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1. Novel genetic variants associated with mortality after unrelated donor allogeneic hematopoietic cell transplantation

Author

Hahn, Theresa, Wang, Junke, Preus, Leah M., Karaesmen, Ezgi, Rizvi, Abbas, Clay-Gilmour, Alyssa I., Zhu, Qianqian, Wang, Yiwen, Yan, Li, Liu, Song, Stram, Daniel O., Pooler, Loreall, Sheng, Xin, Haiman, Christopher A., Berg, David Van Den, Webb, Amy, Brock, Guy, Spellman, Stephen R., Onel, Kenan, McCarthy, Philip L., Pasquini, Marcelo C., and Sucheston-Campbell, Lara E.

Published
2021
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2. Working mechanisms of the use and acceptability of ecological momentary interventions: a realist evaluation of a guided self-help ecological momentary intervention targeting self-esteem.

Author

Postma, Mary Rose, Vrancken, Suzanne, Daemen, Maud, Meulen, Iris Hoes-van der, Volbragt, Nele, Delespaul, Philippe, Haan, Lieuwe de, Pluijm, Marieke van der, Breedvelt, Josefien Johanna Froukje, Gaag, Mark van der, Lindauer, Ramon, Berg, David van den, Bockting, Claudi, Amelsvoort, Therese van, Schwannauer, Matthias, Doi, Lawrence, and Reininghaus, Ulrich

Subjects
PSYCHOTHERAPY, SELF-esteem, MOBILE apps, LIFE skills, ADVERSE childhood experiences
Abstract

Background: Technology improves accessibility of psychological interventions for youth. An ecological momentary intervention (EMI) is a digital intervention geared toward intervening in daily life to enhance the generalizability and ecological validity, and to be able to intervene in moments most needed. Identifying working mechanisms of the use of ecological momentary interventions might generate insights to improve interventions. Methods: The present study investigates the working mechanisms of the use and acceptability of an ecological momentary intervention, named SELFIE, targeting self-esteem in youth exposed to childhood trauma, and evaluates under what circumstances these mechanisms of use and acceptability do or do not come into play. A realist evaluation approach was used for developing initial program theories (data: expert interviews and a stakeholders focus group), and subsequently testing (data: 15 interviews with participants, a focus group with therapists, debriefing questionnaire), and refining them. Results: The SELFIE intervention is offered through a smartphone application enabling constant availability of the intervention and thereby increasing accessibility and feasibility. When the intervention was offered on their personal smartphone, this enhanced a sense of privacy and less hesitance in engaging with the app, leading to increased disclosure and active participation. Further, the smartphone application facilitates the practice of skills in daily life, supporting the repeated practice of exercises in different situations leading to the generalizability of the effect. Buffering against technical malfunction seemed important to decrease its possible negative effects. Conclusions: This study enhanced our understanding of possible working mechanisms in EMIs, such as the constant availability supporting increased accessibility and feasibility, for which the use of the personal smartphone was experienced as a facilitating context. Hereby, the current study contributes to relatively limited research in this field. For the field to move forward, mechanisms of use, and acceptability of EMIs need to be understood. It is strongly recommended that alongside efficacy trials of an EMI on specific target mechanisms, a process evaluation is conducted investigating the working mechanisms of use. Trial registration: The current paper reports on a realist evaluation within the SELFIE trial (Netherlands Trial Register NL7129 (NTR7475)). [ABSTRACT FROM AUTHOR]

Published
2024
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3. Testing the combination of Feeling Safe and Peer Counselling against Formulation-Based Cognitive Behavior Therapy to promote Psychological Wellbeing in People with Persecutory Delusions: Study Protocol for a Randomized Controlled Trial (the Feeling Safe-NL Trial).

