Etiologic heterogeneity in endometrial cancer: Evidence from a Gynecologic Oncology Group trial

Louise A. Brinton, Ashley S. Felix, D. Scott McMeekin, William T. Creasman, Mark E. Sherman, David Mutch, David E. Cohn, Joan L. Walker, Richard G. Moore, Levi S Downs, Robert A. Soslow, Richard Zaino

Research output: Contribution to journalArticlepeer-review

174 Scopus citations


Objective: Although the epidemiology of typical endometrial carcinomas (grades 1-2 endometrioid or Type I) is well established, less is known regarding higher grade endometrioid or non-endometrioid carcinomas (Type II). Within a large Gynecologic Oncology Group trial (GOG-210), which included central pathology review, we investigated the etiologic heterogeneity of endometrial cancers by comparing risk factors for different histologic categories. Methods: Based on epidemiologic questionnaire data, risk factor associations, expressed as odds ratios (OR) with 95% confidence intervals (CI), were estimated comparing grade 3 endometrioid and Type II cancers (including histologic subtypes) to grades 1-2 endometrioid cancers. Results: Compared with 2244 grades 1-2 endometrioid cancers, women with Type II cancers (321 serous, 141 carcinosarcomas, 77 clear cell, 42 mixed epithelial with serous or clear cell components) were older; more often non-white, multiparous, current smokers; and less often obese. Risk factors for grade 3 endometrioid carcinomas (n = 354) were generally similar to those identified for Type II cancers, although patients with grade 3 endometrioid tumors more often had histories of breast cancer without tamoxifen exposure while those with Type II tumors were more frequently treated with tamoxifen. Patients with serous cancers and carcinosarcomas more frequently had breast cancer histories with tamoxifen treatment compared to patients with other tumors. Conclusions: Risk factors for aggressive endometrial cancers, including grade 3 endometrioid and non-endometrioid tumors, appear to differ from lower grade endometrioid carcinomas. Our findings support etiologic differences between Type I and II endometrial cancers as well as additional heterogeneity within Type II cancers.

Original languageEnglish (US)
Pages (from-to)277-284
Number of pages8
JournalGynecologic oncology
Issue number2
StatePublished - May 2013

Bibliographical note

Funding Information:
The following institutions participated in this study: Roswell Park Cancer Institute, University of Alabama at Birmingham, Duke University Medical Center, Abington Memorial Hospital, Walter Reed Army Medical Center, Wayne State University, University of Minnesota Medical School, Northwestern University, University of Mississippi, University of Colorado-Anschutz Cancer Pavilion, University of California at Los Angeles, Fred Hutchinson Cancer Research Center, Penn State Milton S. Hershey Medical Center, University of Cincinnati, University of North Carolina, University of Iowa Hospitals and Clinics, University of Texas Southwestern Medical Center, Indiana University Medical Center, Wake Forest University Health Sciences, University of California Medical Center at Irvine — Orange Campus, Magee Women's Hospital — University of Pittsburgh Medical Center, University of New Mexico, Cleveland Clinic Foundation, State University of New York at Stony Brook, Washington University School of Medicine, Cooper Hospital/University Medical Center, Columbus Cancer Council/Ohio State, University of Massachusetts Memorial Health Care, Fox Chase Cancer Center, Women's Cancer Center of Nevada, University of Oklahoma Health Sciences Center, University of Virginia, University of Chicago, Mayo Clinic, Case Western Reserve University, Moffitt Cancer Center and Research Institute, Yale University, University of Wisconsin Hospital, Women and Infants' Hospital, The Hospital of Central Connecticut at New Britain General, GYN Oncology of West Michigan, PLLC and Community Clinical Oncology Program.


  • Carcinosarcoma
  • Endometrial cancer
  • Epidemiology
  • Etiology
  • Serous endometrial cancer
  • Type II endometrial cancer


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