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7. Epithelial-Mesenchymal Transition (EMT) Gene Variants and Epithelial Ovarian Cancer (EOC) Risk.

Author

Amankwah, Ernest K, Lin, Hui-Yi, Tyrer, Jonathan P, Lawrenson, Kate, Dennis, Joe, Chornokur, Ganna, Aben, Katja KH, Anton-Culver, Hoda, Antonenkova, Natalia, Bruinsma, Fiona, Bandera, Elisa V, Bean, Yukie T, Beckmann, Matthias W, Bisogna, Maria, Bjorge, Line, Bogdanova, Natalia, Brinton, Louise A, Brooks-Wilson, Angela, Bunker, Clareann H, Butzow, Ralf, Campbell, Ian G, Carty, Karen, Chen, Zhihua, Chen, Y Ann, Chang-Claude, Jenny, Cook, Linda S, Cramer, Daniel W, Cunningham, Julie M, Cybulski, Cezary, Dansonka-Mieszkowska, Agnieszka, du Bois, Andreas, Despierre, Evelyn, Dicks, Ed, Doherty, Jennifer A, Dörk, Thilo, Dürst, Matthias, Easton, Douglas F, Eccles, Diana M, Edwards, Robert P, Ekici, Arif B, Fasching, Peter A, Fridley, Brooke L, Gao, Yu-Tang, Gentry-Maharaj, Aleksandra, Giles, Graham G, Glasspool, Rosalind, Goodman, Marc T, Gronwald, Jacek, Harrington, Patricia, Harter, Philipp, Hasmad, Hanis N, Hein, Alexander, Heitz, Florian, Hildebrandt, Michelle AT, Hillemanns, Peter, Hogdall, Claus K, Hogdall, Estrid, Hosono, Satoyo, Iversen, Edwin S, Jakubowska, Anna, Jensen, Allan, Ji, Bu-Tian, Karlan, Beth Y, Jim, Heather, Kellar, Melissa, Kiemeney, Lambertus A, Krakstad, Camilla, Kjaer, Susanne K, Kupryjanczyk, Jolanta, Lambrechts, Diether, Lambrechts, Sandrina, Le, Nhu D, Lee, Alice W, Lele, Shashi, Leminen, Arto, Lester, Jenny, Levine, Douglas A, Liang, Dong, Lim, Boon Kiong, Lissowska, Jolanta, Lu, Karen, Lubinski, Jan, Lundvall, Lene, Massuger, Leon FAG, Matsuo, Keitaro, McGuire, Valerie, McLaughlin, John R, McNeish, Ian, Menon, Usha, Milne, Roger L, Modugno, Francesmary, Moysich, Kirsten B, Ness, Roberta B, Nevanlinna, Heli, Eilber, Ursula, Odunsi, Kunle, Olson, Sara H, Orlow, Irene, Orsulic, Sandra, and Weber, Rachel Palmieri

Subjects
Georgia Chenevix-Trench on behalf of the AOCS management group, Humans, Neoplasms, Glandular and Epithelial, Ovarian Neoplasms, Genetic Predisposition to Disease, Odds Ratio, Risk, Genotype, Polymorphism, Single Nucleotide, Adult, Aged, Middle Aged, European Continental Ancestry Group, Female, Genome-Wide Association Study, Epithelial-Mesenchymal Transition, Carcinoma, Ovarian Epithelial, epithelial-mesenchymal transition, ovarian cancer, single-nucleotide polymorphisms, Neoplasms, Glandular and Epithelial, Polymorphism, Single Nucleotide, Carcinoma, Ovarian Epithelial, Epidemiology, Public Health and Health Services, Genetics
Abstract

Epithelial-mesenchymal transition (EMT) is a process whereby epithelial cells assume mesenchymal characteristics to facilitate cancer metastasis. However, EMT also contributes to the initiation and development of primary tumors. Prior studies that explored the hypothesis that EMT gene variants contribute to epithelial ovarian carcinoma (EOC) risk have been based on small sample sizes and none have sought replication in an independent population. We screened 15,816 single-nucleotide polymorphisms (SNPs) in 296 genes in a discovery phase using data from a genome-wide association study of EOC among women of European ancestry (1,947 cases and 2,009 controls) and identified 793 variants in 278 EMT-related genes that were nominally (P < 0.05) associated with invasive EOC. These SNPs were then genotyped in a larger study of 14,525 invasive-cancer patients and 23,447 controls. A P-value

Published
2015

8. Common Genetic Variation In Cellular Transport Genes and Epithelial Ovarian Cancer (EOC) Risk

Author

Chornokur, Ganna, Lin, Hui-Yi, Tyrer, Jonathan P, Lawrenson, Kate, Dennis, Joe, Amankwah, Ernest K, Qu, Xiaotao, Tsai, Ya-Yu, Jim, Heather SL, Chen, Zhihua, Chen, Ann Y, Permuth-Wey, Jennifer, Aben, Katja KH, Anton-Culver, Hoda, Antonenkova, Natalia, Bruinsma, Fiona, Bandera, Elisa V, Bean, Yukie T, Beckmann, Matthias W, Bisogna, Maria, Bjorge, Line, Bogdanova, Natalia, Brinton, Louise A, Brooks-Wilson, Angela, Bunker, Clareann H, Butzow, Ralf, Campbell, Ian G, Carty, Karen, Chang-Claude, Jenny, Cook, Linda S, Cramer, Daniel W, Cunningham, Julie M, Cybulski, Cezary, Dansonka-Mieszkowska, Agnieszka, du Bois, Andreas, Despierre, Evelyn, Dicks, Ed, Doherty, Jennifer A, Dörk, Thilo, Dürst, Matthias, Easton, Douglas F, Eccles, Diana M, Edwards, Robert P, Ekici, Arif B, Fasching, Peter A, Fridley, Brooke L, Gao, Yu-Tang, Gentry-Maharaj, Aleksandra, Giles, Graham G, Glasspool, Rosalind, Goodman, Marc T, Gronwald, Jacek, Harrington, Patricia, Harter, Philipp, Hein, Alexander, Heitz, Florian, Hildebrandt, Michelle AT, Hillemanns, Peter, Hogdall, Claus K, Hogdall, Estrid, Hosono, Satoyo, Jakubowska, Anna, Jensen, Allan, Ji, Bu-Tian, Karlan, Beth Y, Kelemen, Linda E, Kellar, Mellissa, Kiemeney, Lambertus A, Krakstad, Camilla, Kjaer, Susanne K, Kupryjanczyk, Jolanta, Lambrechts, Diether, Lambrechts, Sandrina, Le, Nhu D, Lee, Alice W, Lele, Shashi, Leminen, Arto, Lester, Jenny, Levine, Douglas A, Liang, Dong, Lim, Boon Kiong, Lissowska, Jolanta, Lu, Karen, Lubinski, Jan, Lundvall, Lene, Massuger, Leon FAG, Matsuo, Keitaro, McGuire, Valerie, McLaughlin, John R, McNeish, Iain, Menon, Usha, Milne, Roger L, Modugno, Francesmary, Moysich, Kirsten B, Ness, Roberta B, Nevanlinna, Heli, Eilber, Ursula, Odunsi, Kunle, Olson, Sara H, and Orlow, Irene

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Genetics, Cancer, Ovarian Cancer, Rare Diseases, 2.1 Biological and endogenous factors, Aetiology, Black or African American, Alleles, Asian, Biological Transport, Carcinoma, Ovarian Epithelial, Carrier Proteins, Case-Control Studies, Female, Genetic Association Studies, Genetic Predisposition to Disease, Genetic Variation, Humans, Neoplasms, Glandular and Epithelial, Odds Ratio, Ovarian Neoplasms, Polymorphism, Single Nucleotide, Risk, Georgia Chenevix-Trench, AOCS management group, General Science & Technology
Abstract