Author

Tolmeijer, Eva, primary, Waite, Felicity, additional, Isham, Louise, additional, Bringmann, Laura, additional, Timmers, Robin, additional, Berg, Arjan van den, additional, Schuurmans, Hanneke, additional, Staring, Anton B. P., additional, de Bont, Paul, additional, Grunsven, Rob van, additional, Stulp, Gert, additional, Wijnen, Ben, additional, Gaag, Mark van der, additional, Freeman, Daniel, additional, and Berg, David van den, additional

Published
2023
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4. Genome-wide association study of prostate cancer in men of African ancestry identifies a susceptibility locus at 17q21

Author

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

Subjects
Biological Sciences, Genetics, Human Genome, Aging, Urologic Diseases, Prevention, Prostate Cancer, Cancer, 2.1 Biological and endogenous factors, Aetiology, Black or African American, Chromosomes, Human, Pair 17, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Male, Polymorphism, Single Nucleotide, Prostatic Neoplasms, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology
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

5. Multi-ancestry epigenome-wide analyses identify methylated sites associated with aortic augmentation index in TOPMed MESA

Author

Manichaikul, Ani, primary, Hu, Xiaowei, additional, Logan, Jeongok, additional, Kwon, Younghoon, additional, Lima, Joao, additional, Jacobs, David, additional, Duprez, Daniel, additional, Brumback, Lyndia, additional, Taylor, Kent, additional, Durda, Peter, additional, Johnson, Craig, additional, Cornell, Elaine, additional, Guo, Xiuqing, additional, Liu, Yongmei, additional, Tracy, Russell, additional, Blackwell, Thomas, additional, Papanicolaou, George, additional, Mitchell, Gary, additional, Rich, Stephen, additional, Rotter, Jerome, additional, Berg, David Van Den, additional, Chirinos, Julio, additional, Hughes, Timothy, additional, and Garrett-Bakelman, Francine, additional

Published
2023
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6. Trauma-focused Therapies for Posttraumatic Stress in Psychosis: study protocol for the RE.PROCESS randomized controlled trial

Author

Burger, Simone Rosanne, primary, Linden, Tineke van der, additional, Hardy, Amy, additional, de Bont, Paul A. J., additional, Vleugel, Berber van der, additional, Staring, Anton B. P., additional, de Roos, Carlijn, additional, Zelst, Catherine van, additional, Gottlieb, Jennifer D., additional, Mueser, Kim, additional, Minnen, Agnes van, additional, de Jongh, Ad, additional, Marcelis, Machteld, additional, Gaag, Mark van der, additional, and Berg, David van den, additional

Published
2022
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9. Additional file of The association of polymorphisms in hormone metabolism pathway genes, menopausal hormone therapy, and breast cancer risk: a nested case-control study in the California Teachers Study cohort

Author

Eunjung Lee, Schumacher, Fredrick, Lewinger, Juan Pablo, Neuhausen, Susan L, Anton-Culver, Hoda, Horn-Ross, Pamela L, Henderson, Katherine D, Ziogas, Argyrios, Berg, David Van Den, Bernstein, Leslie, and Giske Ursin

Abstract

Additional file of The association of polymorphisms in hormone metabolism pathway genes, menopausal hormone therapy, and breast cancer risk: a nested case-control study in the California Teachers Study cohort

Published
2020
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10. Additional file 2 of The association of polymorphisms in hormone metabolism pathway genes, menopausal hormone therapy, and breast cancer risk: a nested case-control study in the California Teachers Study cohort

Author

Eunjung Lee, Schumacher, Fredrick, Lewinger, Juan Pablo, Neuhausen, Susan L, Anton-Culver, Hoda, Horn-Ross, Pamela L, Henderson, Katherine D, Ziogas, Argyrios, Berg, David Van Den, Bernstein, Leslie, and Giske Ursin

Abstract

Additional file 2: Supplementary Figure S1. A word document of Supplementary Figure S1. (DOCX 29 KB)

Published
2020
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11. Additional file 1 of The association of polymorphisms in hormone metabolism pathway genes, menopausal hormone therapy, and breast cancer risk: a nested case-control study in the California Teachers Study cohort

