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Assessment of Multifactor Gene-Environment Interactions and Ovarian Cancer Risk: Candidate Genes, Obesity, and Hormone-Related Risk Factors.
Usset, Joseph L; Raghavan, Rama; Tyrer, Jonathan P; McGuire, Valerie; Sieh, Weiva; Webb, Penelope; Chang-Claude, Jenny; Rudolph, Anja; Anton-Culver, Hoda; Berchuck, Andrew; Brinton, Louise; Cunningham, Julie M; DeFazio, Anna; Doherty, Jennifer A; Edwards, Robert P; Gayther, Simon A; Gentry-Maharaj, Aleksandra; Goodman, Marc T; Høgdall, Estrid; Jensen, Allan; Johnatty, Sharon E; Kiemeney, Lambertus A; Kjaer, Susanne K; Larson, Melissa C; Lurie, Galina; Massuger, Leon; Menon, Usha; Modugno, Francesmary; Moysich, Kirsten B; Ness, Roberta B; Pike, Malcolm C; Ramus, Susan J; Rossing, Mary Anne; Rothstein, Joseph; Song, Honglin; Thompson, Pamela J; van den Berg, David J; Vierkant, Robert A; Wang-Gohrke, Shan; Wentzensen, Nicolas; Whittemore, Alice S; Wilkens, Lynne R; Wu, Anna H; Yang, Hannah; Pearce, Celeste Leigh; Schildkraut, Joellen M; Pharoah, Paul; Goode, Ellen L; Fridley, Brooke L.
Afiliação
  • Usset JL; Department of Biostatistics, University of Kansas Medical Center, Kansas City, Kansas.
  • Raghavan R; Department of Biostatistics, University of Kansas Medical Center, Kansas City, Kansas.
  • Tyrer JP; Department of Oncology, University of Cambridge Strangeways Research Laboratory, Cambridge, United Kingdom.
  • McGuire V; Department of Health Research and Policy - Epidemiology, Stanford University School of Medicine, Stanford, California.
  • Sieh W; Department of Health Research and Policy - Epidemiology, Stanford University School of Medicine, Stanford, California.
  • Webb P; Population Health Department, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia.
  • Chang-Claude J; Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany.
  • Rudolph A; Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany.
  • Anton-Culver H; Department of Epidemiology, University of California Irvine, Irvine, California.
  • Berchuck A; Department of Obstetrics and Gynecology, Duke University Medical Center, Durham, North Carolina.
  • Brinton L; Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland.
  • Cunningham JM; Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota.
  • DeFazio A; Discipline of Obstetrics, Gynecology, and Neonatology, University of Sydney, Westmead Institute for Cancer Research, Westmead Millennium Institute, Westmead, New South Wales, Australia.
  • Doherty JA; Department of Epidemiology, Geisel School of Medicine, Hanover, New Hampshire.
  • Edwards RP; Department of Obstetrics, Gynecology, and Reproductive Sciences, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
  • Gayther SA; Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, California.
  • Gentry-Maharaj A; Women's Cancer, Institute for Women's Health, University College London, London, United Kingdom.
  • Goodman MT; Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, California.
  • Høgdall E; Department of Virus, Lifestyle, and Genes, Danish Cancer Society Research Center, Copenhagen, Denmark. Department of Pathology, Herlev Hospital, University of Copenhagen, Copenhagen, Denmark.
  • Jensen A; Department of Virus, Lifestyle, and Genes, Danish Cancer Society Research Center, Copenhagen, Denmark.
  • Johnatty SE; Division of Genetics and Public Health, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia.
  • Kiemeney LA; Department of Health Evidence, Radboud University Medical Centre, Nijmegen, the Netherlands.
  • Kjaer SK; Department of Gynecology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
  • Larson MC; Department of Health Science Research, Mayo Clinic, Rochester, Minnesota.
  • Lurie G; Cancer Epidemiology Program, University of Hawaii Cancer Center, Honolulu, Hawaii.
  • Massuger L; Department of Obstetrics & Gynecology, Radboud University Medical Center, Nijmegen, the Netherlands.
  • Menon U; Women's Cancer, Institute for Women's Health, University College London, London, United Kingdom.
  • Modugno F; Department of Obstetrics, Gynecology, and Reproductive Sciences, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania. Department of Epidemiology, University of Pittsburgh, Pittsburgh, Pennsylvania.
  • Moysich KB; Department of Cancer Prevention and Control, Roswell Park Cancer Institute, Buffalo, New York.
  • Ness RB; School of Public Health, The University of Texas, Houston, Texas.
  • Pike MC; Department of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York, New York.
  • Ramus SJ; Department of Preventive Medicine, University of Southern California, Los Angeles, California.
  • Rossing MA; Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington. Department of Epidemiology, University of Washington, Seattle, Washington.
  • Rothstein J; Department of Health Research and Policy - Epidemiology, Stanford University School of Medicine, Stanford, California.
  • Song H; Department of Oncology, University of Cambridge Strangeways Research Laboratory, Cambridge, United Kingdom.
  • Thompson PJ; Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, California.
  • van den Berg DJ; Department of Preventive Medicine, University of Southern California, Los Angeles, California.
  • Vierkant RA; Department of Health Science Research, Mayo Clinic, Rochester, Minnesota.
  • Wang-Gohrke S; Department of Obstetrics and Gynecology, University of Ulm, Ulm, Germany.
  • Wentzensen N; Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland.
  • Whittemore AS; Department of Health Research and Policy - Epidemiology, Stanford University School of Medicine, Stanford, California.
  • Wilkens LR; Cancer Epidemiology Program, University of Hawaii Cancer Center, Honolulu, Hawaii.
  • Wu AH; Department of Preventive Medicine, University of Southern California, Los Angeles, California.
  • Yang H; Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland.
  • Pearce CL; Department of Preventive Medicine, University of Southern California, Los Angeles, California. Department of Epidemiology, University of Michigan, Ann Arbor, Michigan.
  • Schildkraut JM; Department of Public Health Sciences, University of Virginia, Charlottesville, Virginia.
  • Pharoah P; Department of Oncology, University of Cambridge Strangeways Research Laboratory, Cambridge, United Kingdom. Department of Public Health and Primary Care, University of Cambridge Strangeways Research Laboratory, Cambridge, United Kingdom.
  • Goode EL; Department of Health Science Research, Mayo Clinic, Rochester, Minnesota.
  • Fridley BL; Department of Biostatistics, University of Kansas Medical Center, Kansas City, Kansas. bfridley@kumc.edu.
Cancer Epidemiol Biomarkers Prev ; 25(5): 780-90, 2016 05.
Article em En | MEDLINE | ID: mdl-26976855
ABSTRACT

BACKGROUND:

Many epithelial ovarian cancer (EOC) risk factors relate to hormone exposure and elevated estrogen levels are associated with obesity in postmenopausal women. Therefore, we hypothesized that gene-environment interactions related to hormone-related risk factors could differ between obese and non-obese women.

METHODS:

We considered interactions between 11,441 SNPs within 80 candidate genes related to hormone biosynthesis and metabolism and insulin-like growth factors with six hormone-related factors (oral contraceptive use, parity, endometriosis, tubal ligation, hormone replacement therapy, and estrogen use) and assessed whether these interactions differed between obese and non-obese women. Interactions were assessed using logistic regression models and data from 14 case-control studies (6,247 cases; 10,379 controls). Histotype-specific analyses were also completed.

RESULTS:

SNPs in the following candidate genes showed notable interaction IGF1R (rs41497346, estrogen plus progesterone hormone therapy, histology = all, P = 4.9 × 10(-6)) and ESR1 (rs12661437, endometriosis, histology = all, P = 1.5 × 10(-5)). The most notable obesity-gene-hormone risk factor interaction was within INSR (rs113759408, parity, histology = endometrioid, P = 8.8 × 10(-6)).

CONCLUSIONS:

We have demonstrated the feasibility of assessing multifactor interactions in large genetic epidemiology studies. Follow-up studies are necessary to assess the robustness of our findings for ESR1, CYP11A1, IGF1R, CYP11B1, INSR, and IGFBP2 Future work is needed to develop powerful statistical methods able to detect these complex interactions. IMPACT Assessment of multifactor interaction is feasible, and, here, suggests that the relationship between genetic variants within candidate genes and hormone-related risk factors may vary EOC susceptibility. Cancer Epidemiol Biomarkers Prev; 25(5); 780-90. ©2016 AACR.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Neoplasias Ovarianas Tipo de estudo: Etiology_studies / Observational_studies / Prognostic_studies / Risk_factors_studies Limite: Female / Humans / Middle aged Idioma: En Revista: Cancer Epidemiol Biomarkers Prev Assunto da revista: BIOQUIMICA / EPIDEMIOLOGIA / NEOPLASIAS Ano de publicação: 2016 Tipo de documento: Article
Texto completo
Adicionar na Minha BVS
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XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Neoplasias Ovarianas Tipo de estudo: Etiology_studies / Observational_studies / Prognostic_studies / Risk_factors_studies Limite: Female / Humans / Middle aged Idioma: En Revista: Cancer Epidemiol Biomarkers Prev Assunto da revista: BIOQUIMICA / EPIDEMIOLOGIA / NEOPLASIAS Ano de publicação: 2016 Tipo de documento: Article