BackgroundDefective cellular transport processes can lead to aberrant accumulation of trace elements, iron, small molecules and hormones in the cell, which in turn may promote the formation of reactive oxygen species, promoting DNA damage and aberrant expression of key regulatory cancer genes. As DNA damage and uncontrolled proliferation are hallmarks of cancer, including epithelial ovarian cancer (EOC), we hypothesized that inherited variation in the cellular transport genes contributes to EOC risk.MethodsIn total, DNA samples were obtained from 14,525 case subjects with invasive EOC and from 23,447 controls from 43 sites in the Ovarian Cancer Association Consortium (OCAC). Two hundred seventy nine SNPs, representing 131 genes, were genotyped using an Illumina Infinium iSelect BeadChip as part of the Collaborative Oncological Gene-environment Study (COGS). SNP analyses were conducted using unconditional logistic regression under a log-additive model, and the FDR q

Published
2015

9. Polymorphisms in Stromal Genes and Susceptibility to Serous Epithelial Ovarian Cancer: A Report from the Ovarian Cancer Association Consortium

Author

Amankwah, Ernest K., Wang, Qinggang, Schildkraut, Joellen M., Tsai, Ya-Yu, Ramus, Susan J., Fridley, Brooke L., Beesley, Jonathan, Johnatty, Sharon E., Webb, Penelope M., Chenevix-Trench, Georgia, Dale, Laura C., Lambrechts, Diether, Amant, Frederic, Despierre, Evelyn, Vergote, Ignace, Gayther, Simon A., Gentry-Maharaj, Aleksandra, Menon, Usha, Chang-Claude, Jenny, Wang-Gohrke, Shan, Anton-Culver, Hoda, Ziogas, Argyrios, Dork, Thilo, Durst, Matthias, Antonenkova, Natalia, Bogdanova, Natalia, Brown, Robert, Flanagan, James M., Kaye, Stanley B., Paul, James, Butzow, Ralf, Nevanlinna, Heli, Campbell, Ian, Eccles, Diana M., Karlan, Beth Y., Gross, Jenny, Walsh, Christine, Pharoah, Paul P., Song, Honglin, Kruger Kjaer, Susanne, H?gdall, Estrid, H?gdall, Claus, Lundvall, Lene, Nedergaard, Lotte, Kiemeney, Lambertus M., Massuger, Leon G., van Altena, Anne M., Vermeulen, Sita M., Le, Nhu D., Brooks-Wilson, Angela, Cook, Linda S., Phelan, Catherine M., Cunningham, Julie M., Vachon, Celine M., Vierkant, Robert A., Iversen, Edwin S., Berchuck, Andrew, Goode, Ellen L., Sellers, Thomas A., and Kelemen, Linda E.

Subjects
growth-factor-beta, genome-wide association, mammary-gland, tgf-beta, oral-contraceptives, expression, decorin, risk, carcinoma, trends
Abstract

Alterations in stromal tissue components can inhibit or promote epithelial tumorigenesis. Decorin (DCN) and lumican (LUM) show reduced stromal expression in serous epithelial ovarian cancer (sEOC). We hypothesized that common variants in these genes associate with risk. Associations with sEOC among Caucasians were estimated with odds ratios (OR) among 397 cases and 920 controls in two U.S.-based studies (discovery set), 436 cases and 1,098 controls in Australia (replication set 1) and a consortium of 15 studies comprising 1,668 cases and 4,249 controls (replication set 2). The discovery set and replication set 1 (833 cases and 2,013 controls) showed statistically homogeneous (Pheterogeneity≥0.48) decreased risks of sEOC at four variants: DCN rs3138165, rs13312816 and rs516115, and LUM rs17018765 (OR = 0.6 to 0.9; Ptrend = 0.001 to 0.03). Results from replication set 2 were statistically homogeneous (Pheterogeneity≥0.13) and associated with increased risks at DCN rs3138165 and rs13312816, and LUM rs17018765: all ORs = 1.2; Ptrend≤0.02. The ORs at the four variants were statistically heterogeneous across all 18 studies (Pheterogeneity≤0.03), which precluded combining. In post-hoc analyses, interactions were observed between each variant and recruitment period (Pinteraction≤0.003), age at diagnosis (Pinteraction = 0.04), and year of diagnosis (Pinteraction = 0.05) in the five studies with available information (1,044 cases, 2,469 controls). We conclude that variants in DCN and LUM are not directly associated with sEOC, and that confirmation of possible effect modification of the variants by non-genetic factors is required.

Published
2011

11. Abstract 6507: E3 ubiquitin-protein ligase, tetratricopeptide repeat domain 3 (TTC3), H4 clustered histone 5 (H4C5), and epithelial cell adhesion molecule (EpCAM) are novel urine-enriched liquid biopsy biomarkers to detect prostate cancer in men

Author

Perera, Ranjan Joseph, primary, Moschovas, Marcio, additional, Perera, Roshane, additional, Lee, Bongyong, additional, Miller, Alexandra, additional, Amankwah, Ernest K., additional, Pokhrel, Rudramani, additional, Pavlovich, Christian, additional, Sonpavde, Guru, additional, and Patel, Vipul, additional

Published
2023
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13. Risk of venous thromboembolism in pediatric hospitalized patients undergoing noncardiac surgery: A report from the Children's Hospital‐Acquired Thrombosis consortium

Author

Stephens, Elizabeth T., primary, Nguyen, Anh Thy H., additional, Jaffray, Julie, additional, Branchford, Brian, additional, Amankwah, Ernest K., additional, Goldenberg, Neil A., additional, Faustino, E. Vincent S., additional, Zakai, Neil A., additional, Stillings, Amy, additional, Krava, Emily, additional, Young, Guy, additional, and Fargo, John H., additional

Published
2022
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14. Cohorts and consortia conference: a summary report (Banff, Canada, June 17-19, 2009)

Author

Boffetta, Paolo, Colditz, Graham A., Potter, John D., Kolonel, Laurence, Robson, Paula J., Malekzadeh, Reza, Seminara, Daniela, Goode, Ellen L., Yoo, Keun-Young, Demers, Paul, Gallagher, Richard, Prentice, Ross, Yasui, Yutaka, O'Doherty, Kieran, Petersen, Gloria M., Ulrich, Cornelia M., Csizmadi, Ilona, Amankwah, Ernest K., Brockton, Nigel T., Kopciuk, Karen, McGregor, S. Elizabeth, and Kelemen, Linda E.

Published
2011

15. Abstract 8999: Impact of Coronavirus 2019 on Pediatric and Adult Heart Transplantation Waitlist Activity and Mortality in the United States

Author

Ashfaq, Awais, primary, Gray, Geoffrey, additional, Carapellucci, Jennifer, additional, Amankwah, Ernest K, additional, Ahumada, Luis M, additional, PUCHALSKI, Michael, additional, Smith, Andrew, additional, Rehman, Mohamed, additional, Quintessenza, James A, additional, and Asante-Korang, Alfred, additional

Published
2021
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16. Corrigendum to ‘Evaluation of Venous Thromboembolism Risk Factors Reveals Subtype Heterogenicity in Children with Central Venous Catheters: A Multi-Center Study from the CHAT Consortium’ [Journal of Thrombosis and Haemostasis 21/9 (2023) 2441 - 2450]

Author

Jaffray, Julie, Mosha, Maua, Branchford, Brian, Goldenberg, Neil A., Silvey, Michael, Croteau, Stacy E., Fargo, John H., Cooper, James D., Bakeer, Nihal, Stillings, Amy, Krava, Emily, Young, Guy, and Amankwah, Ernest K.

Published
2023
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22. Heliox Prescribing Trends for Pediatric Critical Asthma.

Author

Lew, Alicia, Morrison, John M., Amankwah, Ernest K., and Sochet, Anthony A.