Author

Eunjung Lee, Schumacher, Fredrick, Lewinger, Juan Pablo, Neuhausen, Susan L, Anton-Culver, Hoda, Horn-Ross, Pamela L, Henderson, Katherine D, Ziogas, Argyrios, Berg, David Van Den, Bernstein, Leslie, and Giske Ursin

Abstract

Additional file 1: Supplementary Table S1. A word document of Supplementary Table S1. (DOCX 20 KB)

Published
2020
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13. Additional file 1: of Growth factor genes and change in mammographic density after stopping combined hormone therapy in the California Teachers Study

Author

Eunjung Lee, Jianning Luo, Schumacher, Fredrick, Berg, David Van Den, Wu, Anna, Stram, Daniel, Bernstein, Leslie, and Giske Ursin

Abstract

Table S1. Comparison of characteristics of women who were included in the analyses with characteristics of participants who were included in the longitudinal set (i.e. both on-EPT and off-EPT mammograms were available) but excluded from the analyses. (DOCX 14 kb)

Published
2018
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15. The effect of the cyclin D1 (CCND1) A870G polymorphism on colorectal cancer risk is modified by glutathione-S-transferase polymorphisms and isothiocyanate intake in the Singapore Chinese Health Study

Author

Probst-Hensch, Nicole M., Sun, Can-Lan, Berg, David Van Den, Ceschi, Michela, Koh, Woon-Puay, Yu, Mimi C., Probst-Hensch, Nicole M., Sun, Can-Lan, Berg, David Van Den, Ceschi, Michela, Koh, Woon-Puay, and Yu, Mimi C.

Abstract

Cyclin D1 (CCND1) regulates cellular decision between proliferation and growth arrest. Despite the functional relevance of the CCND1 A870G single nucleotide polymorphism (SNP) published results on its association with colorectal cancer (CRC) were inconsistent. We examined the association between this CCND1 genotype and CRC in the Singapore Chinese Health Study, a prospective investigation of diet and cancer in 63 000 Chinese men and women. We explored the hypothesis that inconsistency regarding the CCND1/CRC association may be attributable to the modifying effect of additional CRC risk factors. Since GSTM1/GSTT1 genotype and dietary isothiocyanate (ITC) intake had previously been identified as CRC risk factors in this cohort, we now explored if they influenced the CCND1/CRC association. In a nested case-control study within the Singapore Cohort, genomic DNA collected from 300 incident CRC cases and 1169 controls was examined for CCND1, GSTM1, GSTT1 and GSTP1 polymorphisms. Unconditional logistic regression was used to assess genotype effects on cancer risk. No main effect of CCND1 was observed, yet the CCND1 effect was influenced by ITC intake and GST genotypes. The presence of at least one CCND1 A-allele was associated with increased risk among low dietary ITC consumers (intake below median value for the cohort) with a high-activity GST profile (≥2 of the 3 GST genotypes classified non-null or high-activity) [odds ratio (OR) = 2.05; 95% confidence interval (CI), 1.10-3.82]. In contrast, the presence of at least one A-allele was associated with a decreased risk among all remaining subjects (OR = 0.56; 0.36-0.86) (P for interaction = 0.01). Recent studies indicate that ITCs inhibit cell proliferation and cause apoptosis through pro-oxidant properties. The results of our current study on CRC and those of our previous breast cancer study are compatible with the notion of oxidative stress in target cells as important determinant of direction and magnitude of the CCND1 e

Published
2017

16. 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

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

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 P-Conditional = 2.36 x 10(-8); Region 4: rs2736098, P = 3.87 x 10(-12) and P-Conditional = 5.19 x 10(-6), Region 5: rs13172201, P = 0.041 and P-Conditional = 2.04 x 10(-6); and Region 6: rs10069690, P = 7.49 x 10 215 and P-Conditional = 5.35 x 10(-7)) and one in the neighboring CLPTM1L gene(Region 2: rs451360; P = 1.90 x 10(-18) and P-Conditional = 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

18. Abstract LB-282: Transethnic genome-wide association study of colorectal cancer identifies a new susceptibility locus in VTI1A

Author

Wang, Hansong, primary, Burnett, Terrilea, additional, Kono, Suminori, additional, Haiman, Christopher, additional, Iwasaki, Motoki, additional, Wilkens, Lynne, additional, Loo, Lenora, additional, Berg, David Van Den, additional, Kolonel, Laurence, additional, Henderson, Brian, additional, Keku, Temitope, additional, Sandler, Robert, additional, Signorello, Lisa, additional, Blot, William, additional, Newcomb, Polly, additional, Pande, Mala, additional, Amos, Christopher, additional, West, Dee, additional, Bézieau, Stéphane, additional, Berndt, Sonja, additional, Zanke, Brent, additional, Hsu, Li, additional, Lindor, Noralane, additional, Haile, Robert, additional, Hopper, John, additional, Jenkins, Mark, additional, Gallinger, Steven, additional, Casey, Graham, additional, Stenzel, Stephanie, additional, Schumacher, Fredrick, additional, Peters, Ulrike, additional, Gruber, Stephen, additional, Tsugane, Shoichiro, additional, Stram, Dan, additional, and Marchand, Loic L., additional

Published
2014
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20. Abstract 4647: 4-Aminobiphenyl hemoglobin adducts in relation to risk of bladder cancer among lifelong nonsmokers

Author

Tao, Li, primary, Day, Billy W., additional, Hu, Bibin, additional, Xiang, Yong-Bing, additional, Wang, Renwei, additional, Stern, Mariana C., additional, Gago-Dominguez, Manuela, additional, Cortessis, Victoria K., additional, Conti, David V., additional, Berg, David Van Den, additional, Pike, Malcolm C., additional, Gao, Yu-Tang, additional, Yu, Mimi C., additional, and Yuan, Jian-Min, additional

Published
2011
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24. Role of inducible nitric oxide synthase in asthma risk and lung function growth during adolescence.

Author

Islam, Talat, Breton, Carrie, Salam, Muhammad T., McConnell, Rob, Wenten, Made, Gauderman, W. James, Conti, David, Berg, David Van Den, Peters, John M., and Gilliland, Frank D.

Subjects
NUCLEOTIDE sequence, NITRIC oxide, CHILDREN'S health, GENETIC polymorphisms, ASTHMA risk factors, OXIDATIVE stress, REACTIVE nitrogen species
Abstract

Background Inducible nitric oxide (NO) synthase (iNOS, encoded by NOS2A) produces NO in response to environmental stimuli, which can result in nitrosative stress. Because nitrosative stress affects respiratory health, it was hypothesised that variants in NOS2A are associated with asthma incidence and lung function growth during adolescence. Methods In this prospective study, spirometric testing was performed at school and a presence or absence of asthma was ascertained annually by questionnaire among children participating in the Southern California Children's Health Study. 24 single nucleotide polymorphisms (SNPs) of the NOS2A region (with seven promoter SNPs in one haplotype block), spanning 20 kb upstream and 10 kb downstream were genotyped. Association between the NOS2A region and asthma or lung function growth was tested using genetic blockspecific principal component and haplotype analyses. This study was restricted to children with Latino and Caucasian ancestry for analyses of both asthma (n=1596) and lung function growth (n=2108). Result A pair of "yineyang" haplotypes in the promoter region showed strong association with new-onset asthma and lung function growth. The "yin" haplotype (h0111101) was associated with 44% increased asthma risk (p=0.003) and reduced forced expiratory volume in 1 s (FEV1) growth from 10 to 18 years of age ( 29.46 ml, p=0.07), whereas the "yang"(h1000010) haplotype was associated with 23% reduced asthma risk (p=0.13) and better FEV1 growth (43.84 ml, p=0.01). Furthermore, the increased asthma risk associated with h0111101 was restricted to children with the GSTM1 "null" genotype (interaction p=0.002, HR 1.89, 95% CI 1.34 to 2.60). Conclusion Common haplotypes in the NOS2A promoter are associated with new-onset asthma and lung function growth. These effects are stronger in adolescents with the GSTM1 "null" genotype. [ABSTRACT FROM AUTHOR]

