Gabrielle M Hawkins1, Wesley C Burkett2, Amber N McCoy3, Hazel B Nichols4, Andrew F Olshan5, Russell Broaddus6, Jason D Merker7, Bernard Weissman8, Wendy R Brewster9, Jeffrey Roach10, Temitope O Keku11, Victoria Bae-Jump12. 1. University of North Carolina at Chapel Hill, Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, United States of America. 2. University of North Carolina at Chapel Hill, Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, United States of America. Electronic address: wesley.burkett@unchealth.unc.edu. 3. University of North Carolina at Chapel Hill, Department of Medicine, Center for Gastrointestinal Biology and Disease, United States of America. Electronic address: amber_mccoy@med.unc.edu. 4. University of North Carolina at Chapel Hill, Gillings School of Global Public Health, Department of Epidemiology, United States of America; University of North Carolina at Chapel Hill, Lineberger Comprehensive Cancer Center, United States of America. Electronic address: hbn@email.unc.edu. 5. University of North Carolina at Chapel Hill, Gillings School of Global Public Health, Department of Epidemiology, United States of America; University of North Carolina at Chapel Hill, Lineberger Comprehensive Cancer Center, United States of America. Electronic address: andy_olshan@unc.edu. 6. University of North Carolina at Chapel Hill, Lineberger Comprehensive Cancer Center, United States of America; University of North Carolina at Chapel Hill, Department of Pathology and Laboratory Medicine, United States of America. Electronic address: rbroaddus@med.unc.edu. 7. University of North Carolina at Chapel Hill, Lineberger Comprehensive Cancer Center, United States of America; University of North Carolina at Chapel Hill, Department of Pathology and Laboratory Medicine, United States of America. Electronic address: jason_merker@med.unc.edu. 8. University of North Carolina at Chapel Hill, Lineberger Comprehensive Cancer Center, United States of America; University of North Carolina at Chapel Hill, Department of Pathology and Laboratory Medicine, United States of America. Electronic address: bernard_weissman@med.unc.edu. 9. University of North Carolina at Chapel Hill, Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, United States of America; University of North Carolina at Chapel Hill, Lineberger Comprehensive Cancer Center, United States of America. Electronic address: wrbrewst@med.unc.edu. 10. University of North Carolina at Chapel Hill, Department of Medicine, Center for Gastrointestinal Biology and Disease, United States of America. Electronic address: jeff_roach@unc.edu. 11. University of North Carolina at Chapel Hill, Department of Medicine, Center for Gastrointestinal Biology and Disease, United States of America. Electronic address: temitope_keku@med.unc.edu. 12. University of North Carolina at Chapel Hill, Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, United States of America; University of North Carolina at Chapel Hill, Lineberger Comprehensive Cancer Center, United States of America. Electronic address: victoria_baejump@med.unc.edu.
Abstract
OBJECTIVE: Black women suffer a higher mortality from endometrial cancer (EC) than White women. Potential biological causes for this disparity include a higher prevalence of obesity and more lethal histologic/molecular subtypes. We hypothesize that another biological factor driving this racial disparity could be the EC microbiome. METHODS: Banked tumor specimens of postmenopausal, Black and White women undergoing hysterectomy for early stage endometrioid EC were identified. The microbiota of the tumors were characterized by bacterial 16S rRNA sequencing. The microbial component of endometrioid ECs in The Cancer Genome Atlas (TCGA) database were assessed for comparison. RESULTS: 95 early stage ECs were evaluated: 23 Black (24%) and 72 White (76%). Microbial diversity was increased (p < 0.001), and Firmicutes, Cyanobacteria and OD1 phyla abundance was higher in tumors from Black versus White women (p < 0.001). Genus level abundance of Dietzia and Geobacillus were found to be lower in tumors of obese Black versus obese White women (p < 0.001). Analysis of early stage ECs in TCGA found that microbial diversity was higher in ECs from Black versus White women (p < 0.05). When comparing ECs from obese Black versus obese White women, 5 bacteria distributions were distinct, with higher abundance of Lactobacillus acidophilus in ECs from Black women being the most striking difference. Similarly in TCGA, Dietzia and Geobacillus were more common in ECs from White women compared to Black. CONCLUSION: Increased microbial diversity and the distinct microbial profiles between ECs of obese Black versus obese White women suggests that intra-tumoral bacteria may contribute to EC disparities and pathogenesis.
OBJECTIVE: Black women suffer a higher mortality from endometrial cancer (EC) than White women. Potential biological causes for this disparity include a higher prevalence of obesity and more lethal histologic/molecular subtypes. We hypothesize that another biological factor driving this racial disparity could be the EC microbiome. METHODS: Banked tumor specimens of postmenopausal, Black and White women undergoing hysterectomy for early stage endometrioid EC were identified. The microbiota of the tumors were characterized by bacterial 16S rRNA sequencing. The microbial component of endometrioid ECs in The Cancer Genome Atlas (TCGA) database were assessed for comparison. RESULTS: 95 early stage ECs were evaluated: 23 Black (24%) and 72 White (76%). Microbial diversity was increased (p < 0.001), and Firmicutes, Cyanobacteria and OD1 phyla abundance was higher in tumors from Black versus White women (p < 0.001). Genus level abundance of Dietzia and Geobacillus were found to be lower in tumors of obese Black versus obese White women (p < 0.001). Analysis of early stage ECs in TCGA found that microbial diversity was higher in ECs from Black versus White women (p < 0.05). When comparing ECs from obese Black versus obese White women, 5 bacteria distributions were distinct, with higher abundance of Lactobacillus acidophilus in ECs from Black women being the most striking difference. Similarly in TCGA, Dietzia and Geobacillus were more common in ECs from White women compared to Black. CONCLUSION: Increased microbial diversity and the distinct microbial profiles between ECs of obese Black versus obese White women suggests that intra-tumoral bacteria may contribute to EC disparities and pathogenesis.
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