title: Microbes and Cancer.
abstract: Commensal microorganisms (the microbiota) live on all the surface barriers of our body and are particularly abundant and diverse in the distal gut. The microbiota and its larger host represent a metaorganism in which the cross talk between microbes and host cells is necessary for health, survival, and regulation of physiological functions locally, at the barrier level, and systemically. The ancestral molecular and cellular mechanisms stemming from the earliest interactions between prokaryotes and eukaryotes have evolved to mediate microbe-dependent host physiology and tissue homeostasis, including innate and adaptive resistance to infections and tissue repair. Mostly because of its effects on metabolism, cellular proliferation, inflammation, and immunity, the microbiota regulates cancer at the level of predisposing conditions, initiation, genetic instability, susceptibility to host immune response, progression, comorbidity, and response to therapy. Here, we review the mechanisms underlying the interaction of the microbiota with cancer and the evidence suggesting that the microbiota could be targeted to improve therapy while attenuating adverse reactions.
authors.affiliation: Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, email: trinchig@mail.nih.gov.
authors.forename: Amiran
authors.initials: A
authors.lastname: Dzutsev
authors.affiliation: Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, email: trinchig@mail.nih.gov.
authors.forename: Jonathan H
authors.initials: JH
authors.lastname: Badger
authors.affiliation: Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, email: trinchig@mail.nih.gov.
authors.forename: Ernesto
authors.initials: E
authors.lastname: Perez-Chanona
authors.affiliation: Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, email: trinchig@mail.nih.gov.
authors.forename: Soumen
authors.initials: S
authors.lastname: Roy
authors.affiliation: Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, email: trinchig@mail.nih.gov.
authors.forename: Rosalba
authors.initials: R
authors.lastname: Salcedo
authors.affiliation: Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, email: trinchig@mail.nih.gov.
authors.forename: Carolyne K
authors.initials: CK
authors.lastname: Smith
authors.affiliation: Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, email: trinchig@mail.nih.gov.
authors.forename: Giorgio
authors.initials: G
authors.lastname: Trinchieri
mesh_terms: D056704:Adaptive Immunity; D000818:Animals; D000970:Antineoplastic Agents / Q000627:therapeutic use; D063646:Carcinogenesis; D006801:Humans; D007113:Immunity, Innate; D007167:Immunotherapy / Q000379:methods*; D007249:Inflammation; D007413:Intestinal Mucosa / Q000276:immunology*; D064307:Microbiota / Q000276:immunology*; D009369:Neoplasms / Q000276:immunology* / Q000382:microbiology / Q000628:therapy; D014945:Wound Healing
chemical_list: D000970:Antineoplastic Agents
keywords: cachexia; cancer; carcinogenesis; chemotherapy; immunotherapy; metabolism and cancer; microbiota