Published
2010
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25. Trans-ethnic genome-wide association study of colorectal cancer identifies a new susceptibility locus in VTI1A

Author

Wang, Hansong, Burnett, Terrilea, Kono, Suminori, Haiman, Christopher A., Iwasaki, Motoki, Wilkens, Lynne R., Loo, Lenora W.M., Berg, David Van Den, Kolonel, Laurence N., Henderson, Brian E., Keku, Temitope O., Sandler, Robert S., Signorello, Lisa B., Blot, William J., Newcomb, Polly A., Pande, Mala, Amos, Christopher I., West, Dee W., Bézieau, Stéphane, Berndt, Sonja I., Zanke, Brent W., Hsu, Li, Lindor, Noralane M., Haile, Robert W., Hopper, John L., Jenkins, Mark A., Gallinger, Steven, Casey, Graham, Stenzel, Stephanie L., Schumacher, Fredrick R., Peters, Ulrike, Gruber, Stephen B., Tsugane, Shoichiro, Stram, Daniel O., and Marchand, Loïc Le

Abstract

The genetic basis of sporadic colorectal cancer (CRC) is not well explained by known risk polymorphisms. Here we perform a meta-analysis of two genome-wide association studies in 2,627 cases and 3,797 controls of Japanese ancestry and 1,894 cases and 4,703 controls of African ancestry, to identify genetic variants that contribute to CRC susceptibility. We replicate genome-wide statistically significant associations (P < 5×10−8) in 16,823 cases and 18,211 controls of European ancestry. This study reveals a new pan-ethnic CRC risk locus at 10q25 (rs12241008, intronic to VTI1A; P=1.4×10−9), providing additional insight into the etiology of CRC and highlighting the value of association mapping in diverse populations.

Published
2014
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26. GWAS meta-analysis and replication identifies three new susceptibility loci for ovarian cancer

