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Christina M. Nagle (Population Health Department QIMR Berghofer Medical Research Institute Royal Brisbane Hospital Br) Christina M. Nagle (Population Health Department QIMR Berghofer Medical Research Institute Royal Brisbane Hospital Br) Tracy A. O'Mara (Genetics & Computational Biology Department QIMR Berghofer Medical Research Institute Royal Bri) Yen Tan (Genetics & Computational Biology Department QIMR Berghofer Medical Research Institute Royal Bri) Daniel D. Buchanan (Colorectal Oncogenomics Group Genetic Epidemiology Laboratory Department of Pathology The Univers) Andreas Obermair (Queensland Centre of Gynaecological Research Royal Brisbane and Women's Hospital Herston Australi) Penny Blomfield (The Royal Hobart Hospital) Michael A. Quinn (Department of Obstetrics and Gynaecology University of Melbourne Parkville Australia) Penelope M. Webb (Population Health Department QIMR Berghofer Medical Research Institute Royal Brisbane Hospital Br) Amanda B. Spurdle (Genetics & Computational Biology Department QIMR Berghofer Medical Research Institute Royal Bri) Australian Endometrial Cancer Study Group (Australian Endometrial Cancer Study Group)
저널정보
대한부인종양학회 Journal of Gynecologic Oncology Journal of Gynecologic Oncology Vol.29 No.3
발행연도
2018.1
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1 - 14 (14page)

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Objective: The risk of developing endometrial cancer (EC) and/or survival following a diagnosis of EC might differ by tumor DNA mismatch repair (MMR) status. We assessed the association between tumor MMR status (classified as MMR-proficient, somatic MMR-deficient, germline MMR-deficient) and the risk of developing EC and survival following a diagnosis of EC. Methods: We analyzed data from women who participated in the Australian National Endometrial Cancer Study (ANECS) conducted between 2005 and 2007. Risk analyses (698 cases/691 population controls) utilized sociodemographic and lifestyle information obtained from telephone interviews at recruitment. For survival analyses (728 cases), patients' clinical data was abstracted from medical records, and survival data were obtained via linkage with the Australian National Death Index. We used logistic regression analysis to evaluate the associations between tumor MMR status and EC risk, and proportional hazards models to perform survival analyses with adjustment of known prognostic factors. Results: Established risk factors for EC did not differ significantly by tumor MMR status. In analyses including all EC subtypes, overall and EC-specific survival did not differ by tumor MMR status. Among women with the most common endometrioid subtype, EC-specific survival was worse for women with somatic MMR-deficient EC compared to women with MMR-proficient EC (hazard ratio [HR]=2.18; 95% confidence interval [CI]=1.19–4.01). Conclusion: The risk of EC is not associated with MMR status. Accurate separation of germline from somatic causes of MMR deficiency suggests that patients with endometrioid subtype somatic MMR-deficient tumors have poorer EC-specific survival than those with MMR-proficient tumors, after accounting for other prognostic factors.

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