Lung and Gut Microbiota as Potential Hidden Driver of Immunotherapy Efficacy in Lung Cancer.
Journal
Mediators of inflammation
ISSN: 1466-1861
Titre abrégé: Mediators Inflamm
Pays: United States
ID NLM: 9209001
Informations de publication
Date de publication:
2019
2019
Historique:
received:
22
05
2019
revised:
12
09
2019
accepted:
26
09
2019
entrez:
13
12
2019
pubmed:
13
12
2019
medline:
2
6
2020
Statut:
epublish
Résumé
Lung cancer is one of the deadliest and most common malignancies in the world, representing one of the greatest challenges in cancer treatment. Immunotherapy is rapidly changing standard treatment schedule and outcomes for patients with advanced malignancies. However, several ongoing studies are still attempting to elucidate the biomarkers that could predict treatment response as well as the new strategies to improve antitumor immune system response ameliorating immunotherapy efficacy. The complex of bacteria, fungi, and other microorganisms, termed microbiota, that live on the epithelial barriers of the host, are involved in the initiation, progression, and dissemination of cancer. The functional role of microbiota has attracted an accumulating attention recently. Indeed, it has been demonstrated that commensal microorganisms are required for the maturation, education, and function of the immune system regulating the efficacy of immunotherapy in the anticancer response. In this review, we discuss some of the major findings depicting bacteria as crucial gatekeeper for the immune response against tumor and their role as driver of immunotherapy efficacy in lung cancer with a special focus on the distinctive role of gut and lung microbiota in the efficacy of immunotherapy treatment.
Identifiants
pubmed: 31827379
doi: 10.1155/2019/7652014
pmc: PMC6885300
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
7652014Informations de copyright
Copyright © 2019 Carmine Carbone et al.
Déclaration de conflit d'intérêts
E.B. received honoraria or speakers' fee from MSD, Astra-Zeneca, Celgene, Pfizer, Helsinn, Eli-Lilly, BMS, Novartis, and Roche; E.B. also received research grants from I.A.S.L.C. (International Association for the Study of Lung Cancer), L.I.L.T. (Lega Italiana per la Lotta contro i Tumori), Fondazione Cariverona, Astra-Zeneca, Roche, and Open Innovation, not related to the submitted work. S.P. reports personal fees from Astra-Zeneca, Eli-Lilly, BMS, Boehringer Ingelheim, Roche, MSD, and Istituto Gentili, outside the submitted work. G.T. reports grants and others from Celgene, Novartis, Roche, Incyte, and Merck Serono and grants from Fondazione Cariverona, outside the submitted work. The remaining authors have nothing to disclose.
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