). A multiancestry PRS of 278 risk variants conferred strong associations with PCa risk in African ancestry studies (odds ratios [ORs] >3 and >5 for men in the top PRS decile and percentile, respectively). More importantly, compared with men in the 40-60% PRS category, men in the top PRS decile had a significantly higher risk of aggressive PCa (OR = 1.23, 95% confidence interval = 1.10-1.38, p = 4.4 × 10-4).Conclusions: This study demonstrates the importance of large-scale genetic studies in men of African ancestry for a better understanding of PCa susceptibility in this high-risk population and suggests a potential clinical utility of PRS in differentiating between the risks of developing aggressive and nonaggressive disease in men of African ancestry.Patient summary: In this large genetic study in men of African ancestry, we discovered nine novel prostate cancer (PCa) risk variants. We also showed that a multiancestry polygenic risk score was effective in stratifying PCa risk, and was able to differentiate risk of aggressive and nonaggressive disease.

Published
2023

9. A Germline Variant at 8q24 Contributes to Familial Clustering of Prostate Cancer in Men of African Ancestry

Author

Luc Multigner, William J. Blot, Alexander Lubwama, Stephen Watya, Peter E. Clark, Lucy Xia, Sara S. Strom, Adam S. Kibel, Jong Y. Park, Adam B. Murphy, Jennifer Cullen, Christopher A. Haiman, Florence Menegaux, Shiv Srivastava, Loreall Pooler, Mariana C. Stern, Anand P. Chokkalingam, Eric A. Klein, Wei Zheng, Thomas A. Sellers, Anselm Hennis, Dana C. Crawford, James L. Mohler, Jack A. Taylor, Esther M. John, Robin J. Leach, Sonja I. Berndt, Laurent Brureau, John D. Carpten, Susan Gundell, David V. Conti, Barbara Nemesure, Rosalind A. Eeles, Graham Casey, Pascal Blanchet, Benjamin A. Rybicki, Chad D. Huff, Maureen Sanderson, Stephen J. Chanock, Melinda C. Aldrich, Jay H. Fowke, Jennifer J. Hu, Diptasri Mandal, Sue A. Ingles, Kosj Yamoah, Kathleen A. Cooney, K. Govindasami, Ian M. Thompson, Patrick C. Walsh, Xin Sheng, Zsofia Kote-Jarai, Janet L. Stanford, Marie-Élise Parent, Christine Neslund-Dudas, Jianfeng Xu, William S. Bush, Phyllis J. Goodman, Meredith Yeager, Burcu F. Darst, Gary J. Smith, Victoria L. Stevens, Rick A. Kittles, Elaine A. Ostrander, Olivier Cussenot, Gyorgy Petrovics, Elizabeth T. H. Fontham, William B. Isaacs, Peggy Wan, Geraldine Cancel-Tassin, Susan M. Gapstur, Bettina F. Drake, Jeannette T. Bensen, University of Southern California (USC), Centre de Recherche pour les Pathologies Prostatiques. (CeRePP / UA 3104), CEREPP, CHU Tenon [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut de recherche en santé, environnement et travail (Irset), Université d'Angers (UA)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Centre de recherche en épidémiologie et santé des populations (CESP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris-Sud - Paris 11 (UP11)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), CHU Pointe-à-Pitre/Abymes [Guadeloupe], U19 CA148537, U19 CA214253, R01 CA165862, and K99 CA246063, National Cancer Institute at the National Institutes of Health, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Université d'Angers (UA)-Université de Rennes (UR)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), and Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
Male, Oncology, medicine.medical_specialty, Urology, Family history, Population, 030232 urology & nephrology, Black People, Familial prostate cancer, [SDV.CAN]Life Sciences [q-bio]/Cancer, Familial clustering, Risk Assessment, Article, Germline, 03 medical and health sciences, Prostate cancer, 0302 clinical medicine, Internal medicine, Genetics, Humans, Medicine, education, Genetic variant, Aged, education.field_of_study, business.industry, Genetic Variation, Prostatic Neoplasms, 8q24, Middle Aged, medicine.disease, Health equity, 3. Good health, Disease Hotspot, Germ Cells, Prostate cancer screening, African ancestry, 030220 oncology & carcinogenesis, Health disparities, business
Abstract

International audience; Although men of African ancestry have a high risk of prostate cancer (PCa), no genes or mutations have been identified that contribute to familial clustering of PCa in this population. We investigated whether the African ancestry-specific PCa risk variant at 8q24, rs72725854, is enriched in men with a PCa family history in 9052 cases, 143 cases from high-risk families, and 8595 controls of African ancestry. We found the risk allele to be significantly associated with earlier age at diagnosis, more aggressive disease, and enriched in men with a PCa family history (32% of high-risk familial cases carried the variant vs 23% of cases without a family history and 12% of controls). For cases with two or more first-degree relatives with PCa who had at least one family member diagnosed at age

Published
2020

10. Author Correction: Germline variation at 8q24 and prostate cancer risk in men of European ancestry

Author

Sara Benlloch, Roger L. Milne, Azad Hassan Abdul Razack, José Manuel Ruiz-Dominguez, Steven Joniau, Maria P. Silva, Martin Andreas Røder, Constance Turman, Anne-Maree Haynes, Jin Ling, Robert N. Hoover, Jong Y. Park, Johanna Schleutker, Brian E. Henderson, Amy Hutchinson, Stephanie J. Weinstein, Manolis Kogevinas, Melissa Papargiris, Monique J. Roobol, Gill Barnett, Wayne D. Tilley, Elio Riboli, Samantha E.T. Larkin, Melissa C. Southey, Michelle Guy, Jeanette T. Bensen, Henrik Grönberg, Fredrick R. Schumacher, Karina Dalsgaard Sørensen, Davor Lessel, Carin Cavalli-Bjoerkman, Tomislav Kuliš, Barry S. Rosenstein, Paula Kujala, Michael Davis, Andrzej M. Kierzek, Antonio Finelli, Gerald L. Andriole, Leire Moya, Antonio Gómez-Caamaño, Demetrius Albanes, Jianming Guo, Lisa F. Newcomb, Koveela Govindasami, Ji Lin, Gert De Meerleer, Manuel Luedeke, Richard M. Martin, Zeljko Kastelan, Kay-Tee Khaw, Ruth C. Travis, Rebecca Elliott, Alexandre R. Zlotta, Xin Guo, Kirsi Talala, Yangling Zhang, Lorelei A. Mucci, Marie Sanchez, Paul D.P. Pharoah, Mariona Bustamante, Peter Klarskov, Aleksandrina Vlahova, Srilakshmi Srinivasan, Aik T. Ong, David E. Neal, Sylvie Cénée, Esther M. John, Sonja I. Berndt, Kan Wang, Peter Iversen, Harry Ostrer, Michael Borre, Freddie C. Hamdy, Christopher A. Haiman, Ji Wu, Florence Menegaux, Jacek Marzec, Sara S. Strom, David P. Dearnaley, Jyotsna Batra, Piet Ost, Mariana C. Stern, Kim De Ruyck, Hyun Soo Park, Trina Yeadon, Elenko Popov, Yudong Wu, Svetlana Christova, Thomas Van den Broeck, Loic Le Marchand, Daniel J. Schaid, Babu Zachariah, Sune F. Nielsen, Mary-Anne Kedda, Judith A. Clements, Olivier Cussenot, Robert Szulkin, Shiro Saito, Andrew Evans, Douglas F. Easton, Gemma Castaño-Vinyals, Steve Hazel, Thérèse Truong, Guomin Wang, Katarina Cuk, Ants Toi, Rosalind A. Eeles, Darina Kachakova, Lourdes Mengual, Lisa G. Horvath, Yuan Chun Ding, Catharine M L West, Ana Carballo, Suzanne K. Chambers, Aurelie Vogt, Angela Cox, Daniel W. Lin, Dominika Wokołorczyk, Manuela Gago-Dominguez, Stephen J. Chanock, Federico Canzian, Aleksandra Klim, Tokhir Dadaev, Kathleen Herkommer, Tihomir Dikov, Lovise Maehle, Jasmine Lim, Janet L. Stanford, Martin Eklund, Guido Jenster, Soo-Hwang Teo, Teemu J. Murtola, Torben F. Ørntoft, Stella Koutros, Christa Stegmaier, Sofia Maia, Mitchell J. Machiela, Lisa A. Cannon-Albright, Clare Berry, Pamela Saunders, Lluís Cecchini, Jeri Kim, Radka Kaneva, Brigitte Trétarre, Anne George, Meir J. Stampfer, Marija Gamulin, Meng H. Tan, Angela Morgan, Jenny L Donovan, Graham G. Giles, Geraldine Cancel-Tassin, Neil Fleshner, Shannon K. McDonnell, Hardeep Ranu, Naomi Livni, Kimmo Taari, Sarah L. Kerns, Csilla Sipeky, Alicja Wolk, Edward Giovannucci, Ninghan Feng, Marta Cardoso, Jan-Erik Johansson, Catherine M. Tangen, Guangwen Cao, Adam S. Kibel, Robert J. MacInnis, Bernd Holleczek, Sarah J Lewis, Bo Zhou, Michael Broms, Maria Elena Martinez, Renea A. Taylor, Børge G. Nordestgaard, Fritz H. Schröder, Ali Amin Al Olama, Sue A. Ingles, Markus Aly, Jie Li, Lori S. Tillmans, Ana Vega, Patricia Calvo, Christopher J. Logothetis, David V. Conti, Miguel Aguado, Inés Gómez-Acebo, Tobias Nordström, Meiling Li, Elaine A. Ostrander, C.H. Bangma, Cyril Fisher, Joanne F. Aitken, Matthew Parliament, Gail P. Risbridger, John L. Hopper, Takashi Imai, Belynda Hicks, Victoria L. Stevens, Cezary Cybulski, G Marsden, Brian D. Carter, Vanessa M. Hayes, Nawaid Usmani, Vanio Mitev, Shan-Chao Zhao, Margaret Cook, Milan S. Geybels, Phyllis J. Goodman, Mark N. Brook, Nora Pashayan, Timothy J. Key, Yongwei Yu, Xavier Rebillard, David J. Hunter, Laura Fachal, Javier Llorca, Afshan Siddiq, Claire Aukim-Hastie, Trinidad Dierssen-Sotos, Walther Vogel, Angel Carracedo, Laura E. Beane Freeman, Julio M. Pow-Sang, Hardev Pandha, Robert A. Gardiner, Shaun M. Riska, Yong-Jie Lu, Zan Sun, Ramón Lobato-Busto, Ami Karlsson, Hongwei Zhang, Guoping Ren, Jing Ma, Huihai Wu, Søren M. Bentzen, John Pedersen, Claire Mulot, Girish S. Kulkarni, Jan Lubinski, Antonio Alcaraz, Jose E. Castelao, Athene Lane, Rasmus Bisbjerg, Thomas A. Sellers, Robert J. Hamilton, Jianfeng Xu, Sofie De Langhe, Artitaya Lophatananon, Maren Weisher, Agnieszka Michael, Yves Akoli Koudou, Niclas Håkansson, Alison M. Dunning, Hubert Thierens, Matthew L. Freedman, Kenneth Muir, Ian M. Thompson, Ian Whitmore, Susan L. Neuhausen, Chavdar Slavov, Wojciech Kluzniak, Laurence N. Kolonel, Lisa M. Butler, Teuvo L.J. Tammela, Alison Thwaites, Theodorus van der Kwast, Liesel M. FitzGerald, Thomas J. Schnoeller, Hermann Brenner, Christiane Maier, Amanda B. Spurdle, Jan Adolfsson, Atanaska Mitkova, Peter Kraft, Paula Peleteiro, Pär Stattin, Xin Sheng, Paul D. Brown, Ron H.N. van Schaik, Zsofia Kote-Jarai, Susan M. Gapstur, Paul A. Townsend, Edward J. Saunders, Bettina F. Drake, Stephen N. Thibodeau, Fredrik Wiklund, Paula Paulo, Esther Gracia-Lavedan, Xueying Mao, Marco Matejcic, Neil G. Burnet, A. L. Eckert, Manuel R. Teixeira, Sara Lindström, Weiyang He, Hui-Yi Lin, Suzanne Kolb, Linda Steele, Philipp Bohnert, Anssi Auvinen, Eli Marie Grindedal, Frank Claessens, and Kathryn L. Penney

Subjects
Urologic Diseases, 0301 basic medicine, Oncology, medicine.medical_specialty, Science, MEDLINE, General Physics and Astronomy, 02 engineering and technology, General Biochemistry, Genetics and Molecular Biology, Germline, 03 medical and health sciences, Internal medicine, medicine, PRACTICAL Consortium, lcsh:Science, Cancer, Prostate cancer risk, Multidisciplinary, business.industry, Prostate Cancer, Published Erratum, General Chemistry, 021001 nanoscience & nanotechnology, medicine.disease, Spelling, 3. Good health, 030104 developmental biology, Variation (linguistics), lcsh:Q, 0210 nano-technology, business
Abstract

The original version of this Article contained an error in the spelling of the author Manuela Gago-Dominguez, which was incorrectly given as Manuela G. Dominguez. This has now been corrected in both the PDF and HTML versions of the Article.

Published
2019

11. Publisher Correction: Trans-ancestry genome-wide association meta-analysis of prostate cancer identifies new susceptibility loci and informs genetic risk prediction

Author

Brian D. Carter, Gert De Meerleer, Michael B. Cook, Paul A. Townsend, Kim De Ruyck, Edward J. Saunders, Christopher A. Haiman, Atushi Takahashi, Sonja I. Berndt, Florence Menegaux, Cezary Cybulski, Barbara Nemesure, Loic Le Marchand, Sune F. Nielsen, Demetrius Albanes, Robert J. Hamilton, Ninghan Feng, Stella Koutros, Stephen J. Chanock, Wei Zheng, Thomas A. Sellers, Rick A. Kittles, Craig C. Teerlink, Stephen N. Thibodeau, Marija Gamulin, Artitaya Lophatananon, Niclas Håkansson, Fredrik Wiklund, Roberta McKean-Cowdin, Yuan Chun Ding, Nora Pashayan, Timothy J. Key, Børge G. Nordestgaard, Shannon K. McDonnell, Jong Y. Park, Laura Fachal, Martin Andreas Røder, Johanna Schleutker, Edward Giovannucci, Anssi Auvinen, Hardev Pandha, Maria Elena Martinez, Mitchell J. Machiela, Gill Barnett, Melissa C. Southey, Graham G. Giles, Barry S. Rosenstein, Stephen Watya, Bernd Holleczek, Pascal Blanchet, Agnieszka Michael, William J. Blot, James L. Mohler, Jack A. Taylor, Sarah L. Kerns, Adam S. Kibel, Piet Ost, Ana Vega, Richard M. Martin, Jennifer J. Hu, Nicholas Mancuso, Yukihide Momozawa, Robert J. MacInnis, Sue A. Ingles, Maureen Sanderson, Kai Uwe Saum, Markus Aly, Robert Szulkin, Davor Lessel, Hermann Brenner, Yves Akoli Koudou, Jan Lubinski, Mina Torres, Anselm Hennis, Eli Marie Grindedal, Csilla Sipeky, Susan L. Neuhausen, Alison M. Dunning, Alicja Wolk, Adam B. Murphy, Brandi Weaver, Mariana C. Stern, Paula Paulo, Stephanie J. Weinstein, Xueying Mao, Tobias Nordström, Neil Fleshner, Tokhir Dadaev, Teuvo L.J. Tammela, Jay H. Fowke, Tomislav Kuliš, Steven Joniau, Yudong Wu, Rosalind A. Eeles, Shan Chao Zhao, Kenneth Muir, Mark N. Brook, Hidewaki Nakagawa, Freddie C. Hamdy, Karina Dalsgaard Sørensen, Linda Steele, Alisha Chou, Dominika Wokołorczyk, Peggy Wan, Martin Eklund, Laurent Brureau, Lisa A. Cannon-Albright, Lilit C. Moss, Daniel J. Schaid, Luc Multigner, Benjamin A. Rybicki, Xin Sheng, Constance Turman, Ron H.N. van Schaik, Radka Kaneva, Zsofia Kote-Jarai, Frank Claessens, Katarina Cuk, Kay-Tee Khaw, Chad D. Huff, Henrik Grönberg, Kathryn L. Penney, Geraldine Cancel-Tassin, Eric A. Klein, Masashi Fujita, Jennifer Cullen, Michael Borre, Jenny L Donovan, Dana C. Crawford, Antonio Gómez-Caamaño, David V. Conti, Manuel Luedeke, Maya Ghoussaini, Janet L. Stanford, Peter Kraft, Ian M. Thompson, Koichi Matsuda, Soo-Hwang Teo, Christopher J. Logothetis, Robin J. Leach, Monique J. Roobol, Manuel R. Teixeira, Jose Esteban Castelao, Sara S. Strom, Vanio Mitev, Stig E. Bojesen, David J. Hunter, Wayne D. Tilley, Jyotsna Batra, Gerald L. Andriole, Christine Neslund-Dudas, Sara Lindström, Guido Jenster, Catherine M. Tangen, William S. Bush, Maren Weischer, Chavdar Slavov, Thomas J. Schnoeller, Javier Llorca, Claire Aukim-Hastie, Nawaid Usmani, Lisa G. Horvath, Daniel W. Lin, Esther M. John, Burcu F. Darst, Milan S. Geybels, Phyllis J. Goodman, Lynne R. Wilkens, Ali Amin Al Olama, Lorelei A. Mucci, Peter Iversen, Christiane Maier, Victoria L. Stevens, Andreia Brandão, Graham Casey, Neil G. Burnet, Ann W. Hsing, Hongwei Zhang, Laura E. Beane Freeman, Susan M. Gapstur, Sara Benlloch, James E. Mensah, Marie-Élise Parent, Jianfeng Xu, Bettina F. Drake, Jeannette T. Bensen, Azad Hassan Abdul Razack, Edward D. Yeboah, David E. Neal, John D. Carpten, Ruth C. Travis, Thomas J. Hoffmann, Thomas Van den Broeck, Jeri Kim, Ali Sahimi, Gemma Castaño-Vinyals, Alexander Lubwama, Leire Moya, Elio Riboli, Douglas F. Easton, Suzanne K. Chambers, Yong-Jie Lu, Melinda C. Aldrich, Manuela Gago-Dominguez, John S. Witte, Matthew Parliament, Gail P. Risbridger, Samantha E.T. Larkin, Lisa F. Newcomb, Fredrick R. Schumacher, Shiv Srivastava, Jasmine Lim, Meir J. Stampfer, Harry Ostrer, Judith A. Clements, Thérèse Truong, Catharine M L West, Zan Sun, Olivier Cussenot, Gyorgy Petrovics, Lovise Maehle, Elizabeth T. H. Fontham, William B. Isaacs, Hui Yi Lin, Rohit Varma, Elaine A. Ostrander, Manolis Kogevinas, Robert N. Hoover, Sandeep Singhal, Antonio Finelli, and Stephen K. Van Den Eeden

Subjects
0303 health sciences, business.industry, Published Erratum, MEDLINE, Genome-wide association study, Computational biology, Biology, medicine.disease, 03 medical and health sciences, Prostate cancer, 0302 clinical medicine, Meta-analysis, Genetics, medicine, Susceptibility locus, 06 Biological Sciences, 11 Medical and Health Sciences, Personalized medicine, Genetic risk, business, 030217 neurology & neurosurgery, 030304 developmental biology, Developmental Biology
Abstract

In the version of this article originally published, the names of the equally contributing authors and jointly supervising authors were switched. The correct affiliations are: “These authors contributed equally: David V. Conti, Burcu F. Darst. These authors jointly supervised this work: David V. Conti, Rosalind A. Eeles, Zsofia Kote-Jarai, Christopher A. Haiman.” The error has been corrected in the HTML and PDF versions of the article.