Subjects
DRUG therapy for asthma, ASTHMA-related mortality, RESEARCH, CONFIDENCE intervals, HELIUM, CONTINUING education units, RETROSPECTIVE studies, POPULATION geography, FISHER exact test, MANN Whitney U Test, ARTIFICIAL respiration, T-test (Statistics), DRUG prescribing, DESCRIPTIVE statistics, CHI-squared test, PHYSICIAN practice patterns, DATA analysis software, ODDS ratio, LONGITUDINAL method, CHILDREN, ADOLESCENCE
Abstract

BACKGROUND: Children with asthma exacerbations requiring pediatric ICU (PICU) admission, known as critical asthma (CA), are prescribed a variety of therapeutic interventions including heliox. Delivered invasively and noninvasively, heliox is employed to enhance deposition of aerosolized medications, improve obstructive pulmonary pathophysiology, and avoid complications associated with invasive mechanical ventilation. We used the Virtual Pediatric Systems database to update estimates of heliox prescription and explore for relationships between heliox and mechanical ventilation frequency and duration. METHODS: We performed a retrospective cohort study using data from 97 PICUs among children 3-17 y of age admitted for CA from 2013-2019. The primary outcome was heliox prescribing rates and trends. Subgroup analyses assessed mechanical ventilation rates and duration by heliox exposure. RESULTS: Of 43,238 subjects studied, 1,070 (2.5%) were prescribed heliox. Mean heliox prescribing rates fell from 4.11% in 2013 to 2.37% in 2019. Heliox use was greater from centers in the South (2.6%) and Midwest (3.3%) as compared to the West (1.6%) and Northeast United States (1.6%, P < .001). In the subgroup assessing mechanical ventilation frequency, mechanical ventilation rates were 273/39,739 (0.7%) and greater for those provided heliox (1.9% vs 0.7%, P < .001). In the subgroup assessing mechanical ventilation duration, no differences in median mechanical ventilation duration were observed (4.94 [interquartile range [IQR] 3.04-6.36] vs 4.63 [IQR 3.11-7.30] d; P = .35) for those with and without heliox. In exploratory adjusted models, noninvasive heliox was not associated with mechanical ventilation. Mortality was rare (206/43,238 [0.47%]) and predominantly among subjects intubated prehospitalization (188/206 [91.3%]). CONCLUSIONS: Heliox as adjunctive therapy for children with CA is uncommon (2.5%) and not associated with mechanical ventilation or decreased mechanical ventilation duration in adjusted models. Updated estimates provided herein inform prospective controlled trial development to better define the role of heliox for CA. [ABSTRACT FROM AUTHOR]

Published
2022
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25. Influence of gene expression on survival of clear cell renal cell carcinoma

Author

Berglund, Anders, primary, Amankwah, Ernest K., additional, Kim, Young‐Chul, additional, Spiess, Philippe E, additional, Sexton, Wade J., additional, Manley, Brandon, additional, Park, Hyun Y., additional, Wang, Liang, additional, Chahoud, Jad, additional, Chakrabarti, Ratna, additional, Yeo, Chang D., additional, Luu, Hung N., additional, Pietro, Giuliano D., additional, Parker, Alexander, additional, and Park, Jong Y., additional

Published
2020
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29. Interleukin polymorphisms associated with overall survival, disease-free survival, and recurrence in non-small cell lung cancer patients

Author

Woods, Nicholas T., Monteiro, Alvaro N., Thompson, Zachary J., Amankwah, Ernest K., Naas, Nina, Haura, Eric B., Beg, Amer, and Schabath, Matthew B.

Subjects
Male, Lung Neoplasms, Recurrence, Carcinoma, Non-Small-Cell Lung, Interleukins, Humans, Female, Middle Aged, Polymorphism, Single Nucleotide, Survival Analysis, Article, Aged
Abstract

Biomarkers based on germline DNA variations could have translational implications by identifying prognostic factors and sub-classifying patients to tailored, patient-specific treatment. To investigate the association between germline variations in interleukin (IL) genes and lung cancer outcomes, we genotyped 251 single nucleotide polymorphisms (SNPs) from 33 different IL genes in 651 non-small cell lung cancer (NSCLC) patients. Analyses were performed to investigate overall survival, disease-free survival, and recurrence. Our analyses revealed 24 different IL SNPs significantly associated with one or more of the lung cancer outcomes of interest. The GG genotype of IL16:rs7170924 was significantly associated with disease-free survival (HR = 0.65; 95% CI 0.50 – 0.83) and was the only SNP that produced a false discovery rate (FDR) of modest confidence that the association is unlikely to represent a false-positive result (FDR = 0.142). Classification and regression tree (CART) analyses were used to identify potential higher-order interactions. We restricted the CART analyses to the five SNPs that were significantly associated with multiple endpoints (IL1A:rs1800587, IL1B:rs1143634, IL8:s12506479, IL12A:rs662959, and IL13:rs1881457) and IL16:rs7170924 which had the lowest FDR. CART analyses did not yield a tree structure for overall survival; separate CART tree structures were identified for recurrence, based on three SNPs (IL13:rs1881457, IL1B:rs1143634, and IL12A:rs662959), and for disease-free survival, based on two SNPs (IL12A:rs662959 and IL16:rs7170924), which may suggest that these candidate IL SNPs have a specific impact on lung cancer progression and recurrence. These data suggests that germline variations in IL genes are associated with clinical outcomes in NSCLC patients.