Author

Pharoah, Paul D. P., Tsai, Ya-Yu, Ramus, Susan J., Phelan, Catherine M., Goode, Ellen L., Lawrenson, Kate, Price, Melissa, Fridley, Brooke L., Tyrer, Jonathan P., Shen, Howard, Weber, Rachel, Karevan, Rod, Larson, Melissa C., Song, Honglin, Tessier, Daniel C., Bacot, François, Vincent, Daniel, Cunningham, Julie M., Dennis, Joe, Dicks, Ed, Aben, Katja K., Anton-Culver, Hoda, Antonenkova, Natalia, Armasu, Sebastian M., Baglietto, Laura, Bandera, Elisa V., Beckmann, Matthias W., Birrer, Michael J., Bloom, Greg, Bogdanova, Natalia, Brenton, James D., Brinton, Louise A., Brooks-Wilson, Angela, Brown, Robert, Butzow, Ralf, Campbell, Ian, Carney, Michael E, Carvalho, Renato S., Chang-Claude, Jenny, Chen, Y. Anne, Chen, Zhihua, Chow, Wong-Ho, Cicek, Mine S., Coetzee, Gerhard, Cook, Linda S., Cramer, Daniel W., Cybulski, Cezary, Dansonka-Mieszkowska, Agnieszka, Despierre, Evelyn, Doherty, Jennifer A, Dörk, Thilo, du Bois, Andreas, Dürst, Matthias, Eccles, Diana, Edwards, Robert, Ekici, Arif B., Fasching, Peter A., Fenstermacher, David, Flanagan, James, Gao, Yu-Tang, Garcia-Closas, Montserrat, Gentry-Maharaj, Aleksandra, Giles, Graham, Gjyshi, Anxhela, Gore, Martin, Gronwald, Jacek, Guo, Qi, Halle, Mari K, Harter, Philipp, Hein, Alexander, Heitz, Florian, Hillemanns, Peter, Hoatlin, Maureen, Høgdall, Estrid, Høgdall, Claus K., Hosono, Satoyo, Jakubowska, Anna, Jensen, Allan, Kalli, Kimberly R., Karlan, Beth Y., Kelemen, Linda E., Kiemeney, Lambertus A., Kjaer, Susanne Krüger, Konecny, Gottfried E., Krakstad, Camilla, Kupryjanczyk, Jolanta, Lambrechts, Diether, Lambrechts, Sandrina, Le, Nhu D., Lee, Nathan, Lee, Janet, Leminen, Arto, Lim, Boon Kiong, Lissowska, Jolanta, Lubiński, Jan, Lundvall, Lene, Lurie, Galina, Massuger, Leon F.A.G., Matsuo, Keitaro, McGuire, Valerie, McLaughlin, John R, Menon, Usha, Modugno, Francesmary, Moysich, Kirsten B., Nakanishi, Toru, Narod, Steven A., Ness, Roberta B., Nevanlinna, Heli, Nickels, Stefan, Noushmehr, Houtan, Odunsi, Kunle, Olson, Sara, Orlow, Irene, Paul, James, Pejovic, Tanja, Pelttari, Liisa M, Permuth-Wey, Jenny, Pike, Malcolm C, Poole, Elizabeth M, Qu, Xiaotao, Risch, Harvey A., Rodriguez-Rodriguez, Lorna, Rossing, Mary Anne, Rudolph, Anja, Runnebaum, Ingo, Rzepecka, Iwona K, Salvesen, Helga B., Schwaab, Ira, Severi, Gianluca, Shen, Hui, Shridhar, Vijayalakshmi, Shu, Xiao-Ou, Sieh, Weiva, Southey, Melissa C., Spellman, Paul, Tajima, Kazuo, Teo, Soo-Hwang, Terry, Kathryn L., Thompson, Pamela J, Timorek, Agnieszka, Tworoger, Shelley S., van Altena, Anne M., Berg, David Van Den, Vergote, Ignace, Vierkant, Robert A., Vitonis, Allison F., Wang-Gohrke, Shan, Wentzensen, Nicolas, Whittemore, Alice S., Wik, Elisabeth, Winterhoff, Boris, Woo, Yin Ling, Wu, Anna H, Yang, Hannah P., Zheng, Wei, Ziogas, Argyrios, Zulkifli, Famida, Goodman, Marc T., Hall, Per, Easton, Douglas F, Pearce, Celeste L, Berchuck, Andrew, Chenevix-Trench, Georgia, Iversen, Edwin, Monteiro, Alvaro N.A., Gayther, Simon A., Schildkraut, Joellen M., and Sellers, Thomas A.

Abstract

Genome wide association studies (GWAS) have identified four susceptibility loci for epithelial ovarian cancer (EOC) with another two loci being close to genome-wide significance. We pooled data from a GWAS conducted in North America with another GWAS from the United Kingdom. We selected the top 24,551 SNPs for inclusion on the iCOGS custom genotyping array. Follow-up genotyping was carried out in 18,174 cases and 26,134 controls from 43 studies from the Ovarian Cancer Association Consortium. We validated the two loci at 3q25 and 17q21 previously near genome-wide significance and identified three novel loci associated with risk; two loci associated with all EOC subtypes, at 8q21 (rs11782652, P=5.5×10-9) and 10p12 (rs1243180; P=1.8×10-8), and another locus specific to the serous subtype at 17q12 (rs757210; P=8.1×10-10). An integrated molecular analysis of genes and regulatory regions at these loci provided evidence for functional mechanisms underlying susceptibility that implicates CHMP4C in the pathogenesis of ovarian cancer.

Published
2013
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27. Interaction molecular QTL mapping discovers cellular and environmental modifiers of genetic regulatory effects.