Published
2021

12. Trans-ancestry genome-wide association meta-analysis of prostate cancer identifies new susceptibility loci and informs genetic risk prediction

Author

Paul A. Townsend, Edward J. Saunders, Hidewaki Nakagawa, Manuel R. Teixeira, Graham Casey, Demetrius Albanes, Christine Neslund-Dudas, Sara Lindström, William S. Bush, Maren Weischer, Lisa A. Cannon-Albright, Rick A. Kittles, Peggy Wan, Martin Eklund, Stephen N. Thibodeau, Burcu F. Darst, Fredrik Wiklund, Nicholas Mancuso, Jeri Kim, Jong Y. Park, Johanna Schleutker, Maureen Sanderson, Samantha E.T. Larkin, Radka Kaneva, Hongwei Zhang, Daniel J. Schaid, Luc Multigner, Marie-Élise Parent, Robert Szulkin, Fredrick R. Schumacher, Geraldine Cancel-Tassin, Jianfeng Xu, Gill Barnett, Melissa C. Southey, Yuan Chun Ding, Alexander Lubwama, Maria Elena Martinez, Manolis Kogevinas, Linda Steele, Laurent Brureau, Shiv Srivastava, Maya Ghoussaini, Alison M. Dunning, Adam B. Murphy, Kenneth Muir, Edward Giovannucci, Mitchell J. Machiela, James L. Mohler, Jack A. Taylor, Robert N. Hoover, Sandeep Singhal, Chavdar Slavov, Guido Jenster, Frank Claessens, Neil Fleshner, Sara Benlloch, Gert De Meerleer, Michael B. Cook, Zan Sun, Harry Ostrer, Pascal Blanchet, Lynne R. Wilkens, Ali Amin Al Olama, Sue A. Ingles, Markus Aly, Jay H. Fowke, Agnieszka Michael, Yves Akoli Koudou, Victoria L. Stevens, Kathryn L. Penney, Ana Vega, Xin Sheng, Ron H.N. van Schaik, Zsofia Kote-Jarai, Kim De Ruyck, Christopher A. Haiman, Atushi Takahashi, Florence Menegaux, Judith A. Clements, Stephen K. Van Den Eeden, Brian D. Carter, Wayne D. Tilley, Antonio Finelli, Jennifer J. Hu, Hermann Brenner, Thomas Van den Broeck, Shan Chao Zhao, Azad Hassan Abdul Razack, Edward D. Yeboah, Sonja I. Berndt, Barbara Nemesure, Mark N. Brook, David V. Conti, Katarina Cuk, Teuvo L.J. Tammela, Ali Sahimi, Stephen J. Chanock, Loic Le Marchand, Gemma Castaño-Vinyals, Sune F. Nielsen, Sara S. Strom, Ann W. Hsing, Roberta McKean-Cowdin, David J. Hunter, Ian M. Thompson, Børge G. Nordestgaard, Jyotsna Batra, Paula Paulo, Masashi Fujita, Jennifer Cullen, Susan M. Gapstur, Sarah L. Kerns, Lorelei A. Mucci, Neil G. Burnet, Xueying Mao, Hui Yi Lin, Rohit Varma, Marija Gamulin, Wei Zheng, Thomas A. Sellers, Adam S. Kibel, Robert J. Hamilton, Leire Moya, Ninghan Feng, Laura E. Beane Freeman, James E. Mensah, Catherine M. Tangen, Shannon K. McDonnell, Matthew Parliament, Davor Lessel, Gail P. Risbridger, Mina Torres, Janet L. Stanford, Bettina F. Drake, Soo-Hwang Teo, Robert J. MacInnis, Stig E. Bojesen, Jeannette T. Bensen, William J. Blot, Stella Koutros, Robin J. Leach, Graham G. Giles, Piet Ost, Artitaya Lophatananon, Laura Fachal, Tomislav Kuliš, Peter Kraft, Monique J. Roobol, Elaine A. Ostrander, Niclas Håkansson, Anselm Hennis, Yukihide Momozawa, Anssi Auvinen, Koichi Matsuda, Steven Joniau, Lisa G. Horvath, Javier Llorca, Claire Aukim-Hastie, Bernd Holleczek, Daniel W. Lin, Gerald L. Andriole, John D. Carpten, Eli Marie Grindedal, Rosalind A. Eeles, Elio Riboli, Constance Turman, Martin Andreas Røder, Yong-Jie Lu, Tobias Nordström, Kai Uwe Saum, Esther M. John, Melinda C. Aldrich, Peter Iversen, Henrik Grönberg, John S. Witte, Andreia Brandão, Eric A. Klein, Olivier Cussenot, Barry S. Rosenstein, Stephen Watya, Jan Lubinski, Douglas F. Easton, Dana C. Crawford, Gyorgy Petrovics, Thomas J. Schnoeller, Richard M. Martin, Stephanie J. Weinstein, Jose Esteban Castelao, Suzanne K. Chambers, Tokhir Dadaev, Karina Dalsgaard Sørensen, Antonio Gómez-Caamaño, Lisa F. Newcomb, Csilla Sipeky, Lovise Maehle, Brandi Weaver, Susan L. Neuhausen, Christiane Maier, Alicja Wolk, Vanio Mitev, Thérèse Truong, Manuel Luedeke, Jenny L Donovan, Mariana C. Stern, Catharine M L West, Manuela Gago-Dominguez, Elizabeth T. H. Fontham, William B. Isaacs, David E. Neal, Christopher J. Logothetis, Alisha Chou, Jasmine Lim, Benjamin A. Rybicki, Kay-Tee Khaw, Meir J. Stampfer, Chad D. Huff, Thomas J. Hoffmann, Michael Borre, Freddie C. Hamdy, Nawaid Usmani, Cezary Cybulski, Craig C. Teerlink, Milan S. Geybels, Nora Pashayan, Timothy J. Key, Phyllis J. Goodman, Hardev Pandha, Ruth C. Travis, Yudong Wu, Dominika Wokołorczyk, Lilit C. Moss, University of Southern California (USC), Keck School of Medicine [Los Angeles], CHU Tenon [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, Institut de recherche en santé, environnement et travail (Irset), Université d'Angers (UA)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), CHU Pointe-à-Pitre/Abymes [Guadeloupe], The institute of cancer research [London], U01CA194393, National Institutes of Health, NA, Achievement Rewards for College Scientists Foundation, Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )-Institut National de la Santé et de la Recherche Médicale (INSERM)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Université d'Angers (UA), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Université d'Angers (UA)-Université de Rennes (UR)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Urology, Clinical Chemistry, Darst, Burcu F [0000-0002-6205-4632], Chou, Alisha [0000-0001-7521-6373], Schumacher, Fredrick R [0000-0002-3073-7463], Dadaev, Tokhir [0000-0002-8268-0438], Brook, Mark N [0000-0002-8969-2378], Hoffmann, Thomas J [0000-0001-6893-4449], Takahashi, Atushi [0000-0001-7099-8767], Matsuda, Koichi [0000-0001-7292-2686], Fujita, Masashi [0000-0002-1457-6233], Muir, Kenneth [0000-0001-6429-988X], Stevens, Victoria L [0000-0003-0259-4407], Schleutker, Johanna [0000-0002-1863-0305], Sipeky, Csilla [0000-0002-8853-4722], Auvinen, Anssi [0000-0003-1125-4818], Giles, Graham G [0000-0003-4946-9099], Martin, Richard M [0000-0002-7992-7719], Nordestgaard, Børge G [0000-0002-1954-7220], Bojesen, Stig E [0000-0002-4061-4133], Røder, Martin Andreas [0000-0002-0019-5333], Batra, Jyotsna [0000-0003-4646-6247], Tilley, Wayne [0000-0003-1893-2626], Risbridger, Gail P [0000-0003-3089-4028], Gronberg, Henrik [0000-0002-1073-2753], Eklund, Martin [0000-0001-5032-5266], Nordström, Tobias [0000-0003-4915-7546], Pashayan, Nora [0000-0003-0843-2468], Dunning, Alison M [0000-0001-6651-7166], Travis, Ruth C [0000-0002-9571-0763], Riboli, Elio [0000-0001-6795-6080], Park, Jong Y [0000-0002-6384-6447], Weinstein, Stephanie J [0000-0002-3834-1535], Kraft, Peter [0000-0002-4472-8103], Ostrander, Elaine A [0000-0001-6075-9738], Wolk, Alicja [0000-0001-7387-6845], Håkansson, Niclas [0000-0001-7673-5554], Machiela, Mitchell J [0000-0001-6538-9705], Sørensen, Karina Dalsgaard [0000-0002-4902-5490], Zheng, Wei [0000-0003-1226-070X], Mensah, James E [0000-0003-4133-1722], Lu, Yong-Jie [0000-0001-6174-6621], West, Catharine ML [0000-0002-0839-3449], Cancel-Tassin, Géraldine [0000-0002-9583-6382], Truong, Thérèse [0000-0002-2943-6786], Vega, Ana [0000-0002-7416-5137], Gómez-Caamaño, Antonio [0000-0002-9773-4590], Fachal, Laura [0000-0002-7256-9752], Kerns, Sarah L [0000-0002-6503-0011], Ostrer, Harry [0000-0002-2209-5376], Teixeira, Manuel R [0000-0002-4896-5982], Brandão, Andreia [0000-0003-0938-1543], Cannon-Albright, Lisa [0000-0003-2602-3668], Multigner, Luc [0000-0003-3205-8568], Klein, Eric A [0000-0002-1783-0698], Murphy, Adam B [0000-0001-9977-3473], Michael, Agnieszka [0000-0002-7262-6227], Ost, Piet [0000-0002-2203-4848], Xu, Jianfeng [0000-0002-1343-8752], Teo, Soo-Hwang [0000-0002-0444-590X], Lessel, Davor [0000-0003-4496-244X], Kulis, Tomislav [0000-0002-0895-5691], Joniau, Steven [0000-0003-3195-9890], Bush, William S [0000-0002-9729-6519], Crawford, Dana C [0000-0002-6437-6248], Roobol, Monique J [0000-0001-6967-1708], Jenster, Guido [0000-0002-8658-2552], Van Den Eeden, Stephen K [0000-0002-5599-8387], Easton, Douglas F [0000-0003-2444-3247], Chanock, Stephen J [0000-0002-2324-3393], Wiklund, Fredrik [0000-0002-4623-0544], Eeles, Rosalind A [0000-0002-3698-6241], Haiman, Christopher A [0000-0002-0097-9971], and Apollo - University of Cambridge Repository

Subjects
Male, 8Q24, Genome-wide association study, Continental Population Groups/genetics, VARIANTS, Prostate cancer, 0302 clinical medicine, Risk Factors, Epidemiology, IMPUTATION, Odds Ratio, Prostatic Neoplasms/diagnosis, 0303 health sciences, education.field_of_study, Continental Population Groups, Manchester Cancer Research Centre, Middle Aged, Càncer--Aspectes genètics, 3. Good health, ODDS RATIOS, 06 Biological Sciences, 11 Medical and Health Sciences, medicine.medical_specialty, Population, Biology, prostate cancer, meta-analysis, SEQUENCE, Article, 03 medical and health sciences, Breast cancer, SDG 3 - Good Health and Well-being, Genetics, medicine, BREAST-CANCER, Humans, Genetic Predisposition to Disease, Neoplasm Invasiveness, education, 030304 developmental biology, Genetic association, [SDV.GEN]Life Sciences [q-bio]/Genetics, MUTATIONS, ResearchInstitutes_Networks_Beacons/mcrc, Racial Groups, Prostatic Neoplasms, Molecular Sequence Annotation, Odds ratio, medicine.disease, BRCA2, Pròstata--Càncer, Genetic Loci, 030217 neurology & neurosurgery, Imputation (genetics), Genètica, Demography, Developmental Biology, Genome-Wide Association Study
Abstract

International audience; Prostate cancer is a highly heritable disease with large disparities in incidence rates across ancestry populations. We conducted a multiancestry meta-analysis of prostate cancer genome-wide association studies (107,247 cases and 127,006 controls) and identified 86 new genetic risk variants independently associated with prostate cancer risk, bringing the total to 269 known risk variants. The top genetic risk score (GRS) decile was associated with odds ratios that ranged from 5.06 (95% confidence interval (CI), 4.84-5.29) for men of European ancestry to 3.74 (95% CI, 3.36-4.17) for men of African ancestry. Men of African ancestry were estimated to have a mean GRS that was 2.18-times higher (95% CI, 2.14-2.22), and men of East Asian ancestry 0.73-times lower (95% CI, 0.71-0.76), than men of European ancestry. These findings support the role of germline variation contributing to population differences in prostate cancer risk, with the GRS offering an approach for personalized risk prediction.

Published
2021

13. Discovery and fine-mapping of height loci via high-density imputation of GWASs in individuals of African ancestry

Author

Mariaelisa Graff, Zhaoming Wang, David R. Weir, Ann W. Hsing, Joel N. Hirschhorn, Rebecca S. Fine, Wei Zheng, William Maixner, Adebowale Adeyemo, Rick A. Kittles, Rebecca Rohde, Krista A. Zanetti, Elizabeth K. Speliotes, Keri L. Monda, Ingrid B. Borecki, Yaming Shao, Suhn K. Rhie, Sanjay R. Patel, Richard S. Cooper, Jerome I. Rotter, Michael J. Thun, William J. Blot, Brendan J. Keating, Michèle M. Sale, Scott M. Williams, Yingchang Lu, Margaret A. Tucker, Eric A. Klein, Uma Nayak, Curtis A. Pettaway, Yii-Der Ida Chen, Sailaja Vedantam, Pamela J. Schreiner, Phyllis J. Goodman, Babatunde L. Salako, Christine Neslund-Dudas, Andrew B. Singleton, Michael F. Press, Neil E. Caporaso, Maureen Sanderson, Diane M. Becker, Michele K. Evans, Margaret R. Spitz, Christopher I. Amos, Susan Redline, Kurt Lohman, Ching-Ti Liu, Hampton L. Leonard, Kris Monroe, Sun J. Kang, David Van Den Berg, Janet L. Stanford, Lewis H. Kuller, Traci M. Bartz, J. M. Zmuda, Christopher S. Carlson, Ruth J. F. Loos, Joanne M. Jordan, Guillaume Lettre, Youfang Liu, Lara Sucheston, Mike A. Nalls, Shad B. Smith, Suzanne Kolb, Lisa B. Signorello, Daniel Shriner, Tamara B. Harris, Larry D. Atwood, Wei-Min Chen, Oladosu Ojengbede, Kristin A. Rand, Claudia Schurmann, Guanjie Chen, Sharon L.R. Kardia, Graham Casey, Lawrence F. Bielak, Dena G. Hernandez, Talin Haritunians, Rajiv Nadukuru, Elisa V. Bandera, Matthew A. Allison, Amidou N'Diaye, Donna K. Arnett, Olufunmilayo I. Olopade, Ellen W. Demerath, Babette S. Zemel, Margaret Wrensch, Myriam Fornage, John K. Wiencke, George J. Papanicolaou, Sara S. Strom, Temidayo O. Ogundiran, Gregory L. Burke, Erin B. Ware, Marian L. Neuhouser, James G. Wilson, Dhananjay Vaidya, Nicholette D. Palmer, Marguerite R. Irvin, JoAnn E. Manson, Benjamin A. Rybicki, Laurence N. Kolonel, Chad D. Huff, Jennifer J. Hu, Jennifer A. Brody, L. Keoki Williams, Leslie A. Lange, Qing Duan, David S. Siscovick, Yongmei Liu, Leslie Bernstein, Jennifer A. Smith, Latchezar Dimitrov, Sarah J. Nyante, Sue A. Ingles, Yu Han H. Hsu, Xifeng Wu, Heather M. Ochs-Balcom, Jingzhong Ding, David V. Conti, L. Adrienne Cupples, Gerry A. Coetzee, Thomas H. Mosley, Kristin L. Young, Donald W. Bowden, Edmond K. Kabagambe, Christine B. Ambrosone, Karen C. Johnson, Patricia A. Peyser, Stefan Ambs, Victoria L. Stevens, Minhui Chen, Carl D. Langefeld, Sonja I. Berndt, Andrew F. Olshan, Qiuyin Cai, Jessica D. Faul, Mary F. Feitosa, Brian E. Cade, Esther M. John, Ann G. Schwartz, Yan V. Sun, Xinruo Zhang, Stephen J. Chanock, Jason H. Moore, Alexander P. Reiner, Caroline S. Fox, Charles Kooperberg, Anne E. Justice, Jin Li, Lorna H. McNeill, Alex Stram, Jie Yao, Xiuqing Guo, Mara Z. Vitolins, Edward A. Ruiz-Narváez, Abdullah Kutlar, Charleston W. K. Chiang, Jing Hua Zhao, Lisa R. Yanek, Poorva Mudgal, John D. Carpten, Barbara V. Howard, Anselm Hennis, Charles N. Rotimi, Ulrich Broeckel, Albert M. Levin, Jonathan P. Bradfield, Curtis C. Harris, Regina G. Ziegler, Brian E. Henderson, Bruce M. Psaty, Adeyinka G. Falusi, Katherine L. Nathanson, Barbara McKnight, Melinda C. Aldrich, Herman A. Taylor, Melissa Garcia, Degui Zhi, Dezheng Huo, Barry I. Freedman, D. C. Rao, Sylvia Wassertheil-Smoller, Jie Zhou, Adam B. Murphy, Eric E. Schadt, Sandra L. Deming, John S. Witte, Julie R. Palmer, Neil A. Zakai, Adesola Ogunniyi, Yun Li, Mary Cushman, Victoria L. Buchanan, Jorge L. Rodriguez-Gil, Struan F.A. Grant, Timothy D. Howard, Omri Gottesman, Wei Zhao, Kira C. Taylor, Yan Meng, Hayrettin Okut, Hakon Hakonarson, Xiaofeng Zhu, Elizabeth M. Gillanders, Alan B. Zonderman, Lisa Chu, Badri Padhukasahasram, Vaneet Lotay, W. Ryan Diver, Mary K. Wojczynski, Simin Liu, Erwin P. Bottinger, Cameron D. Palmer, Alessandra Chesi, Elise Lim, Laura J. Rasmussen-Torvik, Eirini Marouli, Kari E. North, Salman M. Tajuddin, Christopher A. Haiman, Barbara Nemesure, Loic Le Marchand, Bamidele O. Tayo, and Maggie C.Y. Ng

Subjects
Male, 0303 health sciences, 030305 genetics & heredity, High density, Black People, Single-nucleotide polymorphism, Genome-wide association study, Biology, Polymorphism, Single Nucleotide, Body Height, Article, Minor allele frequency, Black or African American, Europe, 03 medical and health sciences, Evolutionary biology, Africa, Genetics, Humans, Female, Genotyping, Genetics (clinical), Imputation (genetics), 030304 developmental biology, Genome-Wide Association Study
Abstract

Although many loci have been associated with height in European ancestry populations, very few have been identified in African ancestry individuals. Furthermore, many of the known loci have yet to be generalized to and fine-mapped within a large-scale African ancestry sample. We performed sex-combined and sex-stratified meta-analyses in up to 52,764 individuals with height and genome-wide genotyping data from the African Ancestry Anthropometry Genetics Consortium (AAAGC). We additionally combined our African ancestry meta-analysis results with published European genome-wide association study (GWAS) data. In the African ancestry analyses, we identified three novel loci (SLC4A3, NCOA2, ECD/FAM149B1) in sex-combined results and two loci (CRB1, KLF6) in women only. In the African plus European sex-combined GWAS, we identified an additional three novel loci (RCCD1, G6PC3, CEP95) which were equally driven by AAAGC and European results. Among 39 genome-wide significant signals at known loci, conditioning index SNPs from European studies identified 20 secondary signals. Two of the 20 new secondary signals and none of the 8 novel loci had minor allele frequencies (MAF) < 5%. Of 802 known European height signals, 643 displayed directionally consistent associations with height, of which 205 were nominally significant (p < 0.05) in the African ancestry sex-combined sample. Furthermore, 148 of 241 loci contained ≤20 variants in the credible sets that jointly account for 99% of the posterior probability of driving the associations. In summary, trans-ethnic meta-analyses revealed novel signals and further improved fine-mapping of putative causal variants in loci shared between African and European ancestry populations.

Published
2020

14. A Mixed-Methods Study to Examine the Role of Psychosocial Stress and Air Pollution on Hypertension in Mexican-Origin Hispanics

Author

Melissa L. Bondy, Amal Rammah, Elaine Symanski, Wenyaw Chan, Kristina W. Whitworth, Inkyu Han, Maria Jimenez, and Sara S. Strom

Subjects
Adult, Male, medicine.medical_specialty, Health (social science), Sociology and Political Science, Air pollution, Pilot Projects, Logistic regression, Article, Psychosocial stress, Odds, Cohort Studies, 03 medical and health sciences, Young Adult, 0302 clinical medicine, Residence Characteristics, Risk Factors, Environmental health, Surveys and Questionnaires, Epidemiology, Mexican Americans, Prevalence, Medicine, Humans, 030212 general & internal medicine, Risk factor, 030505 public health, business.industry, Health Policy, Stressor, Public Health, Environmental and Occupational Health, Odds ratio, Middle Aged, Mexican-origin Hispanics, Texas, 3. Good health, Anthropology, Cohort, Hypertension, Female, 0305 other medical science, business, Psychosocial, Stress, Psychological
Abstract

Purpose Independent and combined effects of air pollution and psychosocial stressors on hypertension, a risk factor for cardiovascular disease, among Hispanics are not well studied. Methods We administered a pilot-tested questionnaire on individual- and neighborhood-level psychosocial stressors, developed with community input, to nearly 2500 individuals from the MD Anderson Cancer Center cohort of Mexican-Americans. We used data from local air quality monitors to estimate individual exposures to ozone (O3) and fine particulate matter (PM2.5) for the 12-month period preceding enrollment using inverse distance interpolation. We applied logistic regression models to examine relationships between exposures to psychosocial stressors and air pollution with prevalent hypertension and used stratified analyses to examine the interacting effects of these two exposures on hypertension. RESULTS: There was a positive association between prevalent hypertension and a high frequency of feeling anxious or depressed (prevalence odds ratio (POR) = 1.36, 95% CI [1.06-1.75]) and experiencing aches and pains (POR = 1.29, 95% CI [1.01-1.64]). The odds of having hypertension were also elevated among those worrying about their own health (POR = 1.65, 95% CI [1.30-2.06]) or about not having enough money (POR = 1.27, 95% CI [1.01-1.6]). We observed an inverse association between O3 and hypertension. There was no interaction between psychosocial stressors and O3 on hypertension. Conclusion Our findings add to the evidence of a positive association between individual and family stressors on hypertension among Hispanics and other racial/ethnic groups. Contrary to previous studies reporting positive associations, our results suggest that long-term exposure to O3 may be inversely related to prevalent hypertension.

Published
2018

15. A genome-wide association study of prostate cancer in Latinos

Author

Christopher A. Haiman, Stephen K. Van Den Eeden, Hannah Hopp, Zhaohui Du, Xin Sheng, Sue A. Ingles, Thomas J. Hoffmann, Esther M. John, Robin J. Leach, Sara S. Strom, John S. Witte, Brandi Weaver, Mariana C. Stern, David V. Conti, Ian M. Thompson, and Chad D. Huff

Subjects
Oncology, Male, Cancer Research, medicine.medical_specialty, Multifactorial Inheritance, Genotype, Latino men, Population, Genetic admixture, Locus (genetics), Genome-wide association study, urologic and male genital diseases, Polymorphism, Single Nucleotide, 03 medical and health sciences, Prostate cancer, 0302 clinical medicine, Internal medicine, medicine, Biomarkers, Tumor, Odds Ratio, Humans, GWAS, MSMB, Genetic Predisposition to Disease, education, Alleles, Genetic association, Aged, education.field_of_study, business.industry, Prostatic Neoplasms, Hispanic or Latino, Middle Aged, medicine.disease, prostate cancer, 3. Good health, admixture mapping, 030220 oncology & carcinogenesis, Personalized medicine, business, Cancer Epidemiology, Genome-Wide Association Study
Abstract

Latinos represent, What's new? There is strong evidence for a genetic predisposition to prostate cancer (PrCa). Most of this information has come from European ancestry populations, with Latinos representing less than 1% of samples in cancer genome‐wide association studies (GWAS). In this study, the majority of established PrCa risk variants (83.3%) were consistently associated with PrCa risk in Latinos. A polygenic risk score comprised of GWAS‐identified risk variants could identify 10% of Latino men with a ~three‐fold increase in PrCa risk. These findings suggest that common germline variants for PrCa can stratify risk in Latino men, which has implications for targeted screening and prevention.

Published
2019

16. Assessing the Optimum Use of Androgen-Deprivation Therapy in High-Risk Prostate Cancer Patients Undergoing External Beam Radiation Therapy

Author

Deborah A. Kuban, Jose-Miguel Yamal, Michelle Ludwig, David S. Lopez, Sara S. Strom, and Xianglin L. Du

Subjects
Oncology, medicine.medical_specialty, Health (social science), medicine.medical_treatment, External beam radiation, lcsh:Medicine, Lower risk, Androgen deprivation therapy, 03 medical and health sciences, Prostate cancer, 0302 clinical medicine, Internal medicine, Tumor stage, Medicine, 030212 general & internal medicine, Gynecology, business.industry, lcsh:R, Radiation dose, Public Health, Environmental and Occupational Health, Hormone replacement therapy (menopause), Articles, medicine.disease, 030220 oncology & carcinogenesis, Outcomes research, business
Abstract

The optimum use of androgen deprivation therapy (ADT) in high-risk prostate cancer patients has not been defined in the setting of dose-escalated external beam radiation therapy. A retrospective analysis of 1,290 patients with high-risk prostate cancer from June 1987 through March 2010 treated with external beam radiation therapy was performed. Median follow-up was 7.2 years, and 797 patients received ADT, with 384 patients experiencing a biochemical failure and 145 with distant metastasis. ADT was associated with lower risk of biochemical failure and distant metastasis than no ADT after adjusting for age, prostate-specific antigen (PSA), Gleason score, year of diagnosis, tumor stage, and radiation dose. ADT was associated with a greater reduction in biochemical failure in the low-dose radiation group than in the high-dose group. Patients with >24 months of ADT had a lower risk of PSA failures than those with 24 months of ADT in all patients who received ADT.

Published
2016

17. The Association of Smoking with English and Spanish Language Use as a Proxy of Acculturation Among Mexican-Americans

Author

Ellen R. Gritz, Irene Tamí-Maury, Sara S. Strom, Judy H. Hong, Carrie J. Aigner, Sarah E. Rush, and Alexander V. Prokhorov

Subjects
Adult, Male, medicine.medical_specialty, Alcohol Drinking, Epidemiology, First language, Mexican americans, Article, Proxy (climate), Cohort Studies, 03 medical and health sciences, Sex Factors, 0302 clinical medicine, Mexican Americans, Prevalence, Humans, Medicine, 030212 general & internal medicine, Language, 030505 public health, business.industry, Public health, Smoking, Public Health, Environmental and Occupational Health, Middle Aged, Texas, Acculturation, Constructed language, Socioeconomic Factors, Cohort, Female, 0305 other medical science, business, On Language, Social psychology, Demography
Abstract

To better characterize the relation of acculturation, based on language use, to smoking status among Mexican-Americans, a large study sample from an ongoing cohort of Mexican-American households in Texas was stratified into current smokers and non-smokers. Four language-use groups were created based on Low/High use of Spanish and English, representing different degrees of acculturation. Participants who reported high English but low Spanish use had the highest smoking prevalence (20.1 %), followed by High English/High Spanish (13.6 %), Low English/High Spanish (8.7 %), and Low English/Low Spanish (6.4 %). Current smokers were more likely to be male, have lower than high school education, currently consume alcohol or had consumed alcohol but quit, and report low Spanish/high English use. Consistent with recent models of acculturation, individuals can differ both in their maintenance of the native language and adoption of a new language and both dimensions are important in predicting tobacco use.

Published
2016

18. Family Cohesion and Moderate-to-Vigorous Physical Activity Among Mexican Origin Adolescents: A Longitudinal Perspective

Author

Laura M. Koehly, Abiodun O. Oluyomi, Larkin L. Strong, Vandita Rajesh, Anna V. Wilkinson, Sara S. Strom, and Galya Bigman

Subjects
Male, Adolescent, Ethnic group, Anxiety, Social Environment, Article, Developmental psychology, Mexican Americans, medicine, Humans, Orthopedics and Sports Medicine, Longitudinal Studies, Exercise, Family Characteristics, Sex Characteristics, Data Collection, Social environment, Health Status Disparities, Health equity, Cohort, Linear Models, Female, Family Relations, medicine.symptom, Psychology, Psychosocial, Demography, Social status, Sex characteristics
Abstract

Background:Existing racial/ethnic disparities in physical activity during childhood increase Hispanics’ risk of developing chronic diseases, which serves to increase health disparities. This study examined associations of family cohesion and conflict with self-reported moderate-tovigorous physical activity (MVPA), controlling for psychosocial covariates such as subjective social status, anxiety, and sensation-seeking.Methods:1000 Mexican origin adolescents reported their MVPA levels approximately 2 years apart. Psychosocial covariates, family cohesion and conflict were measured at the first assessment. Generalized Linear Models were used to prospectively examine the relationship between family cohesion and conflict and subsequent MVPA based on 711 participants who had low levels of baseline MVPA.Results:35% of boys and 24% of girls reported adequate MVPA levels at follow-up; girls were less likely to report adequate MVPA (RR = 0.76; 95% CI: 0.61–0.93) than boys. Overall, family cohesion was associated with MVPA (P = .01), but family cohesion was not (P = .41). Gender-based analyses revealed that adequate MVPA was associated with family cohesion (RR = 1.40; 95% CI: 1.03–1.88), sensation seeking (RR = 1.05; 95% CI: 1.00–1.10), and age (RR = 0.85; 95% CI: 0.74–0.98) among girls and with subjective social status (RR = 1.20; 95% CI: 1.08–1.33) among boys.Conclusions:The family social environment and gender differences should be addressed in health promotion programs targeting MVPA.

Published
2015

19. Comprehensive analysis of factors impacting risks and outcomes of therapy-related myeloid neoplasms following breast cancer treatment

Author

JM Reuben, Sara S. Strom, G. Garcia-Manero, Katarina Sevcikova, Hagop M. Kantarjian, L. J. Medeiros, Gabriel N. Hortobagyi, Ricardo H. Alvarez, Joseph D. Khoury, Zuo Zhuang, Constance Albarracin, Guiling Tang, and Michal Mego

Subjects
Adult, Oncology, Cancer Research, medicine.medical_specialty, Myeloid, Breast Neoplasms, 03 medical and health sciences, 0302 clinical medicine, Breast cancer, Internal medicine, Humans, Medicine, skin and connective tissue diseases, Aged, Proportional Hazards Models, Therapy related, business.industry, Hematopoietic Stem Cell Transplantation, Neoplasms, Second Primary, Hematology, Middle Aged, medicine.disease, Myelodysplastic-Myeloproliferative Diseases, Leukemia, Myeloid, Acute, medicine.anatomical_structure, Myelodysplastic Syndromes, 030220 oncology & carcinogenesis, Female, business, 030215 immunology
Abstract

Comprehensive analysis of factors impacting risks and outcomes of therapy-related myeloid neoplasms following breast cancer treatment

Published
2015

20. Relative survival in patients with chronic-phase chronic myeloid leukaemia in the tyrosine-kinase inhibitor era: analysis of patient data from six prospective clinical trials

Author

Naveen Pemmaraju, Marina Konopleva, Sherry Pierce, Koji Sasaki, Preetesh Jain, Susan O'Brien, Sara S. Strom, Naval Daver, Elias Jabbour, Farhad Ravandi, Hagop M. Kantarjian, Jorge E. Cortes, and Gautam Borthakur

Subjects
Adult, Male, medicine.medical_specialty, Adolescent, Population, Young Adult, Internal medicine, Humans, Medicine, Prospective Studies, Prospective cohort study, education, Protein Kinase Inhibitors, Survival rate, Aged, Aged, 80 and over, Clinical Trials as Topic, education.field_of_study, Univariate analysis, Relative survival, business.industry, Hematology, Middle Aged, 3. Good health, Surgery, Survival Rate, Transplantation, Nilotinib, Leukemia, Myeloid, Chronic-Phase, Female, business, Cohort study, medicine.drug
Abstract

Summary Background Tyrosine-kinase inhibitors improve overall survival in patients with chronic myeloid leukaemia in chronic phase (CML-CP). Survival compared with the general population by age, response, and type of tyrosine-kinase inhibitor is not known. With use of data from trials of tyrosine kinase inhibitors, we compared overall survival in patients with newly diagnosed CML-CP to that of general population. Methods In this cohort analysis, we included data from patients with CML-CP enrolled in six consecutive or parallel prospective clinical trials of tyrosine-kinase inhibitors at a single institution from July 30, 2000, to Sept 17, 2012. We analysed data for response and survival with the Kaplan-Meier method. For estimated overall survival in the general population, we obtained data from national vital statistics reports and matched to patients with CML-CP by age, sex, ethnicity, and year at diagnosis. We assessed numbers and causes of death within 1 year of beginning treatment by age group and by response to therapy. We then did univariate analysis and multivariate analysis to investigate factors associated with survival probability. Findings Our analysis included 483 patients, 271 received imatinib, 105 received nilotinib, and 107 received dasatinib. Most patients were younger than 65 years, and no patients were older than 85 years. Median follow-up was 99·4 months (IQR 44·9–121·6), by which time 53 (11%) patients had died. The most common causes of death were progression to advanced disease stage, including complications of stem-cell transplantation (17 [4%] patients), secondary malignancies (nine [2%] patients), and cardiovascular causes (nine [2%] patients). 5-year overall survival in patients with CML-CP decreased in older age categories. For the whole population of patients with CML-CP, 5-year survival was only slightly lower than that of the matched general population (relative survival 94·7% [95% 92·1–97·4]). Individuals of all ages with a report of complete cytogenetic response to treatment or deeper within 1 year had a 5-year survival similar to that of the general population. Interpretation In the era of treatment with tyrosine-kinase inhibitors, patients diagnosed with CML-CP can expect a 5-year survival that is only slightly lower than that of the general population. With access to tyrosine-kinase inhibitors, most patients with chronic myeloid leukaemia could enjoy a near normal life expectancy. Funding MD Anderson Cancer Center, National Cancer Institute.

Published
2015

21. Racial and Ethnic Differences in the Association of Metabolic Syndrome with Prostate-Specific Antigen Levels in U.S. Men: NHANES 2001–2006

Author

David S. Lopez, Shailesh Advani, Konstantinos K. Tsilidis, Mike Hernandez, Elaine Symanski, Sara S. Strom, Arup Sinha, and Steven Canfield

Subjects
Gerontology, National Health and Nutrition Examination Survey, business.industry, Urology, Ethnic group, General Medicine, medicine.disease, World health, Prostate-specific antigen, Race (biology), Medicine, Who criteria, Metabolic syndrome, business, National Cholesterol Education Program, Demography
Abstract

Background: The interplay between metabolic syndrome (MetS) and race/ethnicity on prostate specific antigen (PSA) still remains unclear. The three major definitions of MetS (National Cholesterol Education Program [ATP III], International Diabetes Federation [IDF], and World Health Organization [WHO]) differ in number and type of components, which are linked to race/ethnicity. We proposed to investigate the associations of three major definitions of metabolic syndrome with PSA levels, and to determine whether these associations vary by race and ethnicity. Methods: We used measurements of serum PSA levels (ng/mL) in 3528 adult men >40 years from the National Health and Nutrition Examination Survey 2001–2006. MetS was defined using ATP III, IDF, and WHO criteria. Racial/ethnic groups included non-Hispanic blacks (NHBs), non-Hispanic whites (NHWs), and Mexican Americans (MAs). We computed geometric mean PSA levels from weighted multiple linear regression models. Results: Men classified with MetS-ATP ...

Published
2014

22. Two Novel Susceptibility Loci for Prostate Cancer in Men of African Ancestry

Author

Loreall Pooler, Pascal Blanchet, Sue A. Ingles, Jong Y. Park, William S. Bush, Laurent Brureau, Andrew A. Adjei, Susan Gundell, James L. Mohler, Peter E. Clark, Xin Sheng, Jack A. Taylor, David V. Conti, Fredrick R. Schumacher, Yao Tettey, Dennis J. Hazelett, Rosalind A. Eeles, Shiv Srivastava, Shelley Niwa, Stephen Watya, Zhaoming Wang, Kan Wang, Mariana C. Stern, Victoria L. Stevens, Jennifer Cullen, Graham Casey, Rick A. Kittles, Robin J. Leach, Sonja I. Berndt, Lucy Xia, Alex Stram, Adam S. Kibel, Eric A. Klein, Daniel O. Stram, Dana C. Crawford, Zsofia-Kote Jarai, Anselm Hennis, Stephen J. Chanock, Ian M. Thompson, Marie-Élise Parent, Jianfeng Xu, Practical, Douglas F. Easton, Kosj Yamoah, Koveela Govindasami, Melinda C. Aldrich, John S. Witte, Anand P. Chokkalingam, Sara S. Strom, Christine Neslund-Dudas, Adam B. Murphy, Janet L. Stanford, Brian E. Henderson, Benjamin A. Rybicki, John D. Carpten, Chad D. Huff, Esther M. John, Peggy Wan, Geraldine Cancel-Tassin, Michael B. Cook, Olivier Cussenot, Christopher A. Haiman, Florence Menegaux, Gyorgy Petrovics, Barbara Nemesure, Elizabeth T. H. Fontham, William B. Isaacs, Edward D. Yeboah, Thomas J. Hoffmann, Alexander Lubwama, Ying Han, Ann Truelove, Stephen K. Van Den Eeden, Evelyn Tay, Ann W. Hsing, Susan M. Gapstur, Wei Zheng, Thomas A. Sellers, Bettina F. Drake, Jeannette T. Bensen, William J. Blot, David Van Den Berg, Maureen Sanderson, Luc Multigner, Richard B. Biritwum, Jennifer J. Hu, Jay H. Fowke, Phyllis J. Goodman, and Gary J. Smith

Subjects
0301 basic medicine, Oncology, Male, Cancer Research, Aging, Chromosomes, Human, Pair 22, Genome-wide association study, Prostate cancer, 0302 clinical medicine, Gene Frequency, Medicine, 2.1 Biological and endogenous factors, Pair 13, Aetiology, African Continental Ancestry Group, Cancer, education.field_of_study, Prostate Cancer, Single Nucleotide, Blacks, 3. Good health, 030220 oncology & carcinogenesis, Human, Biotechnology, Urologic Diseases, medicine.medical_specialty, Population, Oncology and Carcinogenesis, Black People, Brief Communication, Polymorphism, Single Nucleotide, Chromosomes, 03 medical and health sciences, Clinical Research, Internal medicine, Genetics, Humans, Genetic Predisposition to Disease, Oncology & Carcinogenesis, Allele, Polymorphism, education, Allele frequency, Chromosomes, Human, Pair 13, business.industry, Prevention, Human Genome, Case-control study, Prostatic Neoplasms, Odds ratio, medicine.disease, Confidence interval, PRACTICAL/ELLIPSE Consortium, Checkpoint Kinase 2, 030104 developmental biology, Genetic Loci, Case-Control Studies, Insulin Receptor Substrate Proteins, Pair 22, business, Genome-Wide Association Study
Abstract

Prostate cancer incidence is 1.6-fold higher in African Americans than in other populations. The risk factors that drive this disparity are unknown and potentially consist of social, environmental, and genetic influences. To investigate the genetic basis of prostate cancer in men of African ancestry, we performed a genome-wide association meta-analysis using two-sided statistical tests in 10 202 case subjects and 10 810 control subjects. We identified novel signals on chromosomes 13q34 and 22q12, with the risk-associated alleles found only in men of African ancestry (13q34: rs75823044, risk allele frequency = 2.2%, odds ratio [OR] = 1.55, 95% confidence interval [CI] = 1.37 to 1.76, P = 6.10 × 10−12; 22q12.1: rs78554043, risk allele frequency = 1.5%, OR = 1.62, 95% CI = 1.39 to 1.89, P = 7.50 × 10−10). At 13q34, the signal is located 5’ of the gene IRS2 and 3’ of a long noncoding RNA, while at 22q12 the candidate functional allele is a missense variant in the CHEK2 gene. These findings provide further support for the role of ancestry-specific germline variation in contributing to population differences in prostate cancer risk.

Published
2017

23. Low serum testosterone is associated with tumor aggressiveness and poor prognosis in prostate cancer

Author

Jeri Kim, Sara S. Strom, Timothy C. Thompson, Yonggang He, Huakang Tu, Xifeng Wu, John W. Davis, Elizabeth A. Wagar, Jian Gu, Qing H. Meng, and Christopher J. Logothetis

Subjects
Oncology, PCA3, Cancer Research, medicine.medical_specialty, Oncogene, business.industry, Proportional hazards model, medicine.drug_class, 030232 urology & nephrology, Cancer, Testosterone (patch), Articles, medicine.disease, Androgen, Molecular medicine, 3. Good health, 03 medical and health sciences, Prostate cancer, 0302 clinical medicine, 030220 oncology & carcinogenesis, Internal medicine, medicine, business
Abstract

Serum testosterone is a potential marker to distinguish between indolent and aggressive prostate cancer (PCa). The present study aimed to investigate whether low levels of total serum testosterone at diagnosis were associated with aggressive PCa and poor clinical outcomes. In total, 762 non-Hispanic Caucasian men with previously untreated PCa were recruited from The University of Texas MD Anderson Cancer Center (Houston, TX, USA). Patients were categorized into three groups based on their total serum testosterone levels according to clinical guidelines [low (350 ng/dl)]. PCa aggressiveness (low-, intermediate- or high-risk, or metastatic) was compared using multinomial logistic regression. Rates of disease progression, mortality from any cause and PCa-specific mortality were compared using the multivariate Cox proportional hazards model. Testosterone levels significantly decreased as PCa aggressiveness increased (P

Published
2017

24. Leveraging population admixture to characterize the heritability of complex traits

Author

Noah Zaitlen, John S. Witte, Nora Franceschini, Benjamin A. Rybicki, Themistocles L. Assimes, Sonja I. Berndt, Alexander Gusev, Sue A. Ingles, Eric A. Whitsel, Stephen J. Chanock, Victoria L. Stevens, Charles Kooperberg, David Reich, Alkes L. Price, William B. Isaacs, Alexander P. Reiner, Jianqi Zhang, William J. Blot, Janet L. Stanford, Hua Tang, Phyllis G Goodman, Ann W. Hsing, Rick A. Kittles, Christopher A. Haiman, Gaurav Bhatia, James G. Wilson, Jianfeng Xu, Bjarni J. Vilhjálmsson, Sriram Sankararaman, Nick Patterson, Jing He, Barbara Nemesure, Arti Tandon, Eric A. Klein, Taylor Young, Sara S. Strom, Bogdan Pasaniuc, Leslie A. Lange, Samuela Pollack, Daniel O. Stram, and Anselm Hennis

Subjects
Male, Multifactorial Inheritance, Population genetics, Genome-wide association study, Medical and Health Sciences, Body Mass Index, Cohort Studies, 0302 clinical medicine, Models, Missing heritability problem, African Continental Ancestry Group, African Americans, Genetics, 0303 health sciences, education.field_of_study, Chromosome Mapping, Single Nucleotide, Statistical, Biological Sciences, Middle Aged, Phenotype, Cardiovascular Diseases, Female, Genotype, Population, Black People, Single-nucleotide polymorphism, Quantitative trait locus, Biology, Polymorphism, Single Nucleotide, Article, Quantitative Trait, 03 medical and health sciences, Quantitative Trait, Heritable, Genetic, Humans, Computer Simulation, Polymorphism, education, Heritable, Aged, 030304 developmental biology, Models, Statistical, Models, Genetic, Prostatic Neoplasms, Reproducibility of Results, Epistasis, Genetic, Heritability, United States, Black or African American, Genetics, Population, Case-Control Studies, Epistasis, 030217 neurology & neurosurgery, Developmental Biology, Genome-Wide Association Study
Abstract

Despite recent progress on estimating the heritability explained by genotyped SNPs (h(2)g), a large gap between h(2)g and estimates of total narrow-sense heritability (h(2)) remains. Explanations for this gap include rare variants or upward bias in family-based estimates of h(2) due to shared environment or epistasis. We estimate h(2) from unrelated individuals in admixed populations by first estimating the heritability explained by local ancestry (h(2)γ). We show that h(2)γ = 2FSTCθ(1 - θ)h(2), where FSTC measures frequency differences between populations at causal loci and θ is the genome-wide ancestry proportion. Our approach is not susceptible to biases caused by epistasis or shared environment. We applied this approach to the analysis of 13 phenotypes in 21,497 African-American individuals from 3 cohorts. For height and body mass index (BMI), we obtained h(2) estimates of 0.55 ± 0.09 and 0.23 ± 0.06, respectively, which are larger than estimates of h(2)g in these and other data but smaller than family-based estimates of h(2).

Published
2014

25. Genome-wide Scan of 29,141 African Americans Finds No Evidence of Directional Selection since Admixture

Author

Michael F. Press, Sarah J. Nyante, Xifeng Wu, Phillip L. De Jager, W. Ryan Diver, Christopher A. Haiman, Leslie Bernstein, Emma K. Larkin, Melinda C. Aldrich, John S. Witte, Regina G. Ziegler, Christopher I. Amos, Benjamin A. Rybicki, Margaret R. Spitz, Sonja I. Berndt, Alkes L. Price, William J. Blot, Sara S. Strom, William B. Isaacs, Stephen J. Chanock, Gaurav Bhatia, Nick Patterson, Graham Casey, Jorge L. Rodriguez-Gil, David Reich, Esther M. John, Ann G. Schwartz, Margaret A. Tucker, Krista A. Zanetti, Cathryn H. Bock, Susan M. Gapstur, Sue A. Ingles, Yuko Yamamura, Christine Neslund-Dudas, Curtis C. Harris, Christine B. Ambrosone, Elizabeth M. Gillanders, Brian E. Henderson, Lisa B. Signorello, Wei Zheng, Arti Tandon, Neil E. Caporaso, Rick A. Kittles, Adam B. Murphy, John K. Wiencke, Elisa V. Bandera, Lorna H. McNeill, Sandra L. Deming, and Robert C. Millikan

Subjects
Black People, Biology, Polymorphism, Single Nucleotide, Genome, White People, Evolution, Molecular, 03 medical and health sciences, 0302 clinical medicine, Gene Frequency, Report, Genetics, Chromosomes, Human, Humans, Genetics(clinical), Selection, Genetic, Allele frequency, Genetics (clinical), Selection (genetic algorithm), 030304 developmental biology, 0303 health sciences, Genome, Human, Directional selection, 1. No poverty, Large sample, Genetics, Population, Haplotypes, Evolutionary biology, 030217 neurology & neurosurgery, Genome-Wide Association Study
Abstract

The extent of recent selection in admixed populations is currently an unresolved question. We scanned the genomes of 29,141 African Americans and failed to find any genome-wide-significant deviations in local ancestry, indicating no evidence of selection influencing ancestry after admixture. A recent analysis of data from 1,890 African Americans reported that there was evidence of selection in African Americans after their ancestors left Africa, both before and after admixture. Selection after admixture was reported on the basis of deviations in local ancestry, and selection before admixture was reported on the basis of allele-frequency differences between African Americans and African populations. The local-ancestry deviations reported by the previous study did not replicate in our very large sample, and we show that such deviations were expected purely by chance, given the number of hypotheses tested. We further show that the previous study’s conclusion of selection in African Americans before admixture is also subject to doubt. This is because the FST statistics they used were inflated and because true signals of unusual allele-frequency differences between African Americans and African populations would be best explained by selection that occurred in Africa prior to migration to the Americas.

Published
2014
Full Text
View/download PDF

26. Imputation and subset-based association analysis across different cancer types identifies multiple independent risk loci in the TERT-CLPTM1L region on chromosome 5p15.33

Author

Hidemi Ito, Stephen K. Van Den Eeden, Abdisamad M. Ibrahim, Ching C. Lau, Preetha Rajaraman, Gloria M. Petersen, Judith Hoffman-Bolton, Colin P.N. Dinney, Chang Hyun Kang, Melinda C. Aldrich, Mark P. Purdue, Xiao-Ou Shu, William J. Blot, Sanjay Shete, Alpa V. Patel, Charles Kooperberg, Paolo Vineis, David Van Den Berg, Chao A. Hsiung, Anthony J. Swerdlow, Qing Lan, Wu Chou Su, Afshan Siddiq, Ulrike Peters, Katia Scotlandi, Sara H. Olson, Kendra Schwartz, Kelly L. Bolton, Chancellor Hohensee, Josep Lloreta, Kevin B. Jacobs, Debra T. Silverman, Rudolf Kaaks, Wei Zheng, Steven Gallinger, Junwen Wang, Angela Carta, Massimo Serra, Petra H.M. Peeters, Victoria L. Stevens, Yasushi Yatabe, Geraldine Cancel-Tassin, Joshua N. Sampson, Young Tae Kim, Graham A. Colditz, Pan-Chyr Yang, Baosen Zhou, Fredrick R. Schumacher, Nicolas Wentzensen, Evelyn Tay, Claudia Maria Hattinger, Chen Wu, Pilar Amiano, Mattias Johansson, Maxwell P. Lee, Christian P. Kratz, Michael B. Cook, Mingfeng Zhang, Kay-Tee Khaw, Jian-Min Yuan, Anne Zeleniuch-Jacquotte, Jinping Jia, Roberto Tirabosco, Jing Ma, Neil E. Caporaso, Christopher A. Haiman, Bu Tian Ji, Adrienne M. Flanagan, Neyssa Marina, Eric J. Jacobs, Sophia S. Wang, Chong-Jen Yu, Edward Giovannucci, Margaret Wrensch, Robert L. Grubb, Bin Zhu, Daniel O. Stram, Manolis Kogevinas, Margaret R. Karagas, Mazda Jenab, Alison M. Mondul, Jun Xu, Preethi S. Raj, Anders Ahlbom, Christine D. Berg, Shelley Niwa, Kala Visvanathan, Loic Le Marchand, Jorge R. Toro, Robert N. Hoover, Heather Spencer Feigelson, Michelle Brotzman, Laurence N. Kolonel, Krista A. Zanetti, Chengfeng Wang, Mary Ann Butler, Ann Truelove, Irene L. Andrulis, Hongbing Shen, H. Dean Hosgood, Ming Shyan Huang, Gee-Chen Chang, Jianjun Liu, John K. Wiencke, Stephanie J. Weinstein, Beatrice Melin, Kouya Shiraishi, Zhihua Yin, Lee E. Moore, Börje Ljungberg, Jolanta Lissowska, Elizabeth M. Gillanders, M. T. Landi, Cari M. Kitahara, Maria Feychting, Kuan-Yu Chen, Matthias Simon, Brian M. Wolpin, Hemang Parikh, Hannah P. Yang, Graham G. Giles, Alison Johnson, Demetrius Albanes, Carlos González, Brian E. Henderson, Xifeng Wu, Harvey A. Risch, Amy Hutchinson, Christopher Hautman, Constance Chen, Zhibin Hu, Donghui Li, Elio Riboli, Julie E. Buring, Curtis C. Harris, Xu Che, Núria Malats, Roger Henriksson, Rosario Tumino, Joanne S. Colt, Alfredo Carrato, Paolo Boffetta, Maria Pik Wong, Hideo Tanaka, Federico Canzian, Alan D. L. Sihoe, Chien-Jen Chen, Kenneth Muir, Chen Ying, Qincheng He, Melissa C. Southey, Marc Sanson, Victoria K. Cortessis, Sharon A. Savage, Wei Hu, Yao Tettey, Daniela S. Gerhard, Sofia Pavanello, Guangwen Cao, H. Barton Grossman, Michael Goggins, Hideo Kunitoh, Peter D. Inskip, Seth P. Lerner, Peter Kraft, David Thomas, Peng Guan, Chung Hsing Chen, I. Shou Chang, Christoffer Johansen, Roberta McKean-Cowdin, Lee J. Helman, Yuh Min Chen, Ana Patiño-García, Pär Stattin, Xiaoping Miao, Tangchun Wu, Jay S. Wunder, Ann W. Hsing, Yu-Tang Gao, Brooke L. Fridley, Tania Carreón, Charles C. Chung, Nan Hu, Yoo Jin Jung, Richard B. Biritwum, Eric J. Duell, Philip R. Taylor, Satu Männistö, Kai Yu, Meredith Yeager, Xia Pu, Vittorio Krogh, Anand P. Chokkalingam, Susan M. Gapstur, W. Ryan Diver, Yuanqing Ye, Keitaro Matsuo, Cecilia Arici, You-Lin Qiao, Alan R. Schned, Dominique S. Michaud, Joanne W. Elena, Christopher Kim, Dongxin Lin, Yun-Chul Hong, Daru Lu, Reina García-Closas, Jonine D. Figueroa, Linda M. Liao, Yi-Long Wu, Heiner Boeing, Mark Lathrop, Göran Hallmans, Elizabeth A. Holly, Carol Giffen, Andrew A. Adjei, Consol Serra, Anne Tjønneland, Joseph F. Fraumeni, Alisa M. Goldstein, Ruth C. Travis, Rebecca Troisi, Dalsu Baris, Nalan Gokgoz, Olivier Cussenot, Xiang Deng, Yeul Hong Kim, Malin Sund, Sonja I. Berndt, E. David Crawford, Edward D. Yeboah, Sook Whan Sung, Françoise Clavel-Chapelon, Woon-Puay Koh, Nilgun Kurucu, Richard B. Hayes, Ashish M. Kamat, Beata Peplonska, Laurie Burdette, Ze Zhang Tang, Alan A. Arslan, Malcolm C. Pike, Sabina Sierri, J. Michael Gaziano, Lorna H. McNeil, Katherine A. McGlynn, Ulla Vogel, Logan G. Spector, H. Bas Bueno-de-Mesquita, Stephen J. Chanock, Jae Yong Park, Jennifer Prescott, Fernando Lecanda, Margaret A. Tucker, Ti Ding, Christian C. Abnet, Jenny Chang-Claude, Dimitrios Trichopoulos, Wei-Yen Lim, Wen Tan, Nick Orr, Jin Hee Kim, Stefano Porru, Chand Khanna, Robert R. McWilliams, Zhaoming Wang, Jeong Seon Ryu, David V. Conti, Alison P. Klein, Adonina Tardón, Robert J. Klein, Rebecca J. Rodabough, Mark H. Greene, Aruna Kamineni, Jie Lin, Rachael Z. Stolzenberg-Solomon, Patricia Hartge, Susan E. Hankinson, Young-Chul Kim, In Sam Kim, Luis Sierrasesúmaga, Roel Vermeulen, Paige M. Bracci, Mariana C. Stern, Louise A. Brinton, Myron D. Gross, Yong-Bing Xiang, Chih Yi Chen, G. A. Gerald Andriole, Paul S. Meltzer, Ying-Huang Tsai, Faith G. Davis, Ulrika Andersson, Paul Brennan, Sara Lindström, Chaoyu Wang, Giuseppe Mastrangelo, Laufey T. Amundadottir, Immaculata De Vivo, Bryan A. Bassig, Elisabete Weiderpass, Takashi Kohno, Nilanjan Chatterjee, Margaret R. Spitz, Pier Alberto Bertazzi, William Wheeler, David J. Hunter, Wei Tang, Qiuyin Cai, Naomi E. Allen, Molly Schwenn, Emily White, Min Shen, Adeline Seow, Laura E. Beane Freeman, James E. Mensah, Howard D. Sesso, Anna Luisa Di Stefano, Amanda Black, Manuela Gago-Dominguez, Christine B. Ambrosone, Avima M. Ruder, Martha S. Linet, Meir J. Stampfer, Robert C. Kurtz, Donald A. Barkauskas, Lisa W. Chu, Montserrat Garcia-Closas, Jason W. Hoskins, Melissa A. Austin, Kyoung Mu Lee, Jianxin Shi, Charles S. Fuchs, Nathaniel Rothman, Richard Gorlick, Piero Picci, Gianluca Severi, Ann G. Schwartz, Jian Gu, Christopher I. Amos, Marie-Christine Boutron-Ruault, Salvatore Panico, Alicja Wolk, Sara S. Strom, Lisa Mirabello, Jin-Hu Fan, Chin-Fu Hsiao, Neal D. Freedman, Geoffrey S. Tobias, Julie M. Gastier-Foster, Wang, Z, Zhu, B, Zhang, M, Parikh, H, Jia, J, Chung, Cc, Sampson, Jn, Hoskins, Jw, Hutchinson, A, Burdette, L, Ibrahim, A, Hautman, C, Raj, P, Abnet, Cc, Adjei, Aa, Ahlbom, A, Albanes, D, Allen, Ne, Ambrosone, Cb, Aldrich, M, Amiano, P, Amos, C, Andersson, U, Andriole G., Jr, Andrulis, Il, Arici, C, Arslan, Aa, Austin, Ma, Baris, D, Barkauskas, Da, Bassig, Ba, Beane Freeman, Le, Berg, Cd, Berndt, Si, Bertazzi, Pa, Biritwum, Rb, Black, A, Blot, W, Boeing, H, Boffetta, P, Bolton, K, Boutron Ruault, Mc, Bracci, Pm, Brennan, P, Brinton, La, Brotzman, M, Bueno de Mesquita, Hb, Buring, Je, Butler, Ma, Cai, Q, Cancel Tassin, G, Canzian, F, Cao, G, Caporaso, Ne, Carrato, A, Carreon, T, Carta, A, Chang, Gc, Chang, I, Chang Claude, J, Che, X, Chen, Cj, Chen, Cy, Chen, Ch, Chen, C, Chen, Ky, Chen, Ym, Chokkalingam, Ap, Chu, Lw, Clavel Chapelon, F, Colditz, Ga, Colt, J, Conti, D, Cook, Mb, Cortessis, Vk, Crawford, Ed, Cussenot, O, Davis, Fg, De Vivo, I, Deng, X, Ding, T, Dinney, Cp, Di Stefano, Al, Diver, Wr, Duell, Ej, Elena, Jw, Fan, Jh, Feigelson, H, Feychting, M, Figueroa, Jd, Flanagan, Am, Fraumeni JF, Jr, Freedman, Nd, Fridley, Bl, Fuchs, C, Gago Dominguez, M, Gallinger, S, Gao, Yt, Gapstur, Sm, Garcia Closas, M, Garcia Closas, R, Gastier Foster, Jm, Gaziano, Jm, Gerhard, D, Giffen, Ca, Giles, Gg, Gillanders, Em, Giovannucci, El, Goggins, M, Gokgoz, N, Goldstein, Am, Gonzalez, C, Gorlick, R, Greene, Mh, Gross, M, Grossman, Hb, Grubb R., 3rd, Gu, J, Guan, P, Haiman, Ca, Hallmans, G, Hankinson, Se, Harris, Cc, Hartge, P, Hattinger, C, Hayes, Rb, He, Q, Helman, L, Henderson, Be, Henriksson, R, Hoffman Bolton, J, Hohensee, C, Holly, Ea, Hong, Yc, Hoover, Rn, Hosgood HD, 3rd, Hsiao, Cf, Hsing, Aw, Hsiung, Ca, Hu, N, Hu, W, Hu, Z, Huang, M, Hunter, Dj, Inskip, Pd, Ito, H, Jacobs, Ej, Jacobs, Kb, Jenab, M, Ji, Bt, Johansen, C, Johansson, M, Johnson, A, Kaaks, R, Kamat, Am, Kamineni, A, Karagas, M, Khanna, C, Khaw, Kt, Kim, C, Kim, I, Kim, Yh, Kim, Yc, Kim, Yt, Kang, Ch, Jung, Yj, Kitahara, Cm, Klein, Ap, Klein, R, Kogevinas, M, Koh, Wp, Kohno, T, Kolonel, Ln, Kooperberg, C, Kratz, Cp, Krogh, V, Kunitoh, H, Kurtz, Rc, Kurucu, N, Lan, Q, Lathrop, M, Lau, Cc, Lecanda, F, Lee, Km, Lee, Mp, Le Marchand, L, Lerner, Sp, Li, D, Liao, Lm, Lim, Wy, Lin, D, Lin, J, Lindstrom, S, Linet, M, Lissowska, J, Liu, J, Ljungberg, B, Lloreta, J, Lu, D, Ma, J, Malats, N, Mannisto, S, Marina, N, Mastrangelo, G, Matsuo, K, Mcglynn, Ka, McKean Cowdin, R, Mcneill, Lh, Mcwilliams, Rr, Melin, B, Meltzer, P, Mensah, Je, Miao, X, Michaud, D, Mondul, Am, Moore, Le, Muir, K, Niwa, S, Olson, Sh, Orr, N, Panico, Salvatore, Park, Jy, Patel, Av, Patino Garcia, A, Pavanello, S, Peeters, Ph, Peplonska, B, Peters, U, Petersen, Gm, Picci, P, Pike, Mc, Porru, S, Prescott, J, Pu, X, Purdue, Mp, Qiao, Yl, Rajaraman, P, Riboli, E, Risch, Ha, Rodabough, Rj, Rothman, N, Ruder, Am, Ryu, J, Sanson, M, Schned, A, Schumacher, Fr, Schwartz, Ag, Schwartz, Kl, Schwenn, M, Scotlandi, K, Seow, A, Serra, C, Serra, M, Sesso, Hd, Severi, G, Shen, H, Shen, M, Shete, S, Shiraishi, K, Shu, Xo, Siddiq, A, Sierrasesumaga, L, Sierri, S, Loon Sihoe, Ad, Silverman, Dt, Simon, M, Southey, Mc, Spector, L, Spitz, M, Stampfer, M, Stattin, P, Stern, Mc, Stevens, Vl, Stolzenberg Solomon, Rz, Stram, Do, Strom, S, Su, Wc, Sund, M, Sung, Sw, Swerdlow, A, Tan, W, Tanaka, H, Tang, W, Tang, Zz, Tardon, A, Tay, E, Taylor, Pr, Tettey, Y, Thomas, Dm, Tirabosco, R, Tjonneland, A, Tobias, G, Toro, Jr, Travis, Rc, Trichopoulos, D, Troisi, R, Truelove, A, Tsai, Yh, Tucker, Ma, Tumino, R, Van Den Berg, D, Van Den Eeden, Sk, Vermeulen, R, Vineis, P, Visvanathan, K, Vogel, U, Wang, C, Wang, J, Wang, S, Weiderpass, E, Weinstein, Sj, Wentzensen, N, Wheeler, W, White, E, Wiencke, Jk, Wolk, A, Wolpin, Bm, Wong, Mp, Wrensch, M, Wu, C, Wu, T, Wu, X, Wu, Yl, Wunder, J, Xiang, Yb, Xu, J, Yang, Hp, Yang, Pc, Yatabe, Y, Ye, Y, Yeboah, Ed, Yin, Z, Ying, C, Yu, Cj, Yu, K, Yuan, Jm, Zanetti, Ka, Zeleniuch Jacquotte, A, Zheng, W, Zhou, B, Mirabello, L, Savage, Sa, Kraft, P, Chanock, Sj, Yeager, M, Landi, Mt, Shi, J, Chatterjee, N, Amundadottir, Lt, Wang, Z., Zhu, B., Zhang, M., Parikh, H., Jia, J., Chung, C.C., Sampson, J.N., Hoskins, J.W., Hutchinson, A., Burdette, L., Ibrahim, A., Hautman, C., Raj, P.S., Abnet, C.C., Adjei, A.A., Ahlbom, A., Albanes, D., Allen, N.E., Ambrosone, C.B., Aldrich, M., Amiano, P., Amos, C., Andersson, U., Gerald Andriole, G.A., Jr., Andrulis, I.L., Arici, C., Arslan, A.A., Austin, M.A., Baris, D., Barkauskas, D.A., Bassig, B.A., Freeman, L.E.B., Berg, C.D., Berndt, S.I., Bertazzi, P.A., Biritwum, R.B., Black, A., Blot, W., Boeing, H., Boffetta, P., Bolton, K., Boutron-Ruault, M.-C., Bracci, P.M., Brennan, P., Brinton, L.A., Brotzman, M., Bueno-de-Mesquita, H.B., Buring, J.E., Butler, M.A., Cai, Q., Cancel-Tassin, G., Canzian, F., Cao, G., Caporaso, N.E., Carrato, A., Carreon, T., Carta, A., Chang, G.-C., Chang, I.-S., Chang-Claude, J., Che, X., Chen, C.-J., Chen, C.-Y., Chen, C.-H., Chen, C., Chen, K.-Y., Chen, Y.-M., Chokkalingam, A.P., Chu, L.W., Clavel-Chapelon, F., Colditz, G.A., Colt, J.S., Conti, D., Cook, M.B., Cortessis, V.K., Crawford, E.D., Cussenot, O., Davis, F.G., De Vivo, I., Deng, X., Ding, T., Dinney, C.P., Di Stefano, A.L., Diver, W.R., Duell, E.J., Elena, J.W., Fan, J.-H., Feigelson, H.S., Feychting, M., Figueroa, J.D., Flanagan, A.M., Fraumeni, J.F., Jr., Freedman, N.D., Fridley, B.L., Fuchs, C.S., Gago-Dominguez, M., Gallinger, S., Gao, Y.-T., Gapstur, S.M., Garcia-Closas, M., Garcia-Closas, R., Gastier-Foster, J.M., Gaziano, J.M., Gerhard, D.S., Giffen, C.A., Giles, G.G., Gillanders, E.M., Giovannucci, E.L., Goggins, M., Gokgoz, N., Goldstein, A.M., Gonzalez, C., Gorlick, R., Greene, M.H., Gross, M., Grossman, H.B., Grubb, R., III and Gu, J., Guan, P., Haiman, C.A., Hallmans, G., Hankinson, S.E., Harris, C.C., Hartge, P., Hattinger, C., Hayes, R.B., He, Q., Helman, L., Henderson, B.E., Henriksson, R., Hoffman-Bolton, J., Hohensee, C., Holly, E.A., Hong, Y.-C., Hoover, R.N., Dean Hosgood, H., Hsiao, C.-F., Hsing, A.W., Hsiung, C.A., Hu, N., Hu, W., Hu, Z., Huang, M.-S., Hunter, D.J., Inskip, P.D., Ito, H., Jacobs, E.J., Jacobs, K.B., Jenab, M., Ji, B.-T., Johansen, C., Johansson, M., Johnson, A., Kaaks, R., Kamat, A.M., Kamineni, A., Karagas, M., Khanna, C., Khaw, K.-T., Kim, C., Kim, I.-S., Kim, J.H., Kim, Y.H., Kim, Y.-C., Kim, Y.T., Kang, C.H., Jung, Y.J., Kitahara, C.M., Klein, A.P., Klein, R., Kogevinas, M., Koh, W.-P., Kohno, T., Kolonel, L.N., Kooperberg, C., Kratz, C.P., Krogh, V., Kunitoh, H., Kurtz, R.C., Kurucu, N., Lan, Q., Lathrop, M., Lau, C.C., Lecanda, F., Lee, K.-M., Lee, M.P., Marchand, L.L., Lerner, S.P., Li, D., Liao, L.M., Lim, W.-Y., Lin, D., Lin, J., Lindstrom, S., Linet, M.S., Lissowska, J., Liu, J., Ljungberg, B., Lloreta, J., Lu, D., Ma, J., Malats, N., Mannisto, S., Marina, N., Mastrangelo, G., Matsuo, K., McGlynn, K.A., McKean-Cowdin, R., McNeil, L.H., McWilliams, R.R., Melin, B.S., Meltzer, P.S., Mensah, J.E., Miao, X., Michaud, D.S., Mondul, A.M., Moore, L.E., Muir, K., Niwa, S., Olson, S.H., Orr, N., Panico, S., Park, J.Y., Patel, A.V., Patino-Garcia, A., Pavanello, S., Peeters, P.H.M., Peplonska, B., Peters, U., Petersen, G.M., Picci, P., Pike, M.C., Porru, S., Prescott, J., Pu, X., Purdue, M.P., Qiao, Y.-L., Rajaraman, P., Riboli, E., Risch, H.A., Rodabough, R.J., Rothman, N., Ruder, A.M., Ryu, J.-S., Sanson, M., Schned, A., Schumacher, F.R., Schwartz, A.G., Schwartz, K.L., Schwenn, M., Scotlandi, K., Seow, A., Serra, C., Serra, M., Sesso, H.D., Severi, G., Shen, H., Shen, M., Shete, S., Shiraishi, K., Shu, X.-O., Siddiq, A., Sierrasesumaga, L., Sierri, S., Sihoe, A.D.L., Silverman, D.T., Simon, M., Southey, M.C., Spector, L., Spitz, M., Stampfer, M., Stattin, P., Stern, M.C., Stevens, V.L., Stolzenberg-Solomon, R.Z., Stram, D.O., Strom, S.S., Su, W.-C., Sund, M., Sung, S.W., Swerdlow, A., Tan, W., Tanaka, H., Tang, W., Tang, Z.-Z., Tardon, A., Tay, E., Taylor, P.R., Tettey, Y., Thomas, D.M., Tirabosco, R., Tjonneland, A., Tobias, G.S., Toro, J.R., Travis, R.C., Trichopoulos, D., Troisi, R., Truelove, A., Tsai, Y.-H., Tucker, M.A., Tumino, R., Van Den Berg, D., Van Den Eeden, S.K., Vermeulen, R., Vineis, P., Visvanathan, K., Vogel, U., Wang, C., Wang, J., Wang, S.S., Weiderpass, E., Weinstein, S.J., Wentzensen, N., Wheeler, W., White, E., Wiencke, J.K., Wolk, A., Wolpin, B.M., Wong, M.P., Wrensch, M., Wu, C., Wu, T., Wu, X., Wu, Y.-L., Wunder, J.S., Xiang, Y.-B., Xu, J., Yang, H.P., Yang, P.-C., Yatabe, Y., Ye, Y., Yeboah, E.D., Yin, Z., Ying, C., Yu, C.-J., Yu, K., Yuan, J.-M., Zanetti, K.A., Zeleniuch-Jacquotte, A., Zheng, W., Zhou, B., Mirabello, L., Savage, S.A., Kraft, P., Chanock, S.J., Yeager, M., Landi, M.T., Shi, J., Chatterjee, N., and Amundadottir, L.T.

Subjects
Male, SINGLE-NUCLEOTIDE POLYMORPHISM, Genome-wide association study, Epigenesis, Genetic, Gene Frequency, Molecular Biology, Genetics, Genetics (clinical), Neoplasms, Odds Ratio, Genome-wide association studies (GWAS), Telomerase, DNA METHYLATION Author Information, Association Studies Articles, General Medicine, PANCREATIC-CANCER, PROSTATE-CANCER, Neoplasm Proteins, POSTMENOPAUSAL BREAST-CANCER, TERT PROMOTER MUTATIONS, Gene Expression Regulation, Neoplastic, 2 SUSCEPTIBILITY LOCI, DNA methylation, Chromosomes, Human, Pair 5, Female, Risk, Locus (genetics), Single-nucleotide polymorphism, TERT and CLPTM1L gene, Biology, Polymorphism, Single Nucleotide, LUNG-CANCER, Humans, Genetic Predisposition to Disease, GENOME-WIDE ASSOCIATION, Allele, Gene, Allele frequency, Alleles, Genetic association, chromosome 5p15.33, Computational Biology, Membrane Proteins, DNA Methylation, Genetic Loci, TELOMERE LENGTH, Genome-Wide Association Study
Abstract

Genome-wide association studies (GWAS) have mapped risk alleles for at least 10 distinct cancers to a small region of 63 000 bp on chromosome 5p15.33. This region harbors the TERT and CLPTM1L genes; the former encodes the catalytic subunit of telomerase reverse transcriptase and the latter may play a role in apoptosis. To investigate further the genetic architecture of common susceptibility alleles in this region, we conducted an agnostic subset-based meta-analysis (association analysis based on subsets) across six distinct cancers in 34 248 cases and 45 036 controls. Based on sequential conditional analysis, we identified as many as six independent risk loci marked by common single-nucleotide polymorphisms: five in the TERT gene (Region 1: rs7726159, P = 2.10 x 10(-39); Region 3: rs2853677, P = 3.30 x 10(-36) and PConditional = 2.36 x 10(-8); Region 4: rs2736098, P = 3.87 x 10(-12) and PConditional = 5.19 x 10(-6), Region 5: rs13172201, P = 0.041 and PConditional = 2.04 x 10(-6); and Region 6: rs10069690, P = 7.49 x 10(-15) and PConditional = 5.35 x 10(-7)) and one in the neighboring CLPTM1L gene (Region 2: rs451360; P = 1.90 x 10(-18) and PConditional = 7.06 x 10(-16)). Between three and five cancers mapped to each independent locus with both risk-enhancing and protective effects. Allele-specific effects on DNA methylation were seen for a subset of risk loci, indicating that methylation and subsequent effects on gene expression may contribute to the biology of risk variants on 5p15.33. Our results provide strong support for extensive pleiotropy across this region of 5p15.33, to an extent not previously observed in other cancer susceptibility loci.

Published
2014

27. Generalizability of established prostate cancer risk variants in men of African ancestry

Author

Rosalind A. Eeles, Benjamin A. Rybicki, John S. Witte, W. Ryan Diver, Esther M. John, Lisa Chu, Sue A. Ingles, Eric A. Klein, Timothy R. Rebbeck, William J. Blot, John D. Carpten, Jong Y. Park, William B. Isaacs, Ying Han, Phyllis J. Goodman, Suh Yuh Wu, Janet L. Stanford, Brian E. Henderson, Sonja I. Berndt, S. Lilly Zheng, Christopher A. Haiman, Kristin A. Rand, Barbara Nemesure, Loic Le Marchand, Curtis A. Pettaway, Stephen J. Chanock, Ann W. Hsing, Graham Casey, Lisa B. Signorello, Susan M. Gapstur, Christine Neslund-Dudas, Suzanne Kolb, Adam B. Murphy, Rick A. Kittles, Douglas F. Easton, Jianfeng Xu, Sara S. Strom, M. Cristina Leske, Fredrick R. Schumacher, David V. Conti, Adam S. Kibel, Daniel O. Stram, and Anselm Hennis

Subjects
Genetics, Oncology, Cancer Research, medicine.medical_specialty, Case-control study, Genome-wide association study, Odds ratio, Biology, medicine.disease, Logistic regression, Prostate cancer, Internal medicine, medicine, Allele, Genetic association, Cohort study
Abstract

Genome-wide association studies have identified more than 80 risk variants for prostate cancer, mainly in European or Asian populations. The generalizability of these variants in other racial/ethnic populations needs to be understood before the loci can be used widely in risk modeling. In our study, we examined 82 previously reported risk variants in 4,853 prostate cancer cases and 4,678 controls of African ancestry. We performed association testing for each variant using logistic regression adjusted for age, study and global ancestry. Of the 82 known risk variants, 68 (83%) had effects that were directionally consistent in their association with prostate cancer risk and 30 (37%) were significantly associated with risk at p < 0.05, with the most statistically significant variants being rs116041037 (p = 3.7 × 10(-26) ) and rs6983561 (p = 1.1 × 10(-16) ) at 8q24, as well as rs7210100 (p = 5.4 × 10(-8) ) at 17q21. By exploring each locus in search of better markers, the number of variants that captured risk in men of African ancestry (p < 0.05) increased from 30 (37%) to 44 (54%). An aggregate score comprised of these 44 markers was strongly associated with prostate cancer risk [per-allele odds ratio (OR) = 1.12, p = 7.3 × 10(-98) ]. In summary, the consistent directions of effects for the vast majority of variants in men of African ancestry indicate common functional alleles that are shared across populations. Further exploration of these susceptibility loci is needed to identify the underlying biologically relevant variants to improve prostate cancer risk modeling in populations of African ancestry.

Published
2014

28. A meta-analysis of 87,040 individuals identifies 23 new susceptibility loci for prostate cancer

Author

Laurie Burdette, Rick A. Kittles, Hidewaki Nakagawa, Janet L. Stanford, Wojciech Kluźniak, Karen Park, Sofia Maia, Lisa A. Cannon-Albright, Douglas F. Easton, Dennis J. Hazelett, Hermann Brenner, Paula Paulo, Peter Klarskov, Zhaoming Wang, Koveela Govindasami, Loic Le Marchand, David V. Conti, Phyllis J. Goodman, Chavdar Slavov, Manuel R. Teixeira, Sara Lindström, Maren Weischer, Suzanne Kolb, Lisa B. Signorello, Jianfeng Xu, W. Ryan Diver, Barbara Nemesure, Fredrick R. Schumacher, Michael B. Cook, Qiyuan Li, William J. Blot, Jyotsna Batra, Malgorzata Tymrakiewicz, Anand P. Chokkalingam, Esther M. John, Christopher A. Haiman, Merideth Yeager, David E. Neal, John D. Carpten, Daniel Leongamornlert, Cezary Cybulski, Kathryn L. Penney, Sara Benlloch, Peter Iversen, Judith A. Clements, Shannon K. McDonnell, Matthew L. Freedman, Adam B. Murphy, Mahbubl Ahmed, Kenneth Muir, Sonja I. Berndt, Aida Karina Dieffenbach, Cristina Leske, William B. Isaacs, Chee Goh, Edward D. Yeboah, Jong Y. Park, Ruth C. Travis, Atsushi Takahashi, Nora Pashayan, Timothy J. Key, Evelyn Tay, Lorelei A. Mucci, Edward Giovannucci, Stephen N. Thibodeau, Fredrik Wiklund, Amanda B. Spurdle, Teuvo L.J. Tammela, Peter Kraft, Johanna Schleutker, Melissa C. Southey, Elio Riboli, Afshan Siddiq, Sara S. Strom, Hardev Pandha, Curtis A. Pettaway, Sue A. Ingles, Demetrius Albanes, Brian E. Henderson, Rosalind A. Eeles, Meir J. Stampfer, Markus Aly, Suh-Yuh Wu, Constance Chen, Sune F. Nielsen, Federico Canzian, Christa Stegmaier, Hui-Yi Lin, Amy K. Hutchinson, John S. Witte, Andrzej M. Kierzek, Elizabeth M. Gillanders, Vanio Mitev, Dominika Wokołorczyk, Ali Amin Al Olama, Richard B. Biritwum, Andrew A. Adjei, Ann Truelove, Daniel J. Schaid, Mitchell J. Machiela, Graham Casey, Børge G. Nordestgaard, Wei Zheng, Tokhir Dadaev, Thomas A. Sellers, Lucy Xia, Antonio Hurtado Coll, Tiina Wahlfors, Paul D.P. Pharoah, Jenny L Donovan, Victoria L. Stevens, Kristin A. Rand, Kai Yu, Alex Stram, Anssi Auvinen, Lisa Chu, Adam S. Kibel, Yao Tettey, Gerhard A. Coetzee, Martin Andreas Røder, Gianluca Severi, Daniel O. Stram, Anselm Hennis, Charles C. Chung, Jing Ma, Stephen J. Chanock, Katri A. Leinonen, Stephanie J. Weinstein, Jonathan Tyrer, Freddie C. Hamdy, Shelley Niwa, Kathleen Herkommer, Beatrice S. Knudsen, Laurence N. Kolonel, David J. Hunter, Christine Neslund-Dudas, Loreall Pooler, Robert N. Hoover, Antje E. Rinckleb, Jarmo Virtamo, Henrik Grönberg, Peggy Wan, Eric A. Klein, Michelle Guy, Manuel Luedeke, Radka Kaneva, Xin Sheng, Zsofia Kote-Jarai, Daniella Seminara, Tapio Visakorpi, Christiane Maier, Ann W. Hsing, Susan M. Gapstur, Sara Jugurnauth-Little, Ying Han, Ed Saunders, Agnieszka Michael, Alan W. Partin, Graham G. Giles, S. Lilly Zheng, Michiaki Kubo, Benjamin A. Rybicki, Kay-Tee Khaw, and Sarah K. Holt

Subjects
Male, Genotype, Single-nucleotide polymorphism, Genome-wide association study, Disease, Biology, ta3111, Polymorphism, Single Nucleotide, Risk Assessment, Article, Prostate cancer, Risk Factors, Genetics, medicine, Humans, Genetic Predisposition to Disease, Genetic association, ta113, ta112, ta1184, ta1182, Cancer, Prostatic Neoplasms, medicine.disease, ta3122, Genetic Loci, Meta-analysis, Genome-Wide Association Study
Abstract

Genome-wide association studies (GWAS) have identified 76 variants associated with prostate cancer risk predominantly in populations of European ancestry. To identify additional susceptibility loci for this common cancer, we conducted a meta-analysis of > 10 million SNPs in 43,303 prostate cancer cases and 43,737 controls from studies in populations of European, African, Japanese and Latino ancestry. Twenty-three new susceptibility loci were identified at association P < 5 × 10(-8); 15 variants were identified among men of European ancestry, 7 were identified in multi-ancestry analyses and 1 was associated with early-onset prostate cancer. These 23 variants, in combination with known prostate cancer risk variants, explain 33% of the familial risk for this disease in European-ancestry populations. These findings provide new regions for investigation into the pathogenesis of prostate cancer and demonstrate the usefulness of combining ancestrally diverse populations to discover risk loci for disease.

Published
2014

29. Dietary Intake of Vegetables, Fruits, and Meats/Beans as Potential Risk Factors of Acute Myeloid Leukemia: A Texas Case-Control Study

Author

Yuko Yamamura, Guillermo Garcia-Manero, Robert Edison Oum, Sara S. Strom, and Kplola Y. Elhor Gbito

Subjects
Adult, Male, Cancer Research, Meat, Adolescent, Medicine (miscellaneous), Young Adult, Risk Factors, Environmental health, Vegetables, Confidence Intervals, Odds Ratio, medicine, Humans, Food science, Young adult, Risk factor, Aged, Aged, 80 and over, Nutrition and Dietetics, business.industry, Case-control study, food and beverages, Fabaceae, Feeding Behavior, Odds ratio, Middle Aged, medicine.disease, Texas, Confidence interval, Diet, Leukemia, Myeloid, Acute, Leukemia, Logistic Models, Seafood, Oncology, Quartile, Case-Control Studies, Fruit, Multivariate Analysis, Red meat, Female, business
Abstract

Diet has been identified as a risk factor for some cancers, but its role in adult de novo acute myeloid leukemia (AML) is unclear. This study was conducted at the University of Texas MD Anderson Cancer Center to evaluate associations between consumption of vegetables, fruits, and meats with AML risk among Texas residents. All participants, 323 adult de novo AML cases and 380 frequency-matched controls, completed demographic and food frequency questionnaires. Overall, AML risk was significantly decreased among those who consumed the most dark green vegetables, seafood, and nuts/seeds; and it was significantly increased among greatest consumers of red meat. Among men, AML risk was lowest among those whose consumption was in the highest quartile for fruits [odds ratio (OR) = 0.25, 95% confidence interval (CI) = 0.10-0.69], poultry (OR = 0.28, 95%CI = 0.10-0.78), and seafood (OR = 0.39, 95%CI = 0.16-0.96) compared to those in the lowest. Among women, risk was lowest among those whose consumption was in the highest quartile of dark-green vegetables (OR = 0.28, 95%CI = 0.12-.68), orange vegetables (OR = 0.40, 95%CI = 0.17-.96) and nuts/beans (OR = 0.26, 95%CI = 0.11-0.60). Based on these findings, interventions can be developed to modify intake of specific dietary components to reduce cancer risk.

Published
2013

30. A meta-analysis identifies new loci associated with body mass index in individuals of African ancestry

Author

Mary Cushman, Shad B. Smith, Patricia A. Peyser, Jorge L. Rodriguez-Gil, Struan F.A. Grant, Regina G. Ziegler, Timothy D. Howard, Imran O. Morhason-Bello, Mariaelisa Graff, Christopher S. Carlson, Cameron D. Palmer, Charleston W. K. Chiang, Evandine Rampersaud, Lisa Chu, Uma Nayak, Curtis A. Pettaway, Ye Feng, Jing Hua Zhao, Barbara V. Howard, Joanne M. Jordan, Gregory L. Burke, Melinda C. Aldrich, Dezheng Huo, Omri Gottesman, Richard S. Cooper, Sonja I. Berndt, Donna K. Arnett, Gary S. Gilkeson, M. Cristina Leske, Ulrich Broeckel, Edmond K. Kabagambe, Stephen J. Chanock, Michael J. Thun, John S. Witte, William Maixner, Adebowale Adeyemo, Oladosu Ojengbede, Sarah J. Nyante, William J. Blot, Nicholette D. Palmer, Jyotika K. Fernandes, Laura J. Rasmussen-Torvik, Julie R. Palmer, Ida J. Spruill, Wei Zheng, Ruth J. F. Loos, Guo Li, Robert C. Millikan, Donald W. Bowden, Ellen W. Demerath, Michèle M. Sale, Neil A. Zakai, Zhaoming Wang, Fang Chen, George J. Papanicolaou, Gary K. Chen, Talin Haritunians, Rajiv Nadukuru, James J. Yang, Brian E. Henderson, Sandra Deming-Halverson, Adesola Ogunniyi, David Van Den Berg, Diane L. Kamen, Phyllis J. Goodman, Eric A. Klein, Yingchang Lu, Thomas W. Winkler, Marguerite R. Irvin, Badri Padhukasahasram, Benjamin A. Rybicki, Yan V. Sun, Yii-Der Ida Chen, Temidayo O. Ogundiran, Andrew B. Singleton, Babatunde L. Salako, Vaneet Lotay, Christine B. Ambrosone, Karen C. Johnson, Michael F. Press, Neil E. Caporaso, Guillaume Lettre, Ingrid B. Borecki, Sue A. Ingles, Yonglan Zheng, Jennifer J. Hu, Leslie Bernstein, Keri L. Monda, Kristine R. Monroe, L. Keoki Williams, Thomas H. Mosley, Shamika Ketkar, Ryan W. Driver, Margaret A. Tucker, Josyf C. Mychaleckyj, Ann W. Hsing, Xiuqing Guo, Lewis H. Kuller, Patricia M. Dubbert, Kelly J. Hunt, JoAnn E. Manson, Joel N. Hirschhorn, Mara Z. Vitolins, Tamara B. Harris, Matthew A. Allison, Abdullah Kutlar, Leslie A. Lange, Yongmei Liu, Ulrike Peters, Hakon Hakonarson, Mary K. Wojczynski, Xiaofeng Zhu, Edward A. Ruiz-Narváez, Todd L. Edwards, Heather M. Ochs-Balcom, Jingzhong Ding, Albert M. Levin, W. Timothy Garvey, Digna R. Velez Edwards, Sun J. Kang, Jie Zhou, Barry I. Freedman, Sanjay R. Patel, Suh Yuh Wu, Sylvia Wassertheil-Smoller, Simin Liu, Daniel Shriner, Elizabeth K. Speliotes, Larry D. Atwood, Graham Casey, Lisa R. Yanek, Susan Redline, Lisa B. Signorello, Wei Zhao, Scott M. Williams, Bamidele O. Tayo, Kira C. Taylor, Angela Britton, Xifeng Wu, Erwin P. Bottinger, Charles N. Rotimi, Mary F. Feitosa, Joseph M. Zmuda, Curtis C. Harris, Christine Neslund-Dudas, Bruce M. Psaty, Alexander P. Reiner, Helen N. Lyon, Youfang Liu, Krista A. Zanetti, Jonathan P. Bradfield, Esther M. John, Ann G. Schwartz, Elizabeth M. Gillanders, Mike A. Nalls, Suzanne Kolb, Cathryn H. Bock, Alan B. Zonderman, David Duggan, Gerhard A. Coetzee, Charles Kooperberg, Sharon L.R. Kardia, Olufunmilayo I. Olopade, Suhn K. Rhie, John D. Carpten, Maggie C.Y. Ng, Kari E. North, Christopher A. Haiman, Barbara Nemesure, Loic Le Marchand, Christopher I. Amos, Adeyinka Ademola, Lara Sucheston, Pamela J. Schreiner, Taylor Young, Sara S. Strom, Carl D. Langefeld, Jason H. Moore, Marian L. Neuhouser, Lawrence F. Bielak, Diane M. Becker, Margaret Wrensch, Janet L. Stanford, Laurence N. Kolonel, Yan A. Meng, Margaret R. Spitz, Brendan J. Keating, Kurt Lohman, Virginia J. Howard, Guanjie Chen, Elisa V. Bandera, Quiyin Cai, Amidou N'Diaye, Stefan Ambs, Adam B. Murphy, Eric E. Schadt, Anselm Hennis, Rick A. Kittles, Caroline S. Fox, John K. Wiencke, Katherine L. Nathanson, Barbara McKnight, Michele K. Evans, Wei-Min Chen, Dena G. Hernandez, Herman A. Taylor, David S. Siscovick, and Lorna H. McNeill

