TY - JOUR
T1 - Anti-Mullerian hormone and endometrial cancer
T2 - A multi-cohort study
AU - Fortner, Renée T.
AU - Schock, Helena
AU - Jung, Seungyoun
AU - Allen, Naomi E.
AU - Arslan, Alan A.
AU - Brinton, Louise A.
AU - Egleston, Brian L.
AU - Falk, Roni T.
AU - Gunter, Marc J.
AU - Helzlsouer, Kathy J.
AU - Idahl, Annika
AU - Johnson, Theron S.
AU - Kaaks, Rudolf
AU - Krogh, Vittorio
AU - Lundin, Eva
AU - Merritt, Melissa A.
AU - Navarro, Carmen
AU - Onland-Moret, N. Charlotte
AU - Palli, Domenico
AU - Shu, Xiao Ou
AU - Sluss, Patrick M.
AU - Staats, Paul N.
AU - Trichopoulou, Antonia
AU - Weiderpass, Elisabete
AU - Zeleniuch-Jacquotte, Anne
AU - Zheng, Wei
AU - Dorgan, Joanne F.
N1 - Funding Information:
This work was supported by US National Institutes of Health (NIH) grant R01 CA163018 to JF Dorgan. RT Fortner was supported by a Marie Curie International Incoming Fellowship of the European Commission’s Seventh Framework Programme (MC-IIF-623984). Cancer incidence data for CLUE were provided by the Maryland Cancer Registry, Center for Cancer Surveillance and Control, Department of Health and Mental Hygiene, 201W. Preston Street, Room 400, Baltimore, MD 21201, http:// phpa.dhmh.maryland.gov/cancer, 410–767–4055. We acknowledge the State of Maryland, the Maryland Cigarette Restitution Fund, and the National Program of Cancer Registries of the Centers for Disease Control and Prevention for the funds that support the collection and availability of the cancer registry data. The NYU Women’s Health Study is supported by grants R01 CA178949, CA098661, UM1 CA182934, and centre grants P30 CA016087 and P30 ES000260. The Shanghai Women’s Health Study is supported by NIH grants R37 CA070867 and UM1 CA182910. The coordination of EPIC is financially supported by the European Commission (DG-SANCO) and the International Agency for Research on Cancer. The national cohorts are supported by Danish Cancer Society (Denmark); Ligue Contre le Cancer, Institut Gustave Roussy, Mutuelle Générale de l’Education Nationale, Institut National de la Santé et de la Recherche Médicale (INSERM; France); German Cancer Aid, German Cancer Research Center (DKFZ), Federal Ministry of Education and Research (BMBF), Deutsche Krebshilfe, Deutsches Krebsforschungszentrum, and Federal Ministry of Education and Research (Germany); the Hellenic Health Foundation (Greece); Associazione Italiana per la Ricerca sul Cancro-AIRC-Italy and National Research Council (Italy); Dutch Ministry of Public Health, Welfare and Sports (VWS), Netherlands Cancer Registry (NKR), LK Research Funds, Dutch Prevention Funds, Dutch ZON (Zorg Onderzoek Nederland), World Cancer Research Fund (WCRF), Statistics Netherlands (the Netherlands); ERC-2009-AdG 232997 and Nordforsk, Nordic Centre of Excellence programme on Food, Nutrition and Health (Norway); Health Research Fund (FIS), PI13/00061 to Granada; PI13/01162 to EPIC-Murcia, Regional Governments of Andalucía, Asturias, Basque Country, Murcia and Navarra, ISCIII RETIC (RD06/0020; Spain); Swedish Cancer Society, Swedish Research Council and County Councils of Skåne and Västerbotten (Sweden); Cancer Research UK (14136 to EPIC-Norfolk; C570/ A16491 and C8221/A19170 to EPIC-Oxford), Medical Research Council (1000143 to EPIC-Norfolk, MR/M012190/1 to EPIC-Oxford; UK).
Publisher Copyright:
© 2017 Cancer Research UK. All Rights Reserved.
PY - 2017
Y1 - 2017
N2 - Background: TheMullerian ducts are the embryological precursors of the female reproductive tract, including the uterus; anti-Mullerian hormone (AMH) has a key role in the regulation of foetal sexual differentiation. Anti-Mullerian hormone inhibits endometrial tumour growth in experimental models by stimulating apoptosis and cell cycle arrest. To date, there are no prospective epidemiologic data on circulating AMH and endometrial cancer risk. Methods: We investigated this association among women premenopausal at blood collection in a multicohort study including participants from eight studies located in the United States, Europe, and China. We identified 329 endometrial cancer cases and 339 matched controls. Anti- Mullerian hormone concentrations in blood were quantified using an enzyme-linked immunosorbent assay. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CI) across tertiles and for a doubling of AMH concentrations (ORlog2). Subgroup analyses were performed by ages at blood donation and diagnosis, oral contraceptive use, and tumour characteristics. Results: Anti-Mullerian hormone was not associated with the risk of endometrial cancer overall (ORlog2: 1.07 (0.99-1.17)), or with any of the examined subgroups. Conclusions: Although experimental models implicate AMH in endometrial cancer growth inhibition, our findings do not support a role for circulating AMH in the aetiology of endometrial cancer.
AB - Background: TheMullerian ducts are the embryological precursors of the female reproductive tract, including the uterus; anti-Mullerian hormone (AMH) has a key role in the regulation of foetal sexual differentiation. Anti-Mullerian hormone inhibits endometrial tumour growth in experimental models by stimulating apoptosis and cell cycle arrest. To date, there are no prospective epidemiologic data on circulating AMH and endometrial cancer risk. Methods: We investigated this association among women premenopausal at blood collection in a multicohort study including participants from eight studies located in the United States, Europe, and China. We identified 329 endometrial cancer cases and 339 matched controls. Anti- Mullerian hormone concentrations in blood were quantified using an enzyme-linked immunosorbent assay. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CI) across tertiles and for a doubling of AMH concentrations (ORlog2). Subgroup analyses were performed by ages at blood donation and diagnosis, oral contraceptive use, and tumour characteristics. Results: Anti-Mullerian hormone was not associated with the risk of endometrial cancer overall (ORlog2: 1.07 (0.99-1.17)), or with any of the examined subgroups. Conclusions: Although experimental models implicate AMH in endometrial cancer growth inhibition, our findings do not support a role for circulating AMH in the aetiology of endometrial cancer.
UR - http://www.scopus.com/inward/record.url?scp=85033397473&partnerID=8YFLogxK
U2 - 10.1038/bjc.2017.299
DO - 10.1038/bjc.2017.299
M3 - Article
C2 - 28873086
AN - SCOPUS:85033397473
SN - 0007-0920
VL - 117
SP - 1412
EP - 1418
JO - British Journal of Cancer
JF - British Journal of Cancer
IS - 9
ER -