Author

Kasela S, Aguet F, Kim-Hellmuth S, Brown BC, Nachun DC, Tracy RP, Durda P, Liu Y, Taylor KD, Craig Johnson W, Berg DVD, Gabriel S, Gupta N, Smith JD, Blackwell TW, Rotter JI, Ardlie KG, Manichaikul A, Rich SS, Graham Barr R, and Lappalainen T

Abstract

Bulk tissue molecular quantitative trait loci (QTLs) have been the starting point for interpreting disease-associated variants, while context-specific QTLs show particular relevance for disease. Here, we present the results of mapping interaction QTLs (iQTLs) for cell type, age, and other phenotypic variables in multi-omic, longitudinal data from blood of individuals of diverse ancestries. By modeling the interaction between genotype and estimated cell type proportions, we demonstrate that cell type iQTLs could be considered as proxies for cell type-specific QTL effects. The interpretation of age iQTLs, however, warrants caution as the moderation effect of age on the genotype and molecular phenotype association may be mediated by changes in cell type composition. Finally, we show that cell type iQTLs contribute to cell type-specific enrichment of diseases that, in combination with additional functional data, may guide future functional studies. Overall, this study highlights iQTLs to gain insights into the context-specificity of regulatory effects., Competing Interests: Declaration of interests T.L. advises Variant Bio, Goldfinch Bio, GlaxoSmithKline, and Pfizer and has equity in Variant Bio.

Published
2023
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28. Genome-wide association studies identify four ER negative-specific breast cancer risk loci.

