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The microbiome and gynecologic cancer: cellular mechanisms and clinical applications
  1. Julia Chalif1,
  2. Heather Wang2,
  3. Daniel Spakowicz3,
  4. Allison Quick4,
  5. Elizabeth K Arthur5,
  6. David O’Malley1 and
  7. Laura M Chambers1
  1. 1Divison of Gynecologic Oncology, The Ohio State University Comprehensive Cancer Center – Arthur G James Cancer Hospital and Richard J Solove Research Institute, Columbus, Ohio, USA
  2. 2Ohio University College of Osteopathic Medicine, Athens, Ohio, USA
  3. 3Division of Medical Oncology, The Ohio State University Comprehensive Cancer Centre, Columbus, Ohio, USA
  4. 4Radiation Oncology, The Ohio State University Wexner Medical Center, Columbus, Ohio, USA
  5. 5The Ohio State University Comprehensive Cancer Center – James Cancer Hospital and Solove Research Institute, Columbus, Ohio, USA
  1. Correspondence to Dr Julia Chalif, Divison of Gynecologic Oncology, The Ohio State University Comprehensive Cancer Center– Arthur G James Cancer Hospital and Richard J Solove Research Institute, Columbus, Ohio, USA; Julia.Chalif{at}gmail.com

Abstract

The microbiome plays a vital function in maintaining human health and homeostasis. Each microbiota has unique characteristics, including those of the gastrointestinal and female reproductive tract. Dysbiosis, or alterations to the composition of the microbial communities, impacts the microbiota–host relationship and is linked to diseases, including cancer. In addition, studies have demonstrated that the microbiota can contribute to a pro-carcinogenic state through altered host immunologic response, modulation of cell proliferation, signaling, gene expression, and dysregulated metabolism of nutrients and hormones.

In recent years, the microbiota of the gut and female reproductive tracts have been linked to many diseases, including gynecologic cancers. Numerous pre-clinical and clinical studies have demonstrated that specific bacteria or microbial communities may contribute to the development of gynecologic cancers. Further, the microbiota may also impact the toxicity and efficacy of cancer therapies, including chemotherapy, immunotherapy, and radiation therapy in women with gynecologic malignancies. The microbiota is highly dynamic and may be altered through various mechanisms, including diet, exercise, medications, and fecal microbiota transplantation. This review provides an overview of the current literature detailing the relationship between gynecologic cancers and the microbiota of the female reproductive and gastrointestinal tracts, focusing on mechanisms of carcinogenesis and strategies for modulating the microbiota for cancer prevention and treatment. Advancing our understanding of the complex relationship between the microbiota and gynecologic cancer will provide a novel approach for prevention and therapeutic modulation in the future.

  • Uterine Cancer
  • Cervical Cancer
  • Ovarian Cancer
  • Gestational Trophoblastic Disease
  • Vulvar and Vaginal Cancer

https://doi.org/10.1136/ijgc-2023-004894

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    Footnotes

    • Twitter @laurajmoulton

    • Contributors JC: conceptualization, investigation, writing - original draft, writing - review and editing, project administration. HW: investigation, writing - original draft, writing - review and editing. DS: investigation, writing - original draft, writing - review and editing. AQ: investigation, writing - original draft, writing - review and editing. EKA: investigation, writing - original draft, writing - review and editing. DOM: conceptualization, investigation, writing - original draft, writing - review and editing, project administration, project supervision. LMC: conceptualization, investigation, writing - original draft, writing - review and editing, project administration, project supervision.

    • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

    • Competing interests JC, HW, DS, AQ, EKA, and LMC have no disclosures. DOM receives institutional research funding from AbbVie, Agenus, Aravive, AstraZeneca, Boston Biomedical, Clovis Oncology, Eisai, Exelixis, Genmab, GOG Foundation, ImmunoGen, IOVANCE Biotherapeutics, Leap Therapeutics, Merck, Mersana Therapeutics, NRG Oncology, OncoQuest, Precision Therapeutics, Regeneron Pharmaceuticals, Rubuis Therapeutics, Sutro Biopharma, TESARO, Advaxis, Alkermes, Arcus Biosciences, BeiGene, Bristol Myers Squibb, Deciphera Pharma, EMB Serono, Genentech, GlaxoSmithKline, Hoffman-La Roche, Incyte Corporation, Karyopharm, Ludwig Institute, Merck Sharp & Dohme Corporation, NCI, NovoCure, OncoC4 Inc., Pfizer Inc., Prelude Therapeutics, RTOG, Seattle Genetics (SeaGen), SWOG, and Verastem Inc. DOM receives consulting fees from AbbVie, Adaptimmune, Agenus Inc., Arquer Diagnostics, Arcus Biosciences Inc., AstraZeneca, Atossa Therapeutics, Boston Biomedical, Cardiff Oncology, Celcuity, Clovis Oncology, Corcept Therapeutics, Duality Bio, Eisai, Elevar, Exelixis, Genentech Inc., Genelux, GlaxoSmithKline, GOG Foundation, Hoffman-La Roche Inc., ImmunoGen Inc., Imvax, InterVenn, INXMED, IOVANCE Biotherapeutics, Janssen, Jazz Pharmaceuticals, Laekna, Leap Therapeutics Inc., Luzsana Biotechnology, Merck & Co, Merck Sharp & Dohme Corporation, Mersana Therapeutics Inc., Myriad, Novartis, NovoCure, OncoC4 Inc., Onconova, Regeneron Pharmaceuticals Inc., Repimmune, R Pharm, Roche Diagnostics, Seattle Genetics (SeaGen), Sorrento, Sutro Biopharma, Tarveda Therapeutics, Toray, Trillium, Umoja, Verastem Inc., VBL Therapeutics, Vincerx Pharma, Xencor, and Zentalis. No research or consulting funding was utilized in the execution or formulation of this study.

    • Provenance and peer review Not commissioned; externally peer reviewed.