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Lynch syndrome and cervical cancer.
Int J Cancer. 2015 Dec 01; 137(11):2757-61.IJ

Abstract

Carriers of germline mutations in DNA mismatch repair (MMR) genes are at increased risk of several cancers including colorectal and gynecologic cancers (Lynch syndrome). There is no substantial evidence that these mutations are associated with an increased risk of cervical cancer. A total of 369 families with at least one carrier of a mutation in a MMR gene (133 MLH1, 174 MSH2, 35 MSH6 and 27 PMS2) were ascertained via population cancer registries or via family cancer clinics in Australia, New Zealand, Canada, and USA. Personal and family histories of cancer were obtained from participant interviews. Modified segregation analysis was used to estimate the hazard ratio (incidence rates for carriers relative to those for the general population), and age-specific cumulative risks of cervical cancer for carriers. A total of 65 cases of cervical cancer were reported (including 10 verified by pathology reports). The estimated incidence was 5.6 fold (95% CI: 2.3-13.8; p = 0.001) higher for carriers than for the general population with a corresponding cumulative risk to 80 years of 4.5% (95% CI: 1.9-10.7%) compared with 0.8% for the general population. The mean age at diagnosis was 43.1 years (95% CI: 40.0-46.2), 3.9 years younger than the reported USA population mean of 47.0 years (p = 0.02). Women with MMR gene mutations were found to have an increased risk of cervical cancer. Due to limited pathology verification we cannot be certain that a proportion of these cases were not lower uterine segment endometrial cancers involving the endocervix, a recognized cancer of Lynch syndrome.

Authors+Show Affiliations

Familial Cancer Centre, Royal Melbourne Hospital, Cabrini Health and Southern Health, Parkville, VIC, Australia.Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Parkville, VIC, Australia.Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Parkville, VIC, Australia.Familial Cancer Centre, Peter MacCallum Cancer Centre, East Melbourne, VIC, Australia.Faculty of Health Sciences and Medicine, Bond University, Gold Coast, QLD, Australia.University of Queensland Centre for Clinical Research, Royal Brisbane Hospital, Herston, Queensland, Australia.Lunenfeld Tanenbaum Research Institute, Mount Sinai Hospital, University of Toronto, Toronto, ON, Canada.Department of Health Science Research, Mayo Clinic Arizona, Scottsdale, AZ.Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI.Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Parkville, VIC, Australia. Department of Epidemiology and Institute of Health and Environment, School of Public Health, Seoul National University, Seoul, Korea.Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA. School of Public Health, University of Washington, Seattle, WA.Division of Oncology, Department of Medicine, Stanford Cancer Institute, Stanford University, CA.Digestive Diseases Institute, Cleveland Clinic, Cleveland, OH.Hereditary Cancer Clinic, Prince of Wales Hospital, Sydney, NSW, Australia.Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Parkville, VIC, Australia. Oncogenomics Group, Genetic Epidemiology Laboratory, Department of Pathology, The University of Melbourne, Parkville, VIC, Australia.Department of Haematology and Oncology, The Queen Elizabeth Hospital, Woodville, SA, Australia. SAHMRI Colorectal Node, Basil Hetzel Institute for Translational Research, Woodville, SA, Australia. School of Medicine, University of Adelaide, SA, Australia.Genetic Medicine and Family Cancer Clinic, Royal Melbourne Hospital, Parkville, VIC, Australia. Department of Medicine, The University of Melbourne, Parkville, VIC, Australia.Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Parkville, VIC, Australia.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26077226

Citation

Antill, Yoland C., et al. "Lynch Syndrome and Cervical Cancer." International Journal of Cancer, vol. 137, no. 11, 2015, pp. 2757-61.
Antill YC, Dowty JG, Win AK, et al. Lynch syndrome and cervical cancer. Int J Cancer. 2015;137(11):2757-61.
Antill, Y. C., Dowty, J. G., Win, A. K., Thompson, T., Walsh, M. D., Cummings, M. C., Gallinger, S., Lindor, N. M., Le Marchand, L., Hopper, J. L., Newcomb, P. A., Haile, R. W., Church, J., Tucker, K. M., Buchanan, D. D., Young, J. P., Winship, I. M., & Jenkins, M. A. (2015). Lynch syndrome and cervical cancer. International Journal of Cancer, 137(11), 2757-61. https://doi.org/10.1002/ijc.29641
Antill YC, et al. Lynch Syndrome and Cervical Cancer. Int J Cancer. 2015 Dec 1;137(11):2757-61. PubMed PMID: 26077226.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Lynch syndrome and cervical cancer. AU - Antill,Yoland C, AU - Dowty,James G, AU - Win,Aung Ko, AU - Thompson,Tina, AU - Walsh,Michael D, AU - Cummings,Margaret C, AU - Gallinger,Steven, AU - Lindor,Noralane M, AU - Le Marchand,Loïc, AU - Hopper,John L, AU - Newcomb,Polly A, AU - Haile,Robert W, AU - Church,James, AU - Tucker,Katherine M, AU - Buchanan,Daniel D, AU - Young,Joanne P, AU - Winship,Ingrid M, AU - Jenkins,Mark A, Y1 - 2015/07/14/ PY - 2015/05/21/received PY - 2015/06/03/accepted PY - 2015/6/17/entrez PY - 2015/6/17/pubmed PY - 2015/12/15/medline KW - Lynch syndrome KW - cervical cancer KW - mismatch repair SP - 2757 EP - 61 JF - International journal of cancer JO - Int. J. Cancer VL - 137 IS - 11 N2 - Carriers of germline mutations in DNA mismatch repair (MMR) genes are at increased risk of several cancers including colorectal and gynecologic cancers (Lynch syndrome). There is no substantial evidence that these mutations are associated with an increased risk of cervical cancer. A total of 369 families with at least one carrier of a mutation in a MMR gene (133 MLH1, 174 MSH2, 35 MSH6 and 27 PMS2) were ascertained via population cancer registries or via family cancer clinics in Australia, New Zealand, Canada, and USA. Personal and family histories of cancer were obtained from participant interviews. Modified segregation analysis was used to estimate the hazard ratio (incidence rates for carriers relative to those for the general population), and age-specific cumulative risks of cervical cancer for carriers. A total of 65 cases of cervical cancer were reported (including 10 verified by pathology reports). The estimated incidence was 5.6 fold (95% CI: 2.3-13.8; p = 0.001) higher for carriers than for the general population with a corresponding cumulative risk to 80 years of 4.5% (95% CI: 1.9-10.7%) compared with 0.8% for the general population. The mean age at diagnosis was 43.1 years (95% CI: 40.0-46.2), 3.9 years younger than the reported USA population mean of 47.0 years (p = 0.02). Women with MMR gene mutations were found to have an increased risk of cervical cancer. Due to limited pathology verification we cannot be certain that a proportion of these cases were not lower uterine segment endometrial cancers involving the endocervix, a recognized cancer of Lynch syndrome. SN - 1097-0215 UR - https://www.unboundmedicine.com/medline/citation/26077226/Lynch_syndrome_and_cervical_cancer_ L2 - https://doi.org/10.1002/ijc.29641 DB - PRIME DP - Unbound Medicine ER -