Author

Garcia-Closas M, Couch FJ, Lindstrom S, Michailidou K, Schmidt MK, Brook MN, Orr N, Rhie SK, Riboli E, Feigelson HS, Le Marchand L, Buring JE, Eccles D, Miron P, Fasching PA, Brauch H, Chang-Claude J, Carpenter J, Godwin AK, Nevanlinna H, Giles GG, Cox A, Hopper JL, Bolla MK, Wang Q, Dennis J, Dicks E, Howat WJ, Schoof N, Bojesen SE, Lambrechts D, Broeks A, Andrulis IL, Guénel P, Burwinkel B, Sawyer EJ, Hollestelle A, Fletcher O, Winqvist R, Brenner H, Mannermaa A, Hamann U, Meindl A, Lindblom A, Zheng W, Devillee P, Goldberg MS, Lubinski J, Kristensen V, Swerdlow A, Anton-Culver H, Dörk T, Muir K, Matsuo K, Wu AH, Radice P, Teo SH, Shu XO, Blot W, Kang D, Hartman M, Sangrajrang S, Shen CY, Southey MC, Park DJ, Hammet F, Stone J, Veer LJ, Rutgers EJ, Lophatananon A, Stewart-Brown S, Siriwanarangsan P, Peto J, Schrauder MG, Ekici AB, Beckmann MW, Dos Santos Silva I, Johnson N, Warren H, Tomlinson I, Kerin MJ, Miller N, Marme F, Schneeweiss A, Sohn C, Truong T, Laurent-Puig P, Kerbrat P, Nordestgaard BG, Nielsen SF, Flyger H, Milne RL, Perez JI, Menéndez P, Müller H, Arndt V, Stegmaier C, Lichtner P, Lochmann M, Justenhoven C, Ko YD, Muranen TA, Aittomäki K, Blomqvist C, Greco D, Heikkinen T, Ito H, Iwata H, Yatabe Y, Antonenkova NN, Margolin S, Kataja V, Kosma VM, Hartikainen JM, Balleine R, Tseng CC, Berg DV, Stram DO, Neven P, Dieudonné AS, Leunen K, Rudolph A, Nickels S, Flesch-Janys D, Peterlongo P, Peissel B, Bernard L, Olson JE, Wang X, Stevens K, Severi G, Baglietto L, McLean C, Coetzee GA, Feng Y, Henderson BE, Schumacher F, Bogdanova NV, Labrèche F, Dumont M, Yip CH, Taib NA, Cheng CY, Shrubsole M, Long J, Pylkäs K, Jukkola-Vuorinen A, Kauppila S, Knight JA, Glendon G, Mulligan AM, Tollenaar RA, Seynaeve CM, Kriege M, Hooning MJ, van den Ouweland AM, van Deurzen CH, Lu W, Gao YT, Cai H, Balasubramanian SP, Cross SS, Reed MW, Signorello L, Cai Q, Shah M, Miao H, Chan CW, Chia KS, Jakubowska A, Jaworska K, Durda K, Hsiung CN, Wu PE, Yu JC, Ashworth A, Jones M, Tessier DC, González-Neira A, Pita G, Alonso MR, Vincent D, Bacot F, Ambrosone CB, Bandera EV, John EM, Chen GK, Hu JJ, Rodriguez-Gil JL, Bernstein L, Press MF, Ziegler RG, Millikan RM, Deming-Halverson SL, Nyante S, Ingles SA, Waisfisz Q, Tsimiklis H, Makalic E, Schmidt D, Bui M, Gibson L, Müller-Myhsok B, Schmutzler RK, Hein R, Dahmen N, Beckmann L, Aaltonen K, Czene K, Irwanto A, Liu J, Turnbull C, Rahman N, Meijers-Heijboer H, Uitterlinden AG, Rivadeneira F, Olswold C, Slager S, Pilarski R, Ademuyiwa F, Konstantopoulou I, Martin NG, Montgomery GW, Slamon DJ, Rauh C, Lux MP, Jud SM, Bruning T, Weaver J, Sharma P, Pathak H, Tapper W, Gerty S, Durcan L, Trichopoulos D, Tumino R, Peeters PH, Kaaks R, Campa D, Canzian F, Weiderpass E, Johansson M, Khaw KT, Travis R, Clavel-Chapelon F, Kolonel LN, Chen C, Beck A, Hankinson SE, Berg CD, Hoover RN, Lissowska J, Figueroa JD, Chasman DI, Gaudet MM, Diver WR, Willett WC, Hunter DJ, Simard J, Benitez J, Dunning AM, Sherman ME, Chenevix-Trench G, Chanock SJ, Hall P, Pharoah PD, Vachon C, Easton DF, Haiman CA, and Kraft P

Subjects
Breast Neoplasms metabolism, Breast Neoplasms pathology, Case-Control Studies, Cooperative Behavior, Female, Genome-Wide Association Study, Genotype, Humans, Meta-Analysis as Topic, Oligonucleotide Array Sequence Analysis, Receptors, Estrogen genetics, Risk Factors, Breast Neoplasms etiology, Genetic Loci genetics, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide genetics, Receptors, Estrogen metabolism
Abstract

Estrogen receptor (ER)-negative tumors represent 20-30% of all breast cancers, with a higher proportion occurring in younger women and women of African ancestry. The etiology and clinical behavior of ER-negative tumors are different from those of tumors expressing ER (ER positive), including differences in genetic predisposition. To identify susceptibility loci specific to ER-negative disease, we combined in a meta-analysis 3 genome-wide association studies of 4,193 ER-negative breast cancer cases and 35,194 controls with a series of 40 follow-up studies (6,514 cases and 41,455 controls), genotyped using a custom Illumina array, iCOGS, developed by the Collaborative Oncological Gene-environment Study (COGS). SNPs at four loci, 1q32.1 (MDM4, P = 2.1 × 10(-12) and LGR6, P = 1.4 × 10(-8)), 2p24.1 (P = 4.6 × 10(-8)) and 16q12.2 (FTO, P = 4.0 × 10(-8)), were associated with ER-negative but not ER-positive breast cancer (P > 0.05). These findings provide further evidence for distinct etiological pathways associated with invasive ER-positive and ER-negative breast cancers.

Published
2013
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