Subjects
Genetics, Single-nucleotide polymorphism, Genome-wide association study, Locus (genetics), Biology, Polymorphism, Single Nucleotide, FTO gene, Linkage Disequilibrium, Article, Body Mass Index, Black or African American, Gene Frequency, Genetic Loci, Case-Control Studies, Meta-analysis, Genetic variation, Humans, Genetic Predisposition to Disease, Obesity, Body mass index, Genome-Wide Association Study, Genetic association
Abstract

Genome-wide association studies (GWAS) have identified 36 loci associated with body mass index (BMI), predominantly in populations of European ancestry. We conducted a meta-analysis to examine the association of3.2 million SNPs with BMI in 39,144 men and women of African ancestry and followed up the most significant associations in an additional 32,268 individuals of African ancestry. We identified one new locus at 5q33 (GALNT10, rs7708584, P = 3.4 × 10(-11)) and another at 7p15 when we included data from the GIANT consortium (MIR148A-NFE2L3, rs10261878, P = 1.2 × 10(-10)). We also found suggestive evidence of an association at a third locus at 6q16 in the African-ancestry sample (KLHL32, rs974417, P = 6.9 × 10(-8)). Thirty-two of the 36 previously established BMI variants showed directionally consistent effect estimates in our GWAS (binomial P = 9.7 × 10(-7)), five of which reached genome-wide significance. These findings provide strong support for shared BMI loci across populations, as well as for the utility of studying ancestrally diverse populations.

Published
2013

31. Prostate Cancer Susceptibility in Men of African Ancestry at 8q24

Author

Fredrick R. Schumacher, Dennis J. Hazelett, Anslem J.M. Hennis, Suh Yuh Wu, Xin Sheng, David V. Conti, Dominique Quinque, Brian E. Henderson, Sara S. Strom, Sue A. Ingles, Yao Tettey, Richard B. Biritwum, Bogdan Pasaniuc, Graham Casey, Lisa B. Signorello, Edward D. Yeboah, Shelley Niwa, Anand P. Chokkalingam, Sonja I. Berndt, John D. Carpten, Michael G. Rosenfeld, Stephen J. Chanock, Phyllis J. Goodman, Ying Han, Wei Zheng, Alex Lubwama, M. Cristina Leske, Dimple Notani, Ann W. Hsing, Andrew A. Adjei, Susan M. Gapstur, William J. Blot, Janet L. Stanford, Stephen Watya, Evelyn Tay, Michael B. Cook, Loreall Pooler, Christopher A. Haiman, Victoria L. Stevens, Benjamin A. Rybicki, Lisa Chu, Barbara Nemesure, Ann Truelove, Nadin Rohland, Christine Neslund-Dudas, William B. Isaacs, John S. Witte, Alex Allen, Adam B. Murphy, Suzanne Kolb, Swapan Mallick, David Reich, Rick A. Kittles, Esther M. John, Jianfeng Xu, S. Lilly Zheng, Ranveer Singh Jayani, Gerhard A. Coetzee, Zhaoming Wang, Arti Tandon, Eric A. Klein, Kristin A. Rand, Daniel O. Stram, and Curtis A. Pettaway

Subjects
0301 basic medicine, Oncology, Male, Cancer Research, Aging, Prostate cancer, Prostate, 80 and over, 2.1 Biological and endogenous factors, Aetiology, Cancer, Aged, 80 and over, Prostate Cancer, PROSTATE CANCER SUSCEPTIBILITY, Single Nucleotide, Middle Aged, Control subjects, medicine.anatomical_structure, Pair 8, RNA, Long Noncoding, Long Noncoding, Chromosomes, Human, Pair 8, Human, Urologic Diseases, medicine.medical_specialty, Oncology and Carcinogenesis, Brief Communication, Polymorphism, Single Nucleotide, Chromosomes, 03 medical and health sciences, Clinical Research, Internal medicine, medicine, Genetics, Humans, Genetic Predisposition to Disease, Oncology & Carcinogenesis, Polymorphism, Aged, business.industry, Prevention, Human Genome, Case-control study, Prostatic Neoplasms, Odds ratio, medicine.disease, Confidence interval, United States, Black or African American, 030104 developmental biology, Case-Control Studies, Risk allele, RNA, business
Abstract

The 8q24 region harbors multiple risk variants for distinct cancers, including >8 for prostate cancer. In this study, we conducted fine mapping of the 8q24 risk region (127.8-128.8Mb) in search of novel associations with common and rare variation in 4853 prostate cancer case patients and 4678 control subjects of African ancestry. All statistical tests were two-sided. We identified three independent associations at P values of less than 5.00×10(-8), all of which were replicated in studies from Ghana and Uganda (combined sample = 5869 case patients, 5615 control subjects; rs114798100: risk allele frequency [RAF] = 0.04, per-allele odds ratio [OR] = 2.31, 95% confidence interval [CI] = 2.04 to 2.61, P = 2.38×10(-40); rs72725879: RAF = 0.33, OR = 1.37, 95% CI = 1.30 to 1.45, P = 3.04×10(-27); and rs111906932: RAF = 0.03, OR = 1.79, 95% CI = 1.53 to 2.08, P = 1.39×10(-13)). Risk variants rs114798100 and rs111906923 are only found in men of African ancestry, with rs111906923 representing a novel association signal. The three variants are located within or near a number of prostate cancer-associated long noncoding RNAs (lncRNAs), including PRNCR1, PCAT1, and PCAT2. These findings highlight ancestry-specific risk variation and implicate prostate-specific lncRNAs at the 8q24 prostate cancer susceptibility region.

Published
2016

32. Incidence and prognostic impact of other cancers in a population of long-term survivors of chronic lymphocytic leukemia

Author

Susan Lerner, X. Wang, A. Ferrajoli, Sara S. Strom, Candida Vitale, Michael J. Keating, William G. Wierda, K.Y. Elhor Gbito, and Lorenzo Falchi

Subjects
Oncology, Adult, Male, medicine.medical_specialty, Lung Neoplasms, Chronic lymphocytic leukemia, Population, Breast Neoplasms, 03 medical and health sciences, Prostate cancer, 0302 clinical medicine, Breast cancer, Cancer Survivors, immune system diseases, Risk Factors, Internal medicine, hemic and lymphatic diseases, medicine, Humans, Lung cancer, education, Aged, Gastrointestinal Neoplasms, Aged, 80 and over, education.field_of_study, business.industry, Cancer, Prostatic Neoplasms, Neoplasms, Second Primary, Hematology, Original Articles, Middle Aged, medicine.disease, Prognosis, Leukemia, Lymphocytic, Chronic, B-Cell, Leukemia, 030220 oncology & carcinogenesis, Female, Skin cancer, business, 030215 immunology, SEER Program
Abstract

BACKGROUND Information on the impact of other cancers (OCs) in long-term survivors (LTSs) of chronic lymphocytic leukemia (CLL) is limited. PATIENTS AND METHODS Patients with CLL who survived >10 years were defined as LTSs of CLL. We calculated standardized incidence ratios (SIRs) to compare the incidence of OC in LTS of CLL versus the general population. A multivariable model was used to identify independent predictors of OC. Overall survival was analyzed as a function of the presence of OC. RESULTS Among 797 LTSs of CLL, the cumulative frequency of OC was 36%, similar between 570 patients (72%) who required treatment for CLL (TRT) and 227 (28%) who remained untreated (UT). The most common OC in both groups was non-melanoma skin cancer, followed by prostate cancer, breast cancer, melanoma, lung cancer, and leukemia in TRT patients, and by prostate cancer, breast cancer, melanoma, lung cancer, and gastrointestinal tumors in the UT group. The SIR for all OC was 1.2 (P = 0.034). It was higher in males (SIR 1.31; P = 0.013) and patients

Published
2016

33. Meta-analysis of genome-wide association studies discovers multiple loci for chronic lymphocytic leukemia

Author

Nathaniel Rothman, Yolanda Benavente, Paul Brennan, Qing Lan, Pierluigi Cocco, Simon Crouch, Anneclaire J. De Roos, Josh Wright, Christine F. Skibola, Mark P. Purdue, Elisabete Weiderpass, James R. Cerhan, Randy D. Gascoyne, Maria Grazia Ennas, Kari E. North, Zhaoming Wang, Jinyan Huang, Julie M. Cunningham, Alain Monnereau, Peter Kraft, Patricia Hartge, Edward Giovannucci, Karen Curtin, Giovanna Masala, Jacqueline Clavel, Neil E. Kay, Jacques Riby, María Dolores Chirlaque, John J. Spinelli, Delphine Casabonne, Jenny Turner, Lucia Conde, Lesley F. Tinker, Martha Glenn, Sara S. Strom, Donna K. Arnett, Rebecca Montalvan, Ju-Hyun Park, Melissa C. Southey, Ann Maria, Karin E. Smedby, Lindsay M. Morton, Marc Maynadié, Laurie Burdett, Amy Hutchinson, Bengt Glimelius, W. Ryan Diver, Elio Riboli, Sonja I. Berndt, Lisa A. Cannon-Albright, Kimberly A. Bertrand, Aaron D. Norman, Sara J. Achenbach, Celine M. Vachon, Angela Cox, Xifeng Wu, Theodore R. Holford, Neil E. Caporaso, Joseph F. Fraumeni, Roel Vermeulen, Rudolph Kaaks, Mads Melbye, Joseph Vijai, Kari G. Chaffee, Lauren R. Teras, Rebecca D. Jackson, Lenka Foretova, J. Brice Weinberg, Paige M. Bracci, Sophia S. Wang, Demetrius Albanes, Stephen J. Chanock, Wendy Cozen, Mark Liebow, Anne J. Novak, Hans-Olov Adami, George J. Weiner, Angela Brooks-Wilson, Kenneth Offit, Anne Kricker, Claire M. Vajdic, James McKay, Ellen T. Chang, Baoshan Ma, Cristine Allmer, Susan L. Slager, Brian K. Link, Elizabeth A. Holly, Anthony Staines, Liming Liang, Jarmo Virtamo, Timothy G. Call, Nicola J. Camp, Ruth C. Travis, Alexandra Nieters, Degui Zhi, Brenda M. Birmann, Tait D. Shanafelt, Rachel S. Kelly, Graham G. Giles, Nilanjan Chatterjee, John A. Snowden, Yuanqing Ye, Núria Sala, Tongzhang Zheng, Paolo Boffetta, Lynn R. Goldin, Danylo J. Villano, Jose F. Leis, Paolo Vineis, Lucia Miligi, Jian Gu, Justin M. Leach, Silvia de Sanjosé, Richard K. Severson, Yawei Zhang, Henrik Hjalgrim, Roger L. Milne, Charles E. Lawrence, Meredith Yeager, Moara Machado, Nikolaus Becker, Joseph M. Connors, Anne Zeleniuch-Jacquotte, Giovanni Maria Ferri, Stephanie J. Weinstein, LS IRAS EEPI GRA (Gezh.risico-analyse), Sub Atmospheric physics and chemistry, dIRAS RA-I&I RA, dIRAS RA-2, Berndt, S.I., Camp, N.J., Skibola, C.F., Vijai, J., Wang, Z., Gu, J., Nieters, A., Kelly, R.S., Smedby, K.E., Monnereau, A., Cozen, W., Cox, A., Wang, S.S., Lan, Q., Teras, L.R., Machado, M., Yeager, M., Brooks-Wilson, A.R., Hartge, P., Purdue, M.P., Birmann, B.M., Vajdic, C.M., Cocco, P., Zhang, Y., Giles, G.G., Zeleniuch-Jacquotte, A., Lawrence, C., Montalvan, R., Burdett, L., Hutchinson, A., Ye, Y., Call, T.G., Shanafelt, T.D., Novak, A.J., Kay, N.E., Liebow, M., Cunningham, J.M., Allmer, C., Hjalgrim, H., Adami, H.-O., Melbye, M., Glimelius, B., Chang, E.T., Glenn, M., Curtin, K., Cannon-Albright, L.A., Diver, W.R., Link, B.K., Weiner, G.J., Conde, L., Bracci, P.M., Riby, J., Arnett, D.K., Zhi, D., Leach, J.M., Holly, E.A., Jackson, R.D., Tinker, L.F., Benavente, Y., Sala, N., Casabonne, D., Becker, N., Boffetta, P., Brennan, P., Foretova, L., Maynadie, M., McKay, J., Staines, A., Chaffee, K.G., Achenbach, S.J., Vachon, C.M., Goldin, L.R., Strom, S.S., Leis, J.F., Weinberg, J.B., Caporaso, N.E., Norman, A.D., De Roos, A.J., Morton, L.M., Severson, R.K., Riboli, E., Vineis, P., Kaaks, R., Masala, G., Weiderpass, E., Chirlaque, M.-D., Vermeulen, R.C.H., Travis, R.C., Southey, M.C., Milne, R.L., Albanes, D., Virtamo, J., Weinstein, S., Clavel, J., Zheng, T., Holford, T.R., Villano, D.J., Maria, A., Spinelli, J.J., Gascoyne, R.D., Connors, J.M., Bertrand, K.A., Giovannucci, E., Kraft, P., Kricker, A., Turner, J., Ennas, M.G., Ferri, G.M., Miligi, L., Liang, L., Ma, B., Huang, J., Crouch, S., Park, J.-H., Chatterjee, N., North, K.E., Snowden, J.A., Wright, J., Fraumeni, J.F., Offit, K., Wu, X., De Sanjose, S., Cerhan, J.R., Chanock, S.J., Rothman, N., Slager, S.L., National Cancer Institute ( NIH ), Centre d'épidémiologie des populations ( CEP ), Université de Bourgogne ( UB ) -Centre Régional de Lutte contre le cancer - Centre Georges-François Leclerc ( CRLCC - CGFL ), Registre des hémopathies malignes de Côte d'Or, Mayo Clinic [Rochester], National Cancer Institute [Bethesda] (NCI-NIH), National Institutes of Health [Bethesda] (NIH), Centre d'épidémiologie des populations (CEP), Université de Bourgogne (UB)-Centre Régional de Lutte contre le cancer Georges-François Leclerc [Dijon] (UNICANCER/CRLCC-CGFL), and UNICANCER-UNICANCER

Subjects
0301 basic medicine, Medicin och hälsovetenskap, Chronic lymphocytic leukemia, General Physics and Astronomy, Genome-wide association study, VARIANTS, Medical and Health Sciences, Malalties hereditàries, [ SDV.MHEP.HEM ] Life Sciences [q-bio]/Human health and pathology/Hematology, Chronic, Genetics, RISK, Leukemia, Multidisciplinary, BANK1, VDP::Medisinske Fag: 700::Helsefag: 800::Samfunnsmedisin, sosialmedisin: 801, Bcl-2-Like Protein 11, Adaptor Proteins, [SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/Hematology, Single Nucleotide, Lymphocytic, 3. Good health, PRIORITIZATION, Multidisciplinary Sciences, medicine.anatomical_structure, Science & Technology - Other Topics, TRANSCRIPTION FACTOR EOMESODERMIN, Genetic disorders, EXPRESSION, SUSCEPTIBILITY LOCI, Science, European Continental Ancestry Group, FAS GENE-MUTATIONS, Locus (genetics), Biology, Polymorphism, Single Nucleotide, General Biochemistry, Genetics and Molecular Biology, CLASSIFICATION, White People, Article, 03 medical and health sciences, Proto-Oncogene Proteins, MD Multidisciplinary, medicine, Genetic predisposition, SNP, Humans, Leucèmia limfocítica crònica, Genetic Predisposition to Disease, Polymorphism, B cell, Serpins, Genetic association, Adaptor Proteins, Signal Transducing, Science & Technology, Signal Transducing, B-Cell, Membrane Proteins, General Chemistry, medicine.disease, Leukemia, Lymphocytic, Chronic, B-Cell, 030104 developmental biology, VDP::Medical disciplines: 700::Health sciences: 800::Community medicine, Social medicine: 801, Apoptosis Regulatory Proteins, T-Box Domain Proteins, FOLLICULAR LYMPHOMA, Genome-Wide Association Study
Abstract

Chronic lymphocytic leukemia (CLL) is a common lymphoid malignancy with strong heritability. To further understand the genetic susceptibility for CLL and identify common loci associated with risk, we conducted a meta-analysis of four genome-wide association studies (GWAS) composed of 3,100 cases and 7,667 controls with follow-up replication in 1,958 cases and 5,530 controls. Here we report three new loci at 3p24.1 (rs9880772, EOMES, P=2.55 × 10−11), 6p25.2 (rs73718779, SERPINB6, P=1.97 × 10−8) and 3q28 (rs9815073, LPP, P=3.62 × 10−8), as well as a new independent SNP at the known 2q13 locus (rs9308731, BCL2L11, P=1.00 × 10−11) in the combined analysis. We find suggestive evidence (P, Chronic lymphocytic leukemia is a highly inheritable cancer. Here the authors conduct a metaanalysis of four genome-wide association studies and identify three novel loci located near EOMES, SERPINB6 and LPP associated with risk of this disease.

