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      Diversification and deleterious role of microbiome in gastric cancer

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          Abstract

          Gut microbiota dictates the fate of several diseases, including cancer. Most gastric cancers (GC) belong to gastric adenocarcinomas (GAC). Helicobacter pylori colonizes the gastric epithelium and is the causative agent of 75% of all stomach malignancies globally. This bacterium has several virulence factors, including cytotoxin‐associated gene A (CagA), vacuolating cytotoxin (VacA), and outer membrane proteins (OMPs), all of which have been linked to the development of gastric cancer. In addition, bacteria such as Escherichia coli, Streptococcus, Clostridium, Haemophilus, Veillonella, Staphylococcus, and Lactobacillus play an important role in the development of gastric cancer. Besides, lactic acid bacteria (LAB) such as Bifidobacterium, Lactobacillus, Lactococcus, and Streptococcus were found in greater abundance in GAC patients. To identify potential diagnostic and therapeutic interventions for GC, it is essential to understand the mechanistic role of H. pylori and other bacteria that contribute to gastric carcinogenesis. Furthermore, understanding bacteria‐host interactions and bacteria‐induced inflammatory pathways in the host is critical for developing treatment targets for gastric cancer.

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          Comprehensive molecular characterization of gastric adenocarcinoma

          Adam J. Bass, Vesteinn Thorsson, Ilya Shmulevich … (2015)
          Gastric cancer is a leading cause of cancer deaths, but analysis of its molecular and clinical characteristics has been complicated by histological and aetiological heterogeneity. Here we describe a comprehensive molecular evaluation of 295 primary gastric adenocarcinomas as part of The Cancer Genome Atlas (TCGA) project. We propose a molecular classification dividing gastric cancer into four subtypes: tumours positive for Epstein–Barr virus, which display recurrent PIK3CA mutations, extreme DNA hypermethylation, and amplification of JAK2, CD274 (also known as PD-L1) and PDCD1LG2 (also knownasPD-L2); microsatellite unstable tumours, which show elevated mutation rates, including mutations of genes encoding targetable oncogenic signalling proteins; genomically stable tumours, which are enriched for the diffuse histological variant and mutations of RHOA or fusions involving RHO-family GTPase-activating proteins; and tumours with chromosomal instability, which show marked aneuploidy and focal amplification of receptor tyrosine kinases. Identification of these subtypes provides a roadmap for patient stratification and trials of targeted therapies.
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            Commensal Bifidobacterium promotes antitumor immunity and facilitates anti-PD-L1 efficacy.

            Ayelet Sivan, Leticia Corrales, Nathaniel A Hubert … (2015)
            T cell infiltration of solid tumors is associated with favorable patient outcomes, yet the mechanisms underlying variable immune responses between individuals are not well understood. One possible modulator could be the intestinal microbiota. We compared melanoma growth in mice harboring distinct commensal microbiota and observed differences in spontaneous antitumor immunity, which were eliminated upon cohousing or after fecal transfer. Sequencing of the 16S ribosomal RNA identified Bifidobacterium as associated with the antitumor effects. Oral administration of Bifidobacterium alone improved tumor control to the same degree as programmed cell death protein 1 ligand 1 (PD-L1)-specific antibody therapy (checkpoint blockade), and combination treatment nearly abolished tumor outgrowth. Augmