Annelise M Wilhite1, Yasmine Baca2, Joanne Xiu2, Rajesh Paladugu3, Adam C ElNaggar4, Jubilee Brown5, Ira S Winer6, Robert Morris6, Britt K Erickson7, Alexander B Olawaiye8, Matthew Powell9, W Michael Korn2, Rodney P Rocconi9, Dineo Khabele10, Nathaniel L Jones3. 1. Mitchell Cancer Institute, University of South Alabama, Division of Gynecologic Oncology Mobile, AL, United States of America. Electronic address: awilhite@health.southalabama.edu. 2. Caris Life Sciences, Pheonix, AZ, United States of America. 3. Mitchell Cancer Institute, University of South Alabama, Division of Gynecologic Oncology Mobile, AL, United States of America. 4. West Cancer Center and Research Institute, Division of Gynecologic Oncology, Memphis, TN, United States of America. 5. Atrium Health, Division of Gynecologic Oncology, Charlotte, NC, United States of America. 6. Wayne State University and Karmanos Cancer Institute, Division of Gynecologic Oncology, Detroit, MI, United States of America. 7. University of Minnesota, Division of Gynecologic Oncology, Minneapolis, MN, United States of America. 8. Magee-Womens Hospital, University of Pittsburgh Medical Center, Division of Gynecologic Oncology, Pittsburgh, PA, United States of America. 9. University of Alabama at Birmingham, Division of Gynecologic Oncology, Birmingham, AL, United States of America. 10. Washington University, Division of Gynecologic Oncology, St. Louis, MO, United States of America.
Abstract
OBJECTIVES: Disparate outcomes exist between Black and White patients with endometrial cancer (EC). One contributing factor is the disproportionately low representation of Black patients in clinical trials and in tumor molecular profiling studies. Our objective was to investigate molecular profiles of ECs in a cohort with a high proportion of tumors from Black patients. METHODS: A total of 248 EC samples and self-reported race data were collected from 6 institutions. Comprehensive tumor profiling and analyses were performed by Caris Life Sciences. RESULTS: Tumors from 105 (42%) Black and 143 (58%) White patients were included. Serous histology (58% vs 36%) and carcinosarcoma (25% vs 16%), was more common among Black patients, and endometrioid was less common (17% vs 48%) (p < 0.01). Differences in gene mutations between cohorts corresponded to observed histologic differences between races. Specifically, TP53 mutations were predominant in serous tumors. In endometrioid tumors, mutations in ARID1A were the most common, and high rates of MSI-H, MMRd, and TMB-H were observed. In carcinosarcoma tumors, hormone receptor expression was high in tumors of Black patients (PR 23.4%, ER 30.8%). When stratified by histology, there were no significant differences between tumors from Black and White women. CONCLUSIONS: This cohort had a high proportion of tumors from Black women. Distinct molecular profiles were driven primarily by more aggressive histologic subtypes among Black women. Continued effort is needed to include Black women and other populations under-represented in EC molecular profiling studies as targeted therapies and personalized medicine become mainstream.
OBJECTIVES: Disparate outcomes exist between Black and White patients with endometrial cancer (EC). One contributing factor is the disproportionately low representation of Black patients in clinical trials and in tumor molecular profiling studies. Our objective was to investigate molecular profiles of ECs in a cohort with a high proportion of tumors from Black patients. METHODS: A total of 248 EC samples and self-reported race data were collected from 6 institutions. Comprehensive tumor profiling and analyses were performed by Caris Life Sciences. RESULTS: Tumors from 105 (42%) Black and 143 (58%) White patients were included. Serous histology (58% vs 36%) and carcinosarcoma (25% vs 16%), was more common among Black patients, and endometrioid was less common (17% vs 48%) (p < 0.01). Differences in gene mutations between cohorts corresponded to observed histologic differences between races. Specifically, TP53 mutations were predominant in serous tumors. In endometrioid tumors, mutations in ARID1A were the most common, and high rates of MSI-H, MMRd, and TMB-H were observed. In carcinosarcoma tumors, hormone receptor expression was high in tumors of Black patients (PR 23.4%, ER 30.8%). When stratified by histology, there were no significant differences between tumors from Black and White women. CONCLUSIONS: This cohort had a high proportion of tumors from Black women. Distinct molecular profiles were driven primarily by more aggressive histologic subtypes among Black women. Continued effort is needed to include Black women and other populations under-represented in EC molecular profiling studies as targeted therapies and personalized medicine become mainstream.