Published
2016

34. Detectable clonal mosaicism from birth to old age and its relationship to cancer

Author

William J. Blot, Christopher I. Amos, Cynthia Regnier, Sara S. Strom, David R. Crosslin, Nadia N. Hansel, Janey L. Wiggs, Cathy C. Laurie, Andrew McDavid, Cecelia A. Laurie, Karl C. Desch, Eleanor Feingold, Kimberly F. Doheny, Lynn R. Goldin, Laura J. Bierut, Jun-Jun Li, Xiuwen Zheng, Hua Ling, Bruce S. Weir, Sarah M. Hartz, Lisa B. Signorello, Jeffrey C. Murray, Jeffrey E. Lee, Rasika A. Mathias, Louis R. Pasquale, Jenna Udren, Kristine R. Monroe, Ingo Ruczinski, Andrew Crenshaw, Bjarke Feenstra, Leila R. Zelnick, Maria Teresa Landi, Neil E. Caporaso, Teri A. Manolio, Kurt N. Hetrick, Terri H. Beaty, Kenneth Rice, Elizabeth W. Pugh, M. Geoffrey Hayes, Robert B. Scharpf, Sarah C. Nelson, Jae H. Kang, Sue A. Ingles, Venkatraman E. Seshan, Sonja I. Berndt, Matthew P. Conomos, Christopher A. Haiman, Li-E Wang, Gail P. Jarvik, Alan F. Scott, David Ginsburg, Loic Le Marchand, Stephen J. Chanock, Mads Melbye, Jess Shen, Brian E. Henderson, John A. Heit, Daniel B. Mirel, David M. Levine, Kathleen C. Barnes, Siiri N. Bennett, William L. Lowe, Qingyi Wei, Sebastian M. Armasu, Patrick J. Heagerty, Denise Daley, Nataliya Sharopova, Neal D. Freedman, Mariza de Andrade, Anastasia L. Wise, Mary L. Marazita, Stephanie M. Gogarten, and Caitlin P. McHugh

Subjects
Adult, Male, Aging, Adolescent, DNA Copy Number Variations, Physiology, Genome-wide association study, Biology, Article, 03 medical and health sciences, 0302 clinical medicine, Neoplasms, Genetics, medicine, Humans, Child, Gene, Aged, 030304 developmental biology, Genetic association, Aged, 80 and over, Chromosome Aberrations, 0303 health sciences, Mosaicism, Infant, Newborn, Chromosome Mapping, Infant, Cancer, Karyotype, Middle Aged, medicine.disease, Confidence interval, Uniparental disomy, 3. Good health, Child, Preschool, 030220 oncology & carcinogenesis, Female, Genome-Wide Association Study, SNP array
Abstract

Clonal mosaicism for large chromosomal anomalies (duplications, deletions and uniparental disomy) was detected using SNP microarray data from over 50,000 subjects recruited for genome-wide association studies. This detection method requires a relatively high frequency of cells (>5–10%) with the same abnormal karyotype (presumably of clonal origin) in the presence of normal cells. The frequency of detectable clonal mosaicism in peripheral blood is low (

Published
2012

35. De novo acute myeloid leukemia risk factors

Author

Yuko Yamamura, Kplola Y. Elhor Gbito, Sara S. Strom, Robert Edison Oum, and Guillermo Garcia-Manero

Subjects
Adult, Male, Oncology, Cancer Research, medicine.medical_specialty, Adolescent, Young Adult, chemistry.chemical_compound, Risk Factors, Occupational Exposure, Surveys and Questionnaires, hemic and lymphatic diseases, Internal medicine, Epidemiology, medicine, Humans, Young adult, neoplasms, Aged, Aged, 80 and over, Chromosome Aberrations, business.industry, Smoking, Case-control study, Cancer, Myeloid leukemia, Odds ratio, Middle Aged, medicine.disease, Leukemia, Myeloid, Acute, Leukemia, chemistry, Case-Control Studies, Immunology, Solvents, Female, Solvent exposure, business
Abstract

BACKGROUND: Acute myeloid leukemia (AML) is comprised of several bone marrow-based cancers and is the most common type of leukemia in the United States. The etiology of AML is not well understood. A case-control study was conducted at The University of Texas M. D. Anderson Cancer Center to investigate associations between lifestyle characteristics and the risk of AML in Texas. METHODS: This study included 638 adult patients with de novo AML (cases) and a group of 636 matched controls. Interviewer-administered questionnaires were used to collect demographic and occupational data. The distribution of cases by World Health Organization (WHO) subtype was 71 patients (11%) with recurrent cytogenetic abnormalities (AML-RCA), 134 patients (21%) with multilineage dysplasia (AML-MD), and 389 patients (61%) with AML not otherwise categorized (AML-NOC). Multivariate logistic regression analyses were performed among all AML cases and among both sexes and each WHO subgroup. RESULTS: Among men, heavy smoking (≥30 pack-years; odds ratio [OR], 1.86) and occupational solvent exposure at low levels (OR, 2.87) or moderate/high levels (OR, 4.13) statistically significantly increased the risk of AML. Among women, obesity (OR, 1.62) and solvent exposure to low levels (OR, 2.73) or moderate/high levels (OR, 3.90) increased the risk of AML. Across WHO subtypes, obesity was associated with a statistically significantly increased risk of AML-RCA (OR, 3.15), whereas solvent exposure increased the risk in all subtypes at low levels (AML-RCA: OR, 4.11; AML-MD: OR, 2.54) and moderate/high levels (AML-RCA: OR, 5.13; AML-MD: OR, 3.02). A joint effect between smoking and solvent exposure was observed, and the highest risk was observed among smokers who had solvent exposure (OR, 4.51). CONCLUSIONS: The current results suggested that several factors play a role in AML predisposition with possible joint effects. Risk profiles for AML differed by sex and WHO subtype. Cancer 2012. © 2012 American Cancer Society.

Published
2012

36. Genome-wide association study of prostate cancer in men of African ancestry identifies a susceptibility locus at 17q21

Author

Iona Cheng, Stephen Watya, Anna M. Ray, Timothy R. Rebbeck, Kristine R. Monroe, John S. Witte, Sara S. Strom, Yuko Yamamura, John D. Carpten, Brian E. Henderson, Ann W. Hsing, Janet L. Stanford, Peggy Wan, M. Cristina Leske, Edder R. Duarte, Sonja I. Berndt, Loreall Pooler, William J. Blot, Charnita Zeigler-Johnson, Zhaoming Wang, Venetta Thomas, Stephen J. Chanock, David Van Den Berg, W. Ryan Diver, Richard B. Hayes, Michael J. Thun, Graham Casey, Benjamin A. Rybicki, Christopher A. Haiman, Sue A. Ingles, Bao Li Chang, Jennifer J. Hu, Kathleen A. Cooney, Qiuyin Cai, Barbara Nemesure, Loic Le Marchand, William B. Isaacs, Gary K. Chen, Jennifer Haslag-Minoff, Esther M. John, S. Lilly Zheng, Glenn O. Allen, Xin Sheng, Suh Yuh Wu, Laurence N. Kolonel, Erin N. Carter, Elaine A. Ostrander, Christine Neslund-Dudas, Suzanne Kolb, Lisa B. Signorello, Yao Tettey, Adam B. Murphy, Rick A. Kittles, Jianfeng Xu, Fredrick R. Schumacher, William Wu, Lucy Xia, Adam S. Kibel, Daniel O. Stram, Anselm Hennis, Edward D. Yeboah, and Serigne Magueye Gueye

Subjects
Male, Genome-wide association study, Disease, Biology, Polymorphism, Single Nucleotide, Article, 03 medical and health sciences, Prostate cancer, 0302 clinical medicine, Genetics, medicine, Humans, Genetic Predisposition to Disease, Allele, 030304 developmental biology, Genetic association, 0303 health sciences, Prostatic Neoplasms, Chromosome, Cancer, Odds ratio, medicine.disease, 3. Good health, Black or African American, 030220 oncology & carcinogenesis, Chromosomes, Human, Pair 17, Genome-Wide Association Study
Abstract

In search of common risk alleles for prostate cancer that could contribute to high rates of the disease in men of African ancestry, we conducted a genome-wide association study, with 1,047,986 SNP markers examined in 3,425 African-Americans with prostate cancer (cases) and 3,290 African-American male controls. We followed up the most significant 17 new associations from stage 1 in 1,844 cases and 3,269 controls of African ancestry. We identified a new risk variant on chromosome 17q21 (rs7210100, odds ratio per allele = 1.51, P = 3.4 × 10(-13)). The frequency of the risk allele is ∼5% in men of African descent, whereas it is rare in other populations (

Published
2011

37. Delayed treatment and continued growth of nonmelanoma skin cancer

Author

Erin S. Gardner, Alfred Rademaker, David J. Margolis, Murad Alam, Leonard Harry Goldberg, Sirunya Silapunt, and Sara S. Strom

Subjects
Male, Pediatrics, medicine.medical_specialty, Delayed Diagnosis, Skin Neoplasms, medicine.medical_treatment, Population, Denial, Psychological, Dermatology, Surveys and Questionnaires, medicine, Mohs surgery, Humans, Medical history, education, Adverse effect, Prospective cohort study, Aged, education.field_of_study, business.industry, Age Factors, Cancer, Middle Aged, Mohs Surgery, medicine.disease, Surgery, Carcinoma, Basal Cell, Private practice, Carcinoma, Squamous Cell, Female, Skin cancer, business, Attitude to Health
Abstract

Background Patients may delay treatment for skin cancer for various reasons. Prior research on treatment delay has focused on melanoma rather than nonmelanoma skin cancer (NMSC), which is much more common. Objective We sought to clarify the reasons for delay in the presentation for diagnosis and treatment of NMSC. Methods This was a prospective cohort study in a Mohs micrographic surgery private practice in an urban setting. Eligible subjects were 982 consecutive patients presenting for Mohs micrographic surgery for NMSC between March and December 2005. No enrolled subjects were withdrawn for adverse effects. The survey was a 4-page written self-administered questionnaire, eliciting patient medical history, skin cancer history, demographic information, initial and subsequent lesion size, and reasons for delay in presentation for evaluation and management. Outcome analyses addressed the: (1) frequency of specific reasons for delayed presentation, as provided by self-report; (2) association between reasons for delay with demographic or other patient-specific factors; and (3) change in lesion diameter from the time of detection by the patient to the time of presentation to the doctor. Results Among the reasons for waiting, denial (including: thought it would go away, thought it wasn't important, too busy, thought they could self-treat, afraid it might be something dangerous) was the most frequent, accounting for 71% of cases; difficulty scheduling was associated with 10% of the instances of delay. Older patients (age >64 years) were more likely to wait to seek care than younger patients (odd ratio [OR] = 0.5; 95% confidence interval [CI] 0.4-0.7). Patients with a prior skin cancer were more likely to wait (OR = 1.4; 95% CI 1.1-2.0), as were patients with major life problems (OR = 2.6; 95% CI 1.6-4.3) and patients with a history of any cancer (OR = 1.8; 95% CI 1.3-2.4). Weighted kappa analysis comparing tumor size at the two time points yielded a kappa of 0.72 (SE = .02; 95% CI 0.68-0.77). When the data were separated into two groups, one including those tumors that had decreased in size or remained the same (698 patients), and those that had increased in size (120 patients), the median delay-to-presentation intervals associated with these two groups (2.5 vs 6.0 months, respectively) were found to be significantly different ( P Limitations This study may have limited generalizability to the extent that it reflects the characteristics only of the subpopulation of patients with skin cancer who eventually received treatment at a referral-based, urban, dermatology private practice. Overall, these patients may have been better insured and be more affluent than the general population. Conclusions Denial is the most common patient-specific factor accounting for delayed presentation for NMSC diagnosis and treatment. Patients younger than 65 years, with a skin cancer history, with major life problems, and with a history of any cancer were most likely to wait to see a doctor. There was a significant increase in tumor size from the time when tumors were noticed by patients to the time when patients presented to a physician. Increased delay was associated with increased tumor growth.

Published
2011

38. Hodgkin lymphoma risk: Role of genetic polymorphisms and gene-gene interactions in DNA repair pathways

Author

Elizabeth A. Rourke, Randa El-Zein, Carol J. Etzel, Claudia M. Monroy, Andrea Cortes, Anas Younes, Mirtha S. Lopez, and Sara S. Strom

Subjects
Genetics, Cancer Research, XRCC1, Candidate gene, XRCC3, DNA repair, Single-nucleotide polymorphism, Base excision repair, Biology, Molecular Biology, Gene, Nucleotide excision repair
Abstract

DNA repair variants may play a potentially important role in an individual's susceptibility to developing cancer. Numerous studies have reported the association between genetic single nucleotide polymorphisms (SNPs) in DNA repair genes and different types of hematologic cancers. However, to date, the effects of such SNPs on modulating Hodgkin lymphoma (HL) risk have not yet been investigated. We hypothesized that gene-gene interaction between candidate genes in direct reversal, nucleotide excision repair (NER), base excision repair (BER) and double strand break (DSB) pathways may contribute to susceptibility to HL. To test this hypothesis, we conducted a study on 200 HL cases and 220 controls to assess associations between HL risk and 21 functional SNPs in DNA repair genes. We evaluated potential gene-gene interactions and the association of multiple polymorphisms in a chromosome region using a multi-analytic strategy combining logistic regression, multi-factor dimensionality reduction and classification and regression tree approaches. We observed that, in combination, allelic variants in the XPC Ala499Val, NBN Glu185Gln, XRCC3 Thr241Me, XRCC1 Arg194Trp, and XRCC1 399Gln polymorphisms modify the risk for developing HL. Moreover, the cumulative genetic risk score revealed a significant trend where the risk for developing HL increases as the number of adverse alleles in BER and DSB genes increase. These findings suggest that DNA repair variants in BER and DSB pathways may play an important role in the development of HL.

Published
2011

39. Baldness, acne and testicular germ cell tumours

Author

Alice J. Sigurdson, Katherine A. McGlynn, Robert J. Amato, Britton Trabert, Sara S. Strom, and Anne M. Sweeney

Subjects
medicine.medical_specialty, business.industry, medicine.drug_class, Urology, Endocrinology, Diabetes and Metabolism, Case-control study, Odds ratio, medicine.disease, Androgen, Endocrinology, Hair loss, Reproductive Medicine, Internal medicine, medicine, Etiology, Male-pattern baldness, Age of onset, business, Acne
Abstract

Androgen levels during critical periods of testicular development may be involved in the aetiology of testicular germ cell tumours (TGCT). We evaluated the roles of adolescent and early adult life correlates of androgen exposure and TGCT in a hospital-based case-control study. TGCT cases (n=187) and controls (n=148), matched on age, race and state of residence, participated in the study. Unconditional logistic regression was used to estimate associations between TGCT and male pattern baldness, severe acne, markers of puberty onset and body size. Cases were significantly less likely to report hair loss than controls [odds ratio (OR): 0.6; 95% confidence interval (CI): 0.4, 1.0]. Amount of hair loss, increasing age at onset and increasing rate of loss were all inversely associated with TGCT (rate of hair loss: p-trend=0.03; age at onset: p-trend=0.03; amount of hair loss: p-trend=0.01). History of severe acne was inversely associated with TGCT (OR: 0.5; 95% CI: 0.3, 0.9) and height was positively associated with TGCT (p-trend=0.02). Increased endogenous androgen levels during puberty and early adulthood may be associated with a decreased risk of TGCT. Additional studies of endogenous hormone levels during puberty and early adult life are warranted, especially studies evaluating the role of androgen synthesis, metabolism and uptake.

Published
2010

40. Survival of patients with multiple primary malignancies: a study of 783 patients with gastrointestinal stromal tumor

Author

J. C. Trent, Robert S. Benjamin, Judy Garber, A. G. Dumont, Joseph A. Ludwig, Vinod Ravi, Sara S. Strom, S. Patel, R. K. Pandurengan, and Dejka M. Araujo

Subjects
Adult, Male, Oncology, medicine.medical_specialty, Pathology, Adolescent, Gastrointestinal Stromal Tumors, Malignant peripheral nerve sheath tumor, Neoplasms, Multiple Primary, Young Adult, Internal medicine, medicine, Humans, Stromal tumor, neoplasms, Survival rate, Aged, Neoplasm Staging, Aged, 80 and over, GiST, business.industry, Cancer, Imatinib, Original Articles, Hematology, Middle Aged, Prognosis, medicine.disease, Combined Modality Therapy, digestive system diseases, Cancer registry, Survival Rate, Imatinib mesylate, Female, business, Follow-Up Studies, medicine.drug
Abstract

Gastrointestinal stromal tumor (GIST) is a rare cancer of the digestive tract that accounts for 0.1%–3.0% of all gastrointestinal neoplasms, 10% of small-bowel tumors, and 10%–15% of all sarcomas [1–4]. There are ∼5000 newly diagnosed cases per year in the USA. Although most of these cases are sporadic, there are reported syndromes of autosomal dominant hereditary GIST that result from inheritance of a germ-line KIT or platelet-derived growth factor receptor (PDGFR) mutation [5]. Additionally, there are predisposition syndromes in which affected individuals may develop GIST as well as other types of cancer. Examples include malignant peripheral nerve sheath tumor in neurofibromatosis [6], paraganglioma and pulmonary chondroma in Carney’s triad [7], and paraganglioma in the Carney–Stratakis syndrome [8]. Recently, Agaimy et al. [9] found that the most common association with GIST is gastric carcinoma (47%), prostate cancer (9%), lymphoma/leukemia (7%), and breast cancer (7%). Au et al. [10] reported that GIST and papillary renal cell carcinoma may occur as familial tumors related to mutations in the proto-oncogenes c-MET and c-KIT. An association has been demonstrated between GIST and acute myeloid leukemia (AML) as well as chronic myelogenous leukemia [11]. The clinical use of imatinib mesylate (imatinib), an oral inhibitor of the Kit receptor tyrosine kinase, has increased the survival of patients with metastatic GIST [12]. Due to the marked success of imatinib in both the adjuvant primary and the metastatic settings, many patients with GIST are treated with imatinib for many years. There are limited data as to the occurrence of additional malignancies after diagnosis of GIST in patients treated with imatinib. Thus, it is critical to investigate the prevalence and type of malignancies that develop before and after diagnosis in the era of increasing use of imatinib for GIST. In this study, we used the University of Texas M. D. Anderson Cancer Center (MDACC) cancer registry to identify additional primary malignancies among our patients with GIST. Furthermore, we have rigorously determined detailed patient demographics, histological type of all malignancies, and whether these additional cancers occurred before or after the diagnosis of GIST. Finally, we estimated the survival of patients with GIST with none, one, or multiple other primary tumors.

Published
2010

41. Targeted prostate cancer screening in men with mutations in BRCA1 and BRCA2 detects aggressive prostate cancer: preliminary analysis of the results of the IMPACT study

Author

A. Abele, Rosalind A. Eeles, Soo Hwang Teo, Marc Tischkowitz, Audrey Ardern-Jones, Ignacio Blanco, Elizabeth Bancroft, Gad Rennert, Nicola Nicolai, Graeme Suthers, R. Doherty, Huw Dorkins, Annelie Liljegren, Cezary Cybulski, S. Townshend, Yolanda Barbachano, L. Maehle, Dorthe G. Crüger, B. Newcombe, Peter R. Wilson, Alan Donaldson, David P. Dearnaley, Virginia E. Clowes, Irene Jobson, C. J. van Asperen, Vincent Khoo, Hans Lilja, Charles Jameson, Zsofia Kote-Jarai, Henrik Grönberg, A. Male, Carole Brewer, Wendy S. Rubinstein, Elizabeth Page, B. Bulman, Clare Moynihan, D G R Evans, T. Ramón y Cajal, Allan D. Spigelman, Jan Lubinski, Louise Izatt, Jorunn E. Eyfjord, Palle Jørn Sloth Osther, Y. J. Bignon, Eitan Friedman, Alan M. F. Stapleton, Fritz H. Schröder, Sara S. Strom, Geoffrey J. Lindeman, Alison Falconer, J Melia, Mónica Salinas, Christopher S. Foster, Colin Mercer, Katherine L. Tucker, Karol Axcrona, Freddie C. Hamdy, Lisa Walker, Judy Kirk, Saundra S. Buys, Susan M. Domchek, Mohnish Suri, Kyriacos Kyriacou, Susan Peock, D. Ilencikova, Chris H. Bangma, Neil K. Aaronson, A. Mitra, Paul Sibley, Fiona Douglas, Douglas F. Easton, Oskar T. Johannsson, Lambertus A. Kiemeney, Diana Eccles, Shirley Hodgson, and Gillian Mitchell

Subjects
Oncology, Gynecology, medicine.medical_specialty, Prostate biopsy, medicine.diagnostic_test, business.industry, Urology, BRCA mutation, Cancer, medicine.disease, Prostate cancer, Prostate-specific antigen, Prostate cancer screening, medicine.anatomical_structure, Prostate, Internal medicine, medicine, Genetic predisposition, skin and connective tissue diseases, business
Abstract

What's known on the subject? and What does the study add? Scientists have found a number of genetic factors that increase prostate cancer risk, including heritable mutations in the genes BRCA1 and BRCA2. These mutations are not common but can have major impact, as a BRCA2 mutation increases risk by up to seven-fold while a BRCA1 mutation is thought to double risk in men under 65. The IMPACT study aims to determine whether targeted screening in men with a known BRCA1 or BRCA2 mutation would lead to earlier diagnosis of prostate cancers. This data from the IMPACT study adds to the increasing evidence that BRCA mutation carriers develop more aggressive disease. Although these are early results, it appears that PSA screening is more accurate at predicting potentially aggressive prostate cancer among men at higher risk of the disease due to a genetic predisposition than general population screening. This study provides support for continued screening in men with genetic mutations. OBJECTIVE To evaluate the role of targeted prostate cancer screening in men with BRCA1 or BRCA2 mutations, an international study, IMPACT (Identification of Men with a genetic predisposition to ProstAte Cancer: Targeted screening in BRCA1/2 mutation carriers and controls), was established. This is the first multicentre screening study targeted at men with a known genetic predisposition to prostate cancer. A preliminary analysis of the data is reported. PATIENTS AND METHODS Men aged 40-69 years from families with BRCA1 or BRCA2 mutations were offered annual prostate specific antigen (PSA) testing, and those with PSA > 3 ng/mL, were offered a prostate biopsy. Controls were men age-matched (+/- 5 years) who were negative for the familial mutation. RESULTS In total, 300 men were recruited (205 mutation carriers; 89 BRCA1, 116 BRCA2 and 95 controls) over 33 months. At the baseline screen (year 1), 7.0% (21/300) underwent a prostate biopsy. Prostate cancer was diagnosed in ten individuals, a prevalence of 3.3%. The positive predictive value of PSA screening in this cohort was 47 center dot 6% (10/21). One prostate cancer was diagnosed at year 2. Of the 11 prostate cancers diagnosed, nine were in mutation carriers, two in controls, and eight were clinically significant. CONCLUSIONS The present study shows that the positive predictive value of PSA screening in BRCA mutation carriers is high and that screening detects clinically significant prostate cancer. These results support the rationale for continued screening in such men.

Published
2010

42. Common occurrence of monoclonal B-cell lymphocytosis among members of high-risk CLL families

Author

Jose F. Leis, Vicki A. Morrison, Martha Glenn, Celine M. Vachon, Gerald E. Marti, J. Brice Weinberg, Sara J. Achenbach, Laura Z. Rassenti, Sara S. Strom, Kari G. Rabe, Lynn R. Goldin, Mark C. Lanasa, James R. Cerhan, Sallie D. Algood, Neil E. Caporaso, Fatima Abbasi, Nicola J. Camp, Timothy G. Call, Susan L. Slager, Laura Fontaine, Curtis A. Hanson, Logan G. Spector, Michelle S. Yau, and Neil E. Kay

Subjects
education.field_of_study, Lymphocytosis, Chronic lymphocytic leukemia, Population, chemical and pharmacologic phenomena, Hematology, Biology, bacterial infections and mycoses, medicine.disease, Asymptomatic, Leukemia, Immunophenotyping, hemic and lymphatic diseases, Immunology, Monoclonal, medicine, Monoclonal B-cell lymphocytosis, medicine.symptom, education
Abstract

Monoclonal B-cell lymphocytosis (MBL) is an asymptomatic haematological condition characterized by low absolute levels of B-cell clones with a surface immunophenotype similar to that of chronic lymphocytic leukaemia (CLL). In the general population, MBL increases with age with a prevalence of 5-9% in individuals over age 60 years. It has been reported to be higher among first-degree relatives from CLL families. We report results of multi-parameter flow cytometry among 505 first-degree relatives with no personal history of lymphoproliferative disease from 140 families having at least two cases of CLL. Seventeen percent of relatives had MBL. Age was the most important determinant where the probability for developing MBL by age 90 years was 61%. MBL clustered in certain families but clustering was independent of the number of known CLL cases in a family. As is the case with CLL, males had a significantly higher risk for MBL than did females (P = 0·04). MBL patients had significantly higher mean absolute lymphocyte counts (2·4 × 10(9) /l) and B-cell counts (0·53 × 10(9) /l) than those with a normal B-cell immuno-phenotype. Our findings show that MBL occurs at a very high rate in high risk CLL families. Both the age and gender distribution of MBL are parallel to CLL, implying a shared inherited risk.

Published
2010

43. Abstract 227: Germline variation at 8q24 and prostate cancer risk in men of European ancestry

Author

Edward J. Saunders, Demetrius Albanes, Henrik Grönberg, Fredrik Wiklund, Peter Kraft, Johanna Schleutker, Douglas F. Easton, Tokhir Dadaev, Karina Dalsgaard Sørensen, Stella Koutros, Sonja I. Berndt, Ana Vega, Zsofia Kote-Jarai, Lorelei A. Mucci, Koveela Govindasami, Manolis Kogevinas, Stephen J. Chanock, Alicja Wolk, David E. Neal, Sara S. Strom, Jyotsna Batra, Rosalind A. Eeles, Mark N. Brook, Adam S. Kibel, Jeanette T. Bensen, Eli Marie Grindedal, Christopher A. Haiman, Jenny L Donovan, Fredrick R. Schumacher, Marco Matejcic, Kenneth Muir, Graham G. Giles, Lovise Maehle, David V. Conti, Judith A. Clements, Sara Benlloch, Freddie C. Hamdy, Robert J. Hamilton, Geraldine Cancel-Tassin, Barry S. Rosenstein, Ruth C. Travis, Apcb, Ali Amin Al Olama, Victoria L. Stevens, Nora Pashayan, Catherine M. Tangen, Yong-Jie Lu, Catharine M L West, Susan M. Gapstur, and Sue A. Ingles

Subjects
Prostate cancer risk, Oncology, Cancer Research, medicine.medical_specialty, Variation (linguistics), business.industry, Internal medicine, medicine, business, Germline
Abstract

We performed an in-depth and well-powered investigation of genetic variation across the cancer susceptibility region at chromosome 8q24 (127.6-129.0 Mb) to search for novel risk variants associated with prostate cancer (PCa) risk in the European ancestry population. We combined genotyped and imputed data from the PRACTICAL/ELLIPSE OncoArray and iCOGS consortia consisting of 71,535 PrCa cases and 52,935 controls of European ancestry. Variants with high imputation quality score (>0.8) were retained for a total of 5,600 overlapping variants between the two datasets. Associations of genetic variants with PCa risk were evaluated using unconditional logistic regression with adjustment for country and ten principal components. The marginal risk estimates for the 5,600 variants that passed quality control were combined by a fixed effects meta-analysis. A meta-stepwise selection was performed on variants marginally associated with PCa risk from the meta results (P Citation Format: Marco Matejcic, Edward J. Saunders, Tokhir Dadaev, Mark Brook, Ali Amin Al Olama, Fredrick R. Schumacher, Sonja I. Berndt, Sara Benlloch, Kenneth Muir, Koveela Govindasami, Victoria L. Stevens, Susan M. Gapstur, Catherine M. Tangen, Jyotsna Batra, Judith Clements, APCB (Australian Prostate Cancer Bio Resource), Henrik Gronberg, Nora Pashayan, Johanna Schleutker, Demetrius Albanes, Alicja Wolk, Catharine West, Lorelei Mucci, Peter Kraft, Géraldine Cancel-Tassin, Stella Koutros, Karina Dalsgaard Sorensen, Lovise Maehle, Eli Marie Grindedal, Sara Strom, David E. Neal, Freddie C. Hamdy, Jenny L. Donovan, Ruth C. Travis, Robert J. Hamilton, Sue Ann Ingles, Barry Rosenstein, Yong-Jie Lu, Graham G. Giles, Adam S. Kibel, Ana Vega, Jeanette Bensen, Manolis Kogevinas, Fredrik Wiklund, Stephen Chanock, Douglas F. Easton, Rosalind A. Eeles, Zsofia Kote-Jarai, David V. Conti, Christopher A. Haiman. Germline variation at 8q24 and prostate cancer risk in men of European ancestry [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 227.

Published
2018

44. Acute myeloid leukemia outcome: role of nucleotide excision repair polymorphisms in intermediate risk patients

Author

Elihu H. Estey, Sara S. Strom, Ubaldo Martinez Outschoorn, and Guillermo Garcia-Manero

Subjects
Oncology, Cancer Research, medicine.medical_specialty, Proportional hazards model, Cytogenetics, Myeloid leukemia, Hematology, Biology, medicine.disease, Leukemia, Internal medicine, Immunology, Genotype, medicine, ERCC1, Survival analysis, Nucleotide excision repair
Abstract

In acute myeloid leukemia (AML), cytogenetics predicts treatment outcome for the favorable and poor subgroups but not for the intermediate subgroup. Polymorphisms within the nucleotide excision repair (NER) pathway may lead to interindividual differences in DNA repair capacity, influencing outcome. We studied the role of six polymorphisms (ERCC1 Gln504Lys, XPD Lys751Gln, XPC Ala499Val, XPC Lys939Gln, XPG Asp1104His, and CCNH Val270Ala) in overall and disease-free survival among 170 adult de novo patients with intermediate cytogenetics (diploid [n = 117]; non-diploid [n = 53]), treated with induction chemotherapy. Kaplan-Meier and Cox proportional hazards models were performed. Diploid patients with the XPD AC/CC genotype survived shorter than those with the wild-type genotype (median survival 22 vs. 40 months, p = 0.03). Diploid patients with XPC CT/TT genotype survived shorter than those with the wild-type genotype (median survival 15 vs. 30 months, p = 0.02). After adjusting for clinical and sociodemographic variables, patients carrying both XPD AC/CC and XPC CT/TT had a greater than two-fold increased risk of dying, compared to those with the wild-type genotypes (HR = 2.49; 95% CI: 1.06-5.85). No associations were observed for disease-free survival. This combined genotype may modulate treatment effect, decreasing overall survival. These findings could in the future help select treatments for patients with normal cytogenetics.

Published
2010

45. Other Malignancies in Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma

Author

William G. Wierda, Susan Lerner, Susan O'Brien, L. Jeffrey Medeiros, Sijin Wen, Apostolia-Maria Tsimberidou, Sara S. Strom, Hagop M. Kantarjian, Peter McLaughlin, Emil J. Freireich, and Michael J. Keating

Subjects
Adult, Male, Oncology, Cancer Research, medicine.medical_specialty, Pathology, Chronic lymphocytic leukemia, Malignancy, Young Adult, Risk Factors, Internal medicine, Epidemiology, medicine, Humans, Aged, Retrospective Studies, Aged, 80 and over, business.industry, Melanoma, Cancer, Neoplasms, Second Primary, Retrospective cohort study, ORIGINAL REPORTS, Middle Aged, medicine.disease, Leukemia, Lymphocytic, Chronic, B-Cell, United States, Lymphoma, Leukemia, Female, business, SEER Program
Abstract

Purpose Other malignancies have been reported to occur with increased frequency in chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL). The aim of this study was to determine the frequency, outcomes, and factors associated with other cancers in patients with CLL/SLL. Patients and Methods We reviewed the records of consecutive patients with previously untreated CLL/SLL seen at The University of Texas M. D. Anderson Cancer Center from 1985 to 2005. The number of second cancers observed was compared with the number expected from the Surveillance, Epidemiology, and End Results database. Results Among 2,028 patients, 324 (16%) had a history of other cancers and 227 (11.2%) developed other malignancies during the follow-up period. Overall, 625 cancers were observed in 551 patients, including skin (30%), prostate (13%), breast (9%), melanoma (8%), lymphoma (8%), gastrointestinal (9%), lung (6%), and other cancers (17%). The risk of a second cancer was 2.2 times higher than the expected risk. The response rates in patients with and without a history of other cancers were 86% and 92%, respectively (P = .04), and the 5-year survival rates were 70% and 82%, respectively (P < .001). In Cox analysis, independent factors predicting development of new cancers were older age, male sex, and elevated levels of β2-microglobulin, lactate dehydrogenase, and creatinine. In patients who were treated for CLL/SLL, the treatment regimen did not affect the risk of subsequent cancer (P = .49). Conclusion Patients with CLL/SLL have more than twice the risk of developing a second cancer and an increased frequency of certain cancer types. Awareness of risk factors could permit early detection.

Published
2009

46. The ratio of matrix metalloproteinase to E-cadherin expression: A pilot study to assess mRNA and protein expression among African American prostate cancer patients

Author

Xuemei Wang, Renduo Song, Patricia Troncoso, Ricardo Sanchez-Ortiz, Sara S. Strom, Philippe E. Spiess, and Curtis A. Pettaway

Subjects
Male, Biochemical recurrence, Pathology, medicine.medical_specialty, Urology, medicine.medical_treatment, Pilot Projects, In situ hybridization, Adenocarcinoma, Article, Cohort Studies, Prostate cancer, Gene expression, Humans, Medicine, RNA, Messenger, Prostatectomy, business.industry, Prostatic Neoplasms, Cancer, Cadherins, Prognosis, medicine.disease, Histologic Progression, Black or African American, Gene Expression Regulation, Neoplastic, Matrix Metalloproteinase 9, Oncology, Disease Progression, Matrix Metalloproteinase 2, Immunohistochemistry, business
Abstract

We assessed the expression of Matrix Metalloproteinase (MMP) to E-cadherin (M/E ratio) to determine the correlation of gene expression with pathologic variables and outcome in a cohort of African American (AA) prostate cancer patients.Tumors from formalin-fixed, paraffin embedded RP specimens were examined. Gleason scores were 6, 7, andor=8 in 7, 16, 13 tumors, respectively. Pathologic stage was organ confined (pT2) in 18 and advanced (pT2) in 18 tumors. A colorimetric mRNA in situ hybridization (ISH) assay was performed using biotinylated anti-sense oligonucleotide probes for MMP 2 and 9, as well as for E-cadherin gene transcripts. Immunohistochemistry (IHC) was performed utilizing specific monoclonal antibodies to detect the above genes. Image analysis was performed to determine the intensity of both mRNA and protein expression. Two reviewers analyzed ISH gene expression independently.The M/E expression ratio was significantly increased at the invasive edge (but not the center) of tumors of higher Gleason score (P = 0.02 and 0.0008) and pathologic stage (P = 0.0001 and0.0001) when examined by both ISH and IHC. Significant variability in ISH staining interpretation was noted within and among the two study reviewers. An M/E ratio2.5 was associated with biochemical recurrence after radical prostatectomy in addition to tumor pathologic stage subsequent to univariate statistical analysis.The M/E ratio characterizes an important aspect of the molecular phenotype associated with the histologic progression of prostate cancer among African American prostate cancer patients. A larger comparative study is required to determine potential racial variation and prognostic significance of gene expression.

Published
2008

47. Prostate cancer in Mexican-Americans: Identification of risk factors

Author

F. Nery Flores-Sandoval, Yuko Yamamura, David S. Lopez, Curtis A. Pettaway, and Sara S. Strom

Subjects
Male, medicine.medical_specialty, Urology, Population, Motor Activity, Logistic regression, Risk Factors, Occupational Exposure, Mexican Americans, Epidemiology, medicine, Humans, Obesity, Risk factor, Family history, education, Life Style, Aged, Gynecology, education.field_of_study, business.industry, Case-control study, Prostatic Neoplasms, Middle Aged, Anthropometry, medicine.disease, Texas, Logistic Models, Oncology, Case-Control Studies, Multivariate Analysis, Agrochemicals, business, Demography
Abstract

BACKGROUND There is a paucity of information regarding prostate cancer (PCa) risk factors among Hispanics, the fastest-growing ethnic group in the United States. METHODS This population-based case-control study included 176 Texas men of Mexican descent with PCa and 174 age- and ethnicity-matched controls. Demographic, lifetime occupational history, family history of cancer, lifestyle (e.g., smoking, alcohol, diet, and recreational physical activity) and anthropometric information were collected by personal interviews. Chemical exposure and physical activity were determined using job-exposure matrices for each reported job. RESULTS Logistic regression models adjusted for relevant covariates were used to evaluate their independent effects. Compared to controls, cases were three times more likely to work in jobs with high agrichemical exposure (OR = 3.44, 95% CI 1.84–6.44), and 54% less likely to work in jobs with moderate/high occupational physical activity (OR = 0.46, 95% CI 0.28–0.77). In analyses stratified by stage, cases with organ-confined PCa were three times more likely to have high agrichemical exposure (OR = 3.39, 9%CI 1.68–6.84), and 56% less likely to have moderate/high levels of occupational physical activity (OR = 0.44, 95% CI 0.26–0.76). Increased risk of being diagnosed with advanced PCa was associated with obesity at time of diagnosis (OR = 2.50, 95% CI 1.20–5.20) and high levels of agrichemical exposure (OR = 4.65, 95% CI 1.97–10.97), but not with occupational physical activity. CONCLUSIONS This case-control study, the first conducted in a homogeneous Hispanic population, identified modifiable PCa risk factors, such as physical activity and agrichemical exposure, which may be useful in developing interventions for this understudied population. Prostate 68: 563–570, 2008. © 2008 Wiley-Liss, Inc.

Published
2008

48. Saturated fat intake predicts biochemical failure after prostatectomy

Author

Yuko Yamamura, Sara S. Strom, Stephanie L. Barrera, John DiGiovanni, Curtis A. Pettaway, and Michele R. Forman

Subjects
Male, Cancer Research, medicine.medical_specialty, Saturated fat, medicine.medical_treatment, Physiology, Diet and obesity, Kaplan-Meier Estimate, Weight Gain, Disease-Free Survival, Body Mass Index, Predictive Value of Tests, Internal medicine, medicine, Humans, Obesity, Treatment Failure, Risk factor, Aged, Proportional Hazards Models, Prostatectomy, business.industry, Proportional hazards model, Fatty Acids, Hazard ratio, Prostatic Neoplasms, Middle Aged, medicine.disease, Dietary Fats, Endocrinology, Oncology, Cohort, Neoplasm Recurrence, Local, Energy Intake, business
Abstract

Previous reports show that obesity predicts biochemical failure after treatment for localized prostate cancer. Since obesity is associated with increased fat consumption, we investigated the role that dietary fat intake plays in modulating obesity-related risk of biochemical failure. We evaluated the association between saturated fat intake and biochemical failure among 390 men from a previously described prostatectomy cohort. Participants completed a food frequency questionnaire collecting nutrient information for the year prior to diagnosis. Because fat and energy intake are highly correlated, the residual method was used to adjust fat (total and saturated) intakes for energy. Biochemical-failure-free-survival rates were calculated using the Kaplan–Meier method. Crude and adjusted effects were estimated using Cox proportional hazards models. During a mean follow-up of 70.6 months, 78 men experienced biochemical failure. Men who consumed high- saturated fat (HSF) diets were more likely to experience biochemical failure (p = 0.006) and had significantly shorter biochemical-failure-free-survival than men with low saturated fat (LSF) diets (26.6 vs. 44.7 months, respectively, p = 0.002). After adjusting for obesity and clinical variables, HSF-diet patients were almost twice as likely to experience biochemical failure (hazard ratio = 1.95, p = 0.008) compared to LSF diet patients. Men who were both obese and consumed HSF diets had the shortest biochemical-failure-free-survival (19 months), and nonobese men who consumed LSF diets had the longest biochemical-failure-free-survival (46 months, p < 0.001). Understanding the interplay between modifiable factors, such as diet and obesity, and disease characteristics may lead to the development of behavioral and/or targeted interventions for patients at increased risk of progression. © 2008 Wiley-Liss, Inc.

Published
2008

49. Randomized Trial of Adjuvant 13-cis-Retinoic Acid and Interferon Alfa for Patients With Aggressive Skin Squamous Cell Carcinoma

Author

J. Jack Lee, Sara S. Strom, Christina A. Meyers, John L. Clifford, Robert L. Collins, Xian Zhou, Mary Jo T. Necesito Reyes, Gary L. Clayman, Abenaa M. Brewster, Anita L. Sabichi, and Scott M. Lippman

Subjects
Adult, Male, Cancer Research, medicine.medical_specialty, Skin Neoplasms, medicine.medical_treatment, Alpha interferon, Interferon alpha-2, Gastroenterology, Internal medicine, Antineoplastic Combined Chemotherapy Protocols, medicine, Carcinoma, Adjuvant therapy, Skin Squamous Cell Carcinoma, Humans, Prospective Studies, Isotretinoin, Survival rate, Interferon alfa, Aged, Aged, 80 and over, Chemotherapy, business.industry, Interferon-alpha, Neoplasms, Second Primary, Middle Aged, Prognosis, medicine.disease, Recombinant Proteins, Surgery, Survival Rate, Oncology, Chemotherapy, Adjuvant, Carcinoma, Squamous Cell, Female, Neoplasm Recurrence, Local, Skin cancer, business, medicine.drug
Abstract

Purpose To conduct a phase III trial of adjuvant 13-cis-retinoic acid (13cRA) plus interferon alfa (IFN-α) for preventing tumor recurrence and second primary tumors (SPTs) of skin squamous cell carcinoma (SCC) among patients with aggressive skin SCC. Patients and Methods Sixty-six patients with aggressive skin SCC were randomly assigned to receive either 6 months of combined 13cRA (1 mg/kg/d orally) and IFN-α (3 × 106 U subcutaneously three times per week) or no adjuvant therapy (control group) after SCC surgery and/or radiation. Results At 21.5 months median follow-up, treatment did not improve the time to tumor recurrence and SPT versus control (hazard ratio [HR], 1.13; 95% CI, 0.53 to 2.41), time to tumor recurrence (HR, 1.08; 95% CI, 0.43 to 2.72), or time to SPT (HR, 0.89; 95% CI, 0.27 to 2.93). Adjuvant 13cRA and IFN-α was moderately tolerable; 29% of patients in the treatment arm required dose reductions for grade 3 or 4 toxicities. Conclusion Results of this phase III trial do not support 13cRA plus IFN-α for adjuvant therapy of aggressive skin SCC. With high rates of tumor recurrence and SPTs, patients with aggressive skin SCC continue to have an unmet medical need, with devastating mortality, morbidity, and financial consequences. Promising agents with preclinical and early clinical results relevant to aggressive skin SCC deserve a high priority for future clinical drug development.

Published
2007

50. 4-Nitroquinoline-1-Oxide-Induced Mutagen Sensitivity and Risk of Nonmelanoma Skin Cancer: A Case–Control Analysis

Author

Randal S. Weber, Scott M. Lippman, Li E. Wang, T. C. Hsu, Ping Xiong, Leonard Harry Goldberg, Gary L. Clayman, Qingyi Wei, Madeleine Duvic, and Sara S. Strom

Subjects
Adult, Male, Pathology, medicine.medical_specialty, Skin Neoplasms, Ultraviolet Rays, 4-Nitroquinoline 1-oxide, Cell, Mutagen, Dermatology, medicine.disease_cause, Biochemistry, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Risk Factors, Humans, Medicine, Basal cell carcinoma, Risk factor, Molecular Biology, Aged, 030304 developmental biology, Aged, 80 and over, 0303 health sciences, integumentary system, business.industry, Case-control study, Chromosome Breakage, Cell Biology, Middle Aged, medicine.disease, 4-Nitroquinoline-1-oxide, 3. Good health, medicine.anatomical_structure, chemistry, Carcinoma, Basal Cell, Case-Control Studies, 030220 oncology & carcinogenesis, Multivariate Analysis, Carcinoma, Squamous Cell, Cancer research, Female, Chromatid, Skin cancer, business, Mutagens
Abstract

The UV radiation-mimetic chemical 4-nitroquinoline-1-oxide (4-NQO) is thought to induce squamous cell carcinoma (SCC) similar to those induced by UV radiation in animals. Therefore, we tested the hypothesis that cellular sensitivity to 4-NQO is associated with risk of developing skin cancer in a case-control study of 191 patients with nonmelanoma skin cancer (NMSC; 81 SCC and 110 basal cell carcinoma (BCC)) and 176 cancer-free controls. Short-term blood cultures were treated with 4-NQO at a final concentration of 10 microM for 24 hours and scored for chromatid breaks in 50 well-spread metaphases. We found that the mean frequency of chromatid breaks per cell (b/c) was significantly higher in the cases (mean+/-SD, 0.46+/-0.43 for SCC and 0.43+/-0.38 for BCC) than in the controls (0.25+/-0.25; P0.001 for both comparisons) and were associated with more-than-twofold increased risk for both SCC and BCC after adjustment for known risk factors. Therefore, our findings support the notion that sensitivity to 4-NQO reflects susceptibility to UV-induced NMSC. However, there is a lack of correlation between UVB-induced b/c and 4-NQO-induced b/c in this study population. Therefore, these findings need to be verified by additional studies.

Published
2007
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results