Published
2015

30. Common Genetic Variation in Circadian Rhythm Genes and Risk of Epithelial Ovarian Cancer (EOC)

Author

Jim, Heather S L, Lin, Hui-Yi, Tyrer, Jonathan P, Lawrenson, Kate, Dennis, Joe, Chornokur, Ganna, Chen, Zhihua, Chen, Y Ann, Permuth-Wey, Jennifer, Aben, Katja Kh, Anton-Culver, Hoda, Antonenkova, Natalia, Bruinsma, Fiona, Bandera, Elisa V, Bean, Yukie T, Beckmann, Matthias W, Bisogna, Maria, Bjorge, Line, Bogdanova, Natalia, Brinton, Louise A, Brooks-Wilson, Angela, Bunker, Clareann H, Butzow, Ralf, Campbell, Ian G, Carty, Karen, Chang-Claude, Jenny, Cook, Linda S, Cramer, Daniel W, Cunningham, Julie M, Cybulski, Cezary, Dansonka-Mieszkowska, Agnieszka, Du Bois, Andreas, Despierre, Evelyn, Sieh, Weiva, Doherty, Jennifer A, Doerk, Thilo, Durst, Matthias, Easton, Douglas F, Eccles, Diana M, Edwards, Robert P, Ekici, Arif B, Fasching, Peter A, Fridley, Brooke L, Gao, Yu-Tang, Gentry-Maharaj, Aleksandra, Giles, Graham, Glasspool, Rosalind M, Goodman, Marc T, Gronwald, Jacek, Harter, Philipp, Hasmad, Hanis N., Hein, Alexander, Heitz, Florian, Hildebrandt, Michelle A T, Hillemanns, Peter, Hogdall, Claus K, Hogdall, Estrid, Hosono, Satoyo, Iversen, Edwin S, Jakubowska, Anna, Jensen, Allan, Ji, Bu-Tian, Karlan, Beth Y, Kellar, Melissa, Kiemeney, Lambertus A, Krakstad, Camilla, Kjaer, Susanne K, Kupryjanczyk, Jolanta, Vierkant, Robert A, Lambrechts, Diether, Lambrechts, Sandrina, Le, Nhu D, Lee, Alice W, Lele, Shashi, Leminen, Arto, Lester, Jenny, Levine, Douglas A, Liang, Dong, Lim, Boon Kiong, Lissowska, Jolanta, Lu, Karen, Lubinski, Jan, Lundvall, Lene, Massuger, Leon F A G, Matsuo, Keitaro, McGuire, Valerie, McLaughlin, John R, McNeish, Ian, Menon, Usha, Milne, Roger L, Modugno, Francesmary, Thomsen, Lotte, Moysich, Kirsten B, Ness, Roberta B, Nevanlinna, Heli, Eilber, Ursula, Odunsi, Kunle, Olson, Sara H, Orlow, Irene, Orsulic, Sandra, Palmieri Weber, Rachel, Paul, James, Pearce, Celeste L, Pejovic, Tanja, Pelttari, Liisa M, Pike, Malcolm C, Poole, Elizabeth M, Schernhammer, Eva, Risch, Harvey A, Rosen, Barry, Rossing, Mary Anne, Rothstein, Joseph H, Rudolph, Anja, Runnebaum, Ingo B, Rzepecka, Iwona K, Salvesen, Helga B, Schwaab, Ira, Shu, Xiao-Ou, Shvetsov, Yurii B, Siddiqui, Nadeem, Song, Honglin, Southey, Melissa C, Spiewankiewicz, Beata, Sucheston-Campbell, Lara, Teo, Soo-Hwang, Terry, Kathryn L, Thompson, Pamela J, Tangen, Ingvild L, Tworoger, Shelley S, van Altena, Anne M, Vergote, Ignace, Walsh, Christine S, Wang-Gohrke, Shan, Wentzensen, Nicolas, Whittemore, Alice S, Wicklund, Kristine G, Wilkens, Lynne R, Wu, Anna H, Wu, Xifeng, Woo, Yin Ling, Yang, Hannah, Zheng, Wei, Ziogas, Argyrios, Amankwah, Ernest K, Berchuck, Andrew, Schildkraut, Joellen M, Kelemen, Linda E, Ramus, Susan J, Monteiro, Alvaro N A, Goode, Ellen L, Narod, Steven A, Gayther, Simon A, Pharoah, Paul P D, Sellers, Thomas A, Phelan, Catherine M, Jim, Heather S L, Lin, Hui-Yi, Tyrer, Jonathan P, Lawrenson, Kate, Dennis, Joe, Chornokur, Ganna, Chen, Zhihua, Chen, Y Ann, Permuth-Wey, Jennifer, Aben, Katja Kh, Anton-Culver, Hoda, Antonenkova, Natalia, Bruinsma, Fiona, Bandera, Elisa V, Bean, Yukie T, Beckmann, Matthias W, Bisogna, Maria, Bjorge, Line, Bogdanova, Natalia, Brinton, Louise A, Brooks-Wilson, Angela, Bunker, Clareann H, Butzow, Ralf, Campbell, Ian G, Carty, Karen, Chang-Claude, Jenny, Cook, Linda S, Cramer, Daniel W, Cunningham, Julie M, Cybulski, Cezary, Dansonka-Mieszkowska, Agnieszka, Du Bois, Andreas, Despierre, Evelyn, Sieh, Weiva, Doherty, Jennifer A, Doerk, Thilo, Durst, Matthias, Easton, Douglas F, Eccles, Diana M, Edwards, Robert P, Ekici, Arif B, Fasching, Peter A, Fridley, Brooke L, Gao, Yu-Tang, Gentry-Maharaj, Aleksandra, Giles, Graham, Glasspool, Rosalind M, Goodman, Marc T, Gronwald, Jacek, Harter, Philipp, Hasmad, Hanis N., Hein, Alexander, Heitz, Florian, Hildebrandt, Michelle A T, Hillemanns, Peter, Hogdall, Claus K, Hogdall, Estrid, Hosono, Satoyo, Iversen, Edwin S, Jakubowska, Anna, Jensen, Allan, Ji, Bu-Tian, Karlan, Beth Y, Kellar, Melissa, Kiemeney, Lambertus A, Krakstad, Camilla, Kjaer, Susanne K, Kupryjanczyk, Jolanta, Vierkant, Robert A, Lambrechts, Diether, Lambrechts, Sandrina, Le, Nhu D, Lee, Alice W, Lele, Shashi, Leminen, Arto, Lester, Jenny, Levine, Douglas A, Liang, Dong, Lim, Boon Kiong, Lissowska, Jolanta, Lu, Karen, Lubinski, Jan, Lundvall, Lene, Massuger, Leon F A G, Matsuo, Keitaro, McGuire, Valerie, McLaughlin, John R, McNeish, Ian, Menon, Usha, Milne, Roger L, Modugno, Francesmary, Thomsen, Lotte, Moysich, Kirsten B, Ness, Roberta B, Nevanlinna, Heli, Eilber, Ursula, Odunsi, Kunle, Olson, Sara H, Orlow, Irene, Orsulic, Sandra, Palmieri Weber, Rachel, Paul, James, Pearce, Celeste L, Pejovic, Tanja, Pelttari, Liisa M, Pike, Malcolm C, Poole, Elizabeth M, Schernhammer, Eva, Risch, Harvey A, Rosen, Barry, Rossing, Mary Anne, Rothstein, Joseph H, Rudolph, Anja, Runnebaum, Ingo B, Rzepecka, Iwona K, Salvesen, Helga B, Schwaab, Ira, Shu, Xiao-Ou, Shvetsov, Yurii B, Siddiqui, Nadeem, Song, Honglin, Southey, Melissa C, Spiewankiewicz, Beata, Sucheston-Campbell, Lara, Teo, Soo-Hwang, Terry, Kathryn L, Thompson, Pamela J, Tangen, Ingvild L, Tworoger, Shelley S, van Altena, Anne M, Vergote, Ignace, Walsh, Christine S, Wang-Gohrke, Shan, Wentzensen, Nicolas, Whittemore, Alice S, Wicklund, Kristine G, Wilkens, Lynne R, Wu, Anna H, Wu, Xifeng, Woo, Yin Ling, Yang, Hannah, Zheng, Wei, Ziogas, Argyrios, Amankwah, Ernest K, Berchuck, Andrew, Schildkraut, Joellen M, Kelemen, Linda E, Ramus, Susan J, Monteiro, Alvaro N A, Goode, Ellen L, Narod, Steven A, Gayther, Simon A, Pharoah, Paul P D, Sellers, Thomas A, and Phelan, Catherine M

Abstract

Disruption in circadian gene expression, whether due to genetic variation or environmental factors (e.g., light at night, shiftwork), is associated with increased incidence of breast, prostate, gastrointestinal and hematologic cancers and gliomas. Circadian genes are highly expressed in the ovaries where they regulate ovulation; circadian disruption is associated with several ovarian cancer risk factors (e.g., endometriosis). However, no studies have examined variation in germline circadian genes as predictors of ovarian cancer risk and invasiveness. The goal of the current study was to examine single nucleotide polymorphisms (SNPs) in circadian genes BMAL1, CRY2, CSNK1E, NPAS2, PER3, REV1 and TIMELESS and downstream transcription factors KLF10 and SENP3 as predictors of risk of epithelial ovarian cancer (EOC) and histopathologic subtypes. The study included a test set of 3,761 EOC cases and 2,722 controls and a validation set of 44,308 samples including 18,174 (10,316 serous) cases and 26,134 controls from 43 studies participating in the Ovarian Cancer Association Consortium (OCAC). Analysis of genotype data from 36 genotyped SNPs and 4600 imputed SNPs indicated that the most significant association was rs117104877 in BMAL1 (OR = 0.79, 95% CI = 0.68-0.90, p = 5.59 × 10(-4)]. Functional analysis revealed a significant down regulation of BMAL1 expression following cMYC overexpression and increasing transformation in ovarian surface epithelial (OSE) cells as well as alternative splicing of BMAL1 exons in ovarian and granulosa cells. These results suggest that variation in circadian genes, and specifically BMAL1, may be associated with risk of ovarian cancer, likely through disruption of hormonal pathways.

