Differences in the microbial profiles of early stage endometrial cancers between Black and White women.


Journal

Gynecologic oncology
ISSN: 1095-6859
Titre abrégé: Gynecol Oncol
Pays: United States
ID NLM: 0365304

Informations de publication

Date de publication:
05 2022
Historique:
received: 20 01 2022
revised: 24 02 2022
accepted: 27 02 2022
pubmed: 13 3 2022
medline: 6 5 2022
entrez: 12 3 2022
Statut: ppublish

Résumé

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. 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. 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. 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.

Identifiants

pubmed: 35277280
pii: S0090-8258(22)00142-1
doi: 10.1016/j.ygyno.2022.02.021
pmc: PMC9093563
mid: NIHMS1791538
pii:
doi:

Substances chimiques

RNA, Ribosomal, 16S 0

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

248-256

Subventions

Organisme : NIEHS NIH HHS
ID : P30 ES010126
Pays : United States
Organisme : NCI NIH HHS
ID : R21 CA220269
Pays : United States
Organisme : NCI NIH HHS
ID : T32 CA244125
Pays : United States

Informations de copyright

Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare no competing financial interest for this manuscript.

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Auteurs

Gabrielle M Hawkins (GM)

University of North Carolina at Chapel Hill, Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, United States of America.

Wesley C Burkett (WC)

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.

Amber N McCoy (AN)

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.

Hazel B Nichols (HB)

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.

Andrew F Olshan (AF)

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.

Russell Broaddus (R)

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.

Jason D Merker (JD)

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.

Bernard Weissman (B)

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.

Wendy R Brewster (WR)

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.

Jeffrey Roach (J)

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.

Temitope O Keku (TO)

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.

Victoria Bae-Jump (V)

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.

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Classifications MeSH