Published
2016

32. Epithelial-Mesenchymal Transition (EMT) Gene Variants and Epithelial Ovarian Cancer (EOC) Risk

Author

Amankwah, Ernest K., Lin, Hui-Yi, Tyrer, Jonathan P., Lawrenson, Kate, Dennis, Joe, Chornokur, Ganna, Aben, Katja K. H., Anton-Culver, Hoda, Antonenkova, Natalia, Bruinsma, Fiona, Bandera, Elisa V., Bean, Yukie T., Beckmann, Matthias W., Bisogna, Maria, Bjorge, Line, Bogdanova, Natalia, Brinton, Louise A., Brooks-Wilson, Angela, Bunker, Clareann H., Butzow, Ralf, Campbell, Ian G., Carty, Karen, Chen, Zhihua, Chen, Y. Ann, Chang-Claude, Jenny, Cook, Linda S., Cramer, Daniel W., Cunningham, Julie M., Cybulski, Cezary, Dansonka-Mieszkowska, Agnieszka, Du Bois, Andreas, Despierre, Evelyn, Dicks, Ed, Doherty, Jennifer A., Doerk, Thilo, Duerst, Matthias, Easton, Douglas F., Eccles, Diana M., Edwards, Robert P., Ekici, Arif B., Fasching, Peter A., Fridley, Brooke L., Gao, Yu-Tang, Gentry-Maharaj, Aleksandra, Giles, Graham G., Glasspool, Rosalind, Goodman, Marc T., Gronwald, Jacek, Harrington, Patricia, Harter, Philipp, Hasmad, Hanis N., Hein, Alexander, Heitz, Florian, Hildebrandt, Michelle A. T., Hillemanns, Peter, Hogdall, Claus K., Hogdall, Estrid, Hosono, Satoyo, Iversen, Edwin S., Jakubowska, Anna, Jensen, Allan, Ji, Bu-Tian, Karlan, Beth Y., Jim, Heather, Kellar, Melissa, Kiemeney, Lambertus A., Krakstad, Camilla, Kjær, Susanne Krüger, Kupryjanczyk, Jolanta, Lambrechts, Diether, Lambrechts, Sandrina, Le, Nhu D., Lee, Alice W., Lele, Shashi, Leminen, Arto, Lester, Jenny, Levine, Douglas A., Liang, Dong, Lim, Boon Kiong, Lissowska, Jolanta, Lu, Karen, Lubinski, Jan, Lundvall, Lene, Massuger, Leon F. A. G., Matsuo, Keitaro, McGuire, Valerie, McLaughlin, John R., McNeish, Ian, Menon, Usha, Milne, Roger L., Modugno, Francesmary, Moysich, Kirsten B., Ness, Roberta B., Nevanlinna, Heli, Eilber, Ursula, Odunsi, Kunle, Olson, Sara H., Orlow, Irene, Orsulic, Sandra, Weber, Rachel Palmieri, Paul, James, Pearce, Celeste L., Pejovic, Tanja, Pelttari, Liisa M., Permuth-Wey, Jennifer, Pike, Malcolm C., Poole, Elizabeth M., Risch, Harvey A., Rosen, Barry, Rossing, Mary Anne, Rothstein, Joseph H., Rudolph, Anja, Runnebaum, Ingo B., Rzepecka, Iwona K., Salvesen, Helga B., Schernhammer, Eva, Schwaab, Ira, Shu, Xiao-Ou, Shvetsov, Yurii B., Siddiqui, Nadeem, Sieh, Weiva, Song, Honglin, Southey, Melissa C., Spiewankiewicz, Beata, Sucheston-Campbell, Lara, Teo, Soo-Hwang, Terry, Kathryn L., Thompson, Pamela J., Thomsen, Lotte, Tangen, Ingvild L., Tworoger, Shelley S., Van Altena, Anne M., Vierkant, Robert A., Vergote, Ignace, Walsh, Christine S., Wang-Gohrke, Shan, Wentzensen, Nicolas, Whittemore, Alice S., Wicklund, Kristine G., Wilkens, Lynne R., Wu, Anna H., Wu, Xifeng, Woo, Yin-Ling, Yang, Hannah, Zheng, Wei, Ziogas, Argyrios, Kelemen, Linda E., Berchuck, Andrew, Chenevix-Trench, Georgia, Grp, Aocs Management, Schildkraut, Joellen M., Ramus, Susan J., Goode, Ellen L., Monteiro, Alvaro N. A., Gayther, Simon A., Narod, Steven A., Pharoah, Paul D. P., Sellers, Thomas A., Phelan, Catherine M., Amankwah, Ernest K., Lin, Hui-Yi, Tyrer, Jonathan P., Lawrenson, Kate, Dennis, Joe, Chornokur, Ganna, Aben, Katja K. H., Anton-Culver, Hoda, Antonenkova, Natalia, Bruinsma, Fiona, Bandera, Elisa V., Bean, Yukie T., Beckmann, Matthias W., Bisogna, Maria, Bjorge, Line, Bogdanova, Natalia, Brinton, Louise A., Brooks-Wilson, Angela, Bunker, Clareann H., Butzow, Ralf, Campbell, Ian G., Carty, Karen, Chen, Zhihua, Chen, Y. Ann, Chang-Claude, Jenny, Cook, Linda S., Cramer, Daniel W., Cunningham, Julie M., Cybulski, Cezary, Dansonka-Mieszkowska, Agnieszka, Du Bois, Andreas, Despierre, Evelyn, Dicks, Ed, Doherty, Jennifer A., Doerk, Thilo, Duerst, Matthias, Easton, Douglas F., Eccles, Diana M., Edwards, Robert P., Ekici, Arif B., Fasching, Peter A., Fridley, Brooke L., Gao, Yu-Tang, Gentry-Maharaj, Aleksandra, Giles, Graham G., Glasspool, Rosalind, Goodman, Marc T., Gronwald, Jacek, Harrington, Patricia, Harter, Philipp, Hasmad, Hanis N., Hein, Alexander, Heitz, Florian, Hildebrandt, Michelle A. T., Hillemanns, Peter, Hogdall, Claus K., Hogdall, Estrid, Hosono, Satoyo, Iversen, Edwin S., Jakubowska, Anna, Jensen, Allan, Ji, Bu-Tian, Karlan, Beth Y., Jim, Heather, Kellar, Melissa, Kiemeney, Lambertus A., Krakstad, Camilla, Kjær, Susanne Krüger, Kupryjanczyk, Jolanta, Lambrechts, Diether, Lambrechts, Sandrina, Le, Nhu D., Lee, Alice W., Lele, Shashi, Leminen, Arto, Lester, Jenny, Levine, Douglas A., Liang, Dong, Lim, Boon Kiong, Lissowska, Jolanta, Lu, Karen, Lubinski, Jan, Lundvall, Lene, Massuger, Leon F. A. G., Matsuo, Keitaro, McGuire, Valerie, McLaughlin, John R., McNeish, Ian, Menon, Usha, Milne, Roger L., Modugno, Francesmary, Moysich, Kirsten B., Ness, Roberta B., Nevanlinna, Heli, Eilber, Ursula, Odunsi, Kunle, Olson, Sara H., Orlow, Irene, Orsulic, Sandra, Weber, Rachel Palmieri, Paul, James, Pearce, Celeste L., Pejovic, Tanja, Pelttari, Liisa M., Permuth-Wey, Jennifer, Pike, Malcolm C., Poole, Elizabeth M., Risch, Harvey A., Rosen, Barry, Rossing, Mary Anne, Rothstein, Joseph H., Rudolph, Anja, Runnebaum, Ingo B., Rzepecka, Iwona K., Salvesen, Helga B., Schernhammer, Eva, Schwaab, Ira, Shu, Xiao-Ou, Shvetsov, Yurii B., Siddiqui, Nadeem, Sieh, Weiva, Song, Honglin, Southey, Melissa C., Spiewankiewicz, Beata, Sucheston-Campbell, Lara, Teo, Soo-Hwang, Terry, Kathryn L., Thompson, Pamela J., Thomsen, Lotte, Tangen, Ingvild L., Tworoger, Shelley S., Van Altena, Anne M., Vierkant, Robert A., Vergote, Ignace, Walsh, Christine S., Wang-Gohrke, Shan, Wentzensen, Nicolas, Whittemore, Alice S., Wicklund, Kristine G., Wilkens, Lynne R., Wu, Anna H., Wu, Xifeng, Woo, Yin-Ling, Yang, Hannah, Zheng, Wei, Ziogas, Argyrios, Kelemen, Linda E., Berchuck, Andrew, Chenevix-Trench, Georgia, Grp, Aocs Management, Schildkraut, Joellen M., Ramus, Susan J., Goode, Ellen L., Monteiro, Alvaro N. A., Gayther, Simon A., Narod, Steven A., Pharoah, Paul D. P., Sellers, Thomas A., and Phelan, Catherine M.

Published
2015

33. Multicenter Study of a Risk Prediction Model for Critically Ill Children at High-Risk for Hospital-Acquired Venous Thromboembolism: Findings from the Children's Hospital-Acquired Thrombosis (CHAT) Consortium

Author

Jaffray, Julie, Mosha, Maua, Branchford, Brian R., Amankwah, Ernest K, Faustino, E. Vincent, Krava, Emily, Stillings, Amy, Young, Guy, and Goldenberg, Neil

Abstract

Introduction:Critically ill children are at high-risk of developing a hospital-acquired venous thromboembolism (HA-VTE) as well as being at an increased risk for bleeding. To better understand which subset of children may benefit from thromboprophylaxis measures, (without contraindications for potential associated hemorrhagic complications), the Children's Hospital Acquired Thrombosis (CHAT) Consortium previously derived a HA-VTE risk assessment model (RAM) for critically ill children from 8 centers. This RAM included five variables: (1) immobility defined using a Braden score ≤2, (2) length of hospitalization prior to PICU admission, (3) central venous catheterization, (4) presence of congenital heart disease (CHD) and (5) history of autoimmune/inflammatory disorder or infection. For this study we aimed to externally evaluate our previous HA-VTE RAM in critically ill children in an independent cohort via the CHAT Consortium.

Published
2023
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35. Epidemiology and therapies for metastatic sarcoma

Author

Amankwah,Ernest K, Conley,Anthony P, Reed,Damon R, Amankwah,Ernest K, Conley,Anthony P, and Reed,Damon R

Abstract

Ernest K Amankwah,1 Anthony P Conley,2 Damon R Reed2 1Department of Cancer Epidemiology, H Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA; 2Sarcoma Department, H Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA Abstract: Sarcomas are cancers arising from the mesenchymal layer that affect children, adolescents, young adults, and adults. Although most sarcomas are localized, many display a remarkable predilection for metastasis to the lungs, liver, bones, subcutaneous tissue, and lymph nodes. Additionally, many sarcoma patients presenting initially with localized disease may relapse at metastatic sites. While localized sarcomas can often be cured through surgery and often radiation, controversies exist over optimal management of patients with metastatic sarcoma. Combinations of chemotherapy are the most effective in many settings, and many promising new agents are under active investigation or are being explored in preclinical models. Metastatic sarcomas are excellent candidates for novel approaches with additional agents as they have demonstrated chemosensitivity and affect a portion of the population that is motivated toward curative therapy. In this paper, we provide an overview on the common sarcomas of childhood (rhabdomyosarcoma), adolescence, and young adults (osteosarcoma, Ewing sarcoma, synovial sarcoma, and malignant peripheral nerve sheath tumor) and older adults (leiomyosarcoma, liposarcoma, and undifferentiated high grade sarcoma) in terms of the epidemiology, current therapy, promising therapeutic directions and outcome with a focus on metastatic disease. Potential advances in terms of promising therapy and biologic insights may lead to more effective and safer therapies; however, more clinical trials and research are needed for patients with metastatic sarcoma. Keywords: chemotherapy, pediatric sarcoma, rhabdomyosarcoma, osteosarcoma, Ewing sarcoma, synovial sarcoma

Published
2013

36. Polymorphisms in Stromal Genes and Susceptibility to Serous Epithelial Ovarian Cancer: A Report from the Ovarian Cancer Association Consortium

Author

University of Helsinki, Department of Pathology, University of Helsinki, Department of Obstetrics and Gynecology, Amankwah, Ernest K., Wang, Qinggang, Schildkraut, Joellen M., Tsai, Ya-Yu, Ramus, Susan J., Fridley, Brooke L., Beesley, Jonathan, Johnatty, Sharon E., Webb, Penelope M., Chenevix-Trench, Georgia, Dale, Laura C., Lambrechts, Diether, Amant, Frederic, Despierre, Evelyn, Vergote, Ignace, Gayther, Simon A., Gentry-Maharaj, Aleksandra, Menon, Usha, Chang-Claude, Jenny, Wang-Gohrke, Shan, Anton-Culver, Hoda, Ziogas, Argyrios, Doerk, Thilo, Duerst, Matthias, Antonenkova, Natalia, Bogdanova, Natalia, Brown, Robert, Flanagan, James M., Kaye, Stanley B., Paul, James, Butzow, Ralf, Nevanlinna, Heli, Campbell, Ian, Eccles, Diana M., Karlan, Beth Y., Gross, Jenny, Walsh, Christine, Pharoah, Paul D. P., Song, Honglin, Kjaer, Susanne Kruger, Hogdall, Estrid, Hogdall, Claus, Lundvall, Lene, Nedergaard, Lotte, Kiemeney, Lambertus A. L. M., Massuger, Leon F. A. G., van Altena, Anne M., Vermeulen, Sita H. H. M., Le, Nhu D., Brooks-Wilson, Angela, Cook, Linda S., Phelan, Catherine M., Cunningham, Julie M., Vachon, Celine M., Vierkant, Robert A., Iversen, Edwin S., Berchuck, Andrew, Goode, Ellen L., Sellers, Thomas A., Kelemen, Linda E., Australian Ovarian Canc Study Grp, University of Helsinki, Department of Pathology, University of Helsinki, Department of Obstetrics and Gynecology, Amankwah, Ernest K., Wang, Qinggang, Schildkraut, Joellen M., Tsai, Ya-Yu, Ramus, Susan J., Fridley, Brooke L., Beesley, Jonathan, Johnatty, Sharon E., Webb, Penelope M., Chenevix-Trench, Georgia, Dale, Laura C., Lambrechts, Diether, Amant, Frederic, Despierre, Evelyn, Vergote, Ignace, Gayther, Simon A., Gentry-Maharaj, Aleksandra, Menon, Usha, Chang-Claude, Jenny, Wang-Gohrke, Shan, Anton-Culver, Hoda, Ziogas, Argyrios, Doerk, Thilo, Duerst, Matthias, Antonenkova, Natalia, Bogdanova, Natalia, Brown, Robert, Flanagan, James M., Kaye, Stanley B., Paul, James, Butzow, Ralf, Nevanlinna, Heli, Campbell, Ian, Eccles, Diana M., Karlan, Beth Y., Gross, Jenny, Walsh, Christine, Pharoah, Paul D. P., Song, Honglin, Kjaer, Susanne Kruger, Hogdall, Estrid, Hogdall, Claus, Lundvall, Lene, Nedergaard, Lotte, Kiemeney, Lambertus A. L. M., Massuger, Leon F. A. G., van Altena, Anne M., Vermeulen, Sita H. H. M., Le, Nhu D., Brooks-Wilson, Angela, Cook, Linda S., Phelan, Catherine M., Cunningham, Julie M., Vachon, Celine M., Vierkant, Robert A., Iversen, Edwin S., Berchuck, Andrew, Goode, Ellen L., Sellers, Thomas A., Kelemen, Linda E., and Australian Ovarian Canc Study Grp

Published
2011

37. Prostate Cancer Susceptibility Polymorphism rs2660753 Is Not Associated with Invasive Ovarian Cancer

Author

Amankwah, Ernest K, Kelemen, Linda E, Wang, Qinggang, Song, Honglin, Chenevix-Trench, Georgia, Beesley, Jonathan, Webb, Penelope M, Pearce, Celeste L, Wu, Anna H, Pike, Malcolm C, Stram, Daniel O, Chang-Claude, Jenny, Wang-Gohrke, Shan, Ness, Roberta B, Goode, Ellen L, Cunningham, Julie M, Fridley, Brooke L, Vierkant, Robert A, Tworoger, Shelley S, Whittemore, Alice S, McGuire, Valerie, Sieh, Weiva, Gayther, Simon A, Gentry-Maharaj, Aleksandra, Menon, Usha, Ramus, Susan J, Rossing, Mary Anne, Doherty, Jennifer A, Goodman, Marc T, Carney, Michael E, Lurie, Galina, Wilkens, Lynne R, Kjær, Susanne Krüger, Høgdall, Estrid, Cramer, Daniel W, Terry, Kathryn L, Garcia-Closas, Montserrat, Yang, Hannah, Lissowska, Jolanta, Anton-Culver, Hoda, Ziogas, Argyrios, Schildkraut, Joellen M, Berchuck, Andrew, Pharoah, Paul D P, Amankwah, Ernest K, Kelemen, Linda E, Wang, Qinggang, Song, Honglin, Chenevix-Trench, Georgia, Beesley, Jonathan, Webb, Penelope M, Pearce, Celeste L, Wu, Anna H, Pike, Malcolm C, Stram, Daniel O, Chang-Claude, Jenny, Wang-Gohrke, Shan, Ness, Roberta B, Goode, Ellen L, Cunningham, Julie M, Fridley, Brooke L, Vierkant, Robert A, Tworoger, Shelley S, Whittemore, Alice S, McGuire, Valerie, Sieh, Weiva, Gayther, Simon A, Gentry-Maharaj, Aleksandra, Menon, Usha, Ramus, Susan J, Rossing, Mary Anne, Doherty, Jennifer A, Goodman, Marc T, Carney, Michael E, Lurie, Galina, Wilkens, Lynne R, Kjær, Susanne Krüger, Høgdall, Estrid, Cramer, Daniel W, Terry, Kathryn L, Garcia-Closas, Montserrat, Yang, Hannah, Lissowska, Jolanta, Anton-Culver, Hoda, Ziogas, Argyrios, Schildkraut, Joellen M, Berchuck, Andrew, and Pharoah, Paul D P

Abstract

BACKGROUND: We previously reported an association between rs2660753, a prostate cancer susceptibility polymorphism, and invasive epithelial ovarian cancer (EOC; OR = 1.2, 95% CI=1.0-1.4, P(trend) = 0.01) that showed a stronger association with the serous histological subtype (OR = 1.3, 95% CI = 1.1-1.5, P(trend) = 0.003). METHODS: We sought to replicate this association in 12 other studies comprising 4,482 cases and 6,894 controls of white non-Hispanic ancestry in the Ovarian Cancer Association Consortium. RESULTS: No evidence for an association with all cancers or serous cancers was observed in a combined analysis of data from the replication studies (all: OR = 1.0, 95% CI = 0.9-1.1, P(trend) = 0.61; serous: OR = 1.0, 95% CI = 0.9-1.1, P(trend) = 0.85) or from the combined analysis of discovery and replication studies (all: OR = 1.0, 95% CI = 1.0-1.1, P(trend) = 0.28; serous: OR = 1.1, 95% CI = 1.0-1.2, P(trend) = 0.11). There was no evidence for statistical heterogeneity in ORs across the studies. CONCLUSIONS: Although rs2660753 is a strong prostate cancer susceptibility polymorphism, the association with another hormonally related cancer, invasive EOC, is not supported by this replication study. Impact: Our findings, based on a larger sample size, emphasize the importance of replicating potentially promising genetic risk associations. Cancer Epidemiol Biomarkers Prev; 20(5); 1028-31. ©2011 AACR.

Published
2011

38. Polymorphisms in stromal genes and susceptibility to serous epithelial ovarian cancer: a report from the Ovarian Cancer Association Consortium

Author

Amankwah, Ernest K, Wang, Qinggang, Schildkraut, Joellen M, Tsai, Ya-Yu, Ramus, Susan J, Fridley, Brooke L, Beesley, Jonathan, Johnatty, Sharon E, Webb, Penelope M, Chenevix-Trench, Georgia, Dale, Laura C, Lambrechts, Diether, Amant, Frederic, Despierre, Evelyn, Vergote, Ignace, Gayther, Simon A, Gentry-Maharaj, Aleksandra, Menon, Usha, Chang-Claude, Jenny, Wang-Gohrke, Shan, Anton-Culver, Hoda, Ziogas, Argyrios, Dörk, Thilo, Dürst, Matthias, Antonenkova, Natalia, Bogdanova, Natalia, Brown, Robert James (Jim), Flanagan, James M, Kaye, Stanley B, Paul, James, Bützow, Ralf, Nevanlinna, Heli, Campbell, Ian, Eccles, Diana M, Karlan, Beth Y, Gross, Jenny, Walsh, Christine, Pharoah, Paul D P, Song, Honglin, Kjær, Susanne, Høgdall, Estrid, Høgdall, Claus, Lundvall, Lene, Nedergaard, Lotte, Kiemeney, Lambertus A L M, Massuger, Leon F A G, van Altena, Anne M, Vermeulen, Sita H H M, Le, Nhu D, Brooks-Wilson, Angela, Amankwah, Ernest K, Wang, Qinggang, Schildkraut, Joellen M, Tsai, Ya-Yu, Ramus, Susan J, Fridley, Brooke L, Beesley, Jonathan, Johnatty, Sharon E, Webb, Penelope M, Chenevix-Trench, Georgia, Dale, Laura C, Lambrechts, Diether, Amant, Frederic, Despierre, Evelyn, Vergote, Ignace, Gayther, Simon A, Gentry-Maharaj, Aleksandra, Menon, Usha, Chang-Claude, Jenny, Wang-Gohrke, Shan, Anton-Culver, Hoda, Ziogas, Argyrios, Dörk, Thilo, Dürst, Matthias, Antonenkova, Natalia, Bogdanova, Natalia, Brown, Robert James (Jim), Flanagan, James M, Kaye, Stanley B, Paul, James, Bützow, Ralf, Nevanlinna, Heli, Campbell, Ian, Eccles, Diana M, Karlan, Beth Y, Gross, Jenny, Walsh, Christine, Pharoah, Paul D P, Song, Honglin, Kjær, Susanne, Høgdall, Estrid, Høgdall, Claus, Lundvall, Lene, Nedergaard, Lotte, Kiemeney, Lambertus A L M, Massuger, Leon F A G, van Altena, Anne M, Vermeulen, Sita H H M, Le, Nhu D, and Brooks-Wilson, Angela

Abstract

Alterations in stromal tissue components can inhibit or promote epithelial tumorigenesis. Decorin (DCN) and lumican (LUM) show reduced stromal expression in serous epithelial ovarian cancer (sEOC). We hypothesized that common variants in these genes associate with risk. Associations with sEOC among Caucasians were estimated with odds ratios (OR) among 397 cases and 920 controls in two U.S.-based studies (discovery set), 436 cases and 1,098 controls in Australia (replication set 1) and a consortium of 15 studies comprising 1,668 cases and 4,249 controls (replication set 2). The discovery set and replication set 1 (833 cases and 2,013 controls) showed statistically homogeneous (P(heterogeneity)=0.48) decreased risks of sEOC at four variants: DCN rs3138165, rs13312816 and rs516115, and LUM rs17018765 (OR¿=¿0.6 to 0.9; P(trend)¿=¿0.001 to 0.03). Results from replication set 2 were statistically homogeneous (P(heterogeneity)=0.13) and associated with increased risks at DCN rs3138165 and rs13312816, and LUM rs17018765: all ORs¿=¿1.2; P(trend)=0.02. The ORs at the four variants were statistically heterogeneous across all 18 studies (P(heterogeneity)=0.03), which precluded combining. In post-hoc analyses, interactions were observed between each variant and recruitment period (P(interaction)=0.003), age at diagnosis (P(interaction)¿=¿0.04), and year of diagnosis (P(interaction)¿=¿0.05) in the five studies with available information (1,044 cases, 2,469 controls). We conclude that variants in DCN and LUM are not directly associated with sEOC, and that confirmation of possible effect modification of the variants by non-genetic factors is required.

Published
2011

40. Gene Variants in Angiogenesis and Lymphangiogenesis and Cutaneous Melanoma Progression

Author

Park, Jong Y., primary, Amankwah, Ernest K., additional, Anic, Gabriella M., additional, Lin, Hui-Yi, additional, Walls, Brooke, additional, Park, Hyun, additional, Krebs, Kevin, additional, Madden, Melissa, additional, Maddox, Kristen, additional, Marzban, Suroosh, additional, Fang, Shenying, additional, Chen, Wei, additional, Lee, Jeffrey E., additional, Wei, Qingyi, additional, Amos, Christopher I., additional, Messina, Jane L., additional, Sondak, Vernon K., additional, Sellers, Thomas A., additional, and Egan, Kathleen M., additional

Published
2013
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46. Regular Multivitamin Supplement Use, Single Nucleotide Polymorphisms in ATIC, SHMT2, and SLC46A1, and Risk of Ovarian Carcinoma

Author

Kelemen, Linda E., primary, Wang, Qinggang, additional, Dinu, Irina, additional, Vierkant, Robert A., additional, Tsai, Ya-Yu, additional, Cunningham, Julie M., additional, Phelan, Catherine M., additional, Fridley, Brooke L., additional, Amankwah, Ernest K., additional, Iversen, Edwin S., additional, Berchuck, Andrew, additional, Schildkraut, Joellen M., additional, Goode, Ellen L., additional, and Sellers, Thomas A., additional

Published
2012
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47. Prostate Cancer Susceptibility Polymorphism rs2660753 Is Not Associated with Invasive Ovarian Cancer

Author

Amankwah, Ernest K., primary, Kelemen, Linda E., additional, Wang, Qinggang, additional, Song, Honglin, additional, Chenevix-Trench, Georgia, additional, Beesley, Jonathan, additional, Webb, Penelope M., additional, Pearce, Celeste L., additional, Wu, Anna H., additional, Pike, Malcolm C., additional, Stram, Daniel O., additional, Chang-Claude, Jenny, additional, Wang-Gohrke, Shan, additional, Ness, Roberta B., additional, Goode, Ellen L., additional, Cunningham, Julie M., additional, Fridley, Brooke L., additional, Vierkant, Robert A., additional, Tworoger, Shelley S., additional, Whittemore, Alice S., additional, McGuire, Valerie, additional, Sieh, Weiva, additional, Gayther, Simon A., additional, Gentry-Maharaj, Aleksandra, additional, Menon, Usha, additional, Ramus, Susan J., additional, Rossing, Mary Anne, additional, Doherty, Jennifer A., additional, Goodman, Marc T., additional, Carney, Michael E., additional, Lurie, Galina, additional, Wilkens, Lynne R., additional, Krüger Kjær, Susanne, additional, Høgdall, Estrid, additional, Cramer, Daniel W., additional, Terry, Kathryn L., additional, Garcia-Closas, Montserrat, additional, Yang, Hannah, additional, Lissowska, Jolanta, additional, Anton-Culver, Hoda, additional, Ziogas, Argyrios, additional, Schildkraut, Joellen M., additional, Berchuck, Andrew, additional, and Pharoah, Paul D.P., additional

Published
2011
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49. Epidemiology and therapies for metastatic sarcoma.

Author

Amankwah, Ernest K., Conley, Anthony P., and Reed, Damon R.

Subjects
SARCOMA, EPIDEMIOLOGY, METASTASIS, LYMPH nodes, CANCER chemotherapy, CANCER treatment
Abstract

Sarcomas are cancers arising from the mesenchymal layer that affect children, adolescents, young adults, and adults. Although most sarcomas are localized, many display a remarkable predilection for metastasis to the lungs, liver, bones, subcutaneous tissue, and lymph nodes. Additionally, many sarcoma patients presenting initially with localized disease may relapse at metastatic sites. While localized sarcomas can often be cured through surgery and often radiation, controversies exist over optimal management of patients with metastatic sarcoma. Combinations of chemotherapy are the most effective in many settings, and many promising new agents are under active investigation or are being explored in preclinical models. Metastatic sarcomas are excellent candidates for novel approaches with additional agents as they have demonstrated chemosensitivity and affect a portion of the population that is motivated toward curative therapy. In this paper, we provide an overview on the common sarcomas of childhood (rhabdomyosarcoma), adolescence, and young adults (osteosarcoma, Ewing sarcoma, synovial sarcoma, and malignant peripheral nerve sheath tumor) and older adults (leiomyosarcoma, liposarcoma, and undifferentiated high grade sarcoma) in terms of the epidemiology, current therapy, promising therapeutic directions and outcome with a focus on metastatic disease. Potential advances in terms of promising therapy and biologic insights may lead to more effective and safer therapies; however, more clinical trials and research are needed for patients with metastatic sarcoma. [ABSTRACT FROM AUTHOR]

Published
2013
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50. Variation in HNF1B and Obesity May Influence Prostate Cancer Risk in African American Men: A Pilot Study.

Author

Chornokur, Ganna, Amankwah, Ernest K., Davis, Stacy N., Phelan, Catherine M., Park, Jong Y., Pow-Sang, Julio, and Kumar, Nagi B.

Subjects
*PROSTATE cancer treatment, *OBESITY, *PROSTATE cancer risk factors, *SOCIOCULTURAL factors, *LIFESTYLES & health, *BODY mass index, *SINGLE nucleotide polymorphisms
Abstract

Background. Prostate cancer (PCa) racial disparity is multifactorial, involving biological, sociocultural, and lifestyle determinants. We investigated the association between selected potentially functional polymorphisms (SNPs) and prostate cancer (PCa) risk in Black (AAM) andWhite (EAM) men. We further explored if these associations varied by the body mass index (BMI) and height. Methods. Age-matched DNA samples from 259 AAM and 269 EAM were genotyped for 10 candidate SNPs in 7 genes using the TaqMan allelic differentiation analysis. The dominant, recessive, and additive age-adjusted unconditional logistic regressionmodels were fitted. Results. Three SNPs showed statistically significant associations with PCa risk: in AAM, HNF1B rs7501939 (OR = 2.42, P = 0.0046) and rs4430796 (OR = 0.57, P = 0.0383); in EAM, CTBP2 rs4962416 (OR = 1.52, P = 0.0384). In addition, high BMI in AAM (OR = 1.06, OR = 0.022) and height in EAM (OR = 0.92, P = 0.0434) showed significant associations. Interestingly, HNF1B rs7501939 was associated with PCa exclusively in obese AAM (OR = 2.14, P = 0.0103). Conclusion. Our results suggest that variation in the HNF1B may influence PCa risk in obese AAM. [ABSTRACT FROM AUTHOR]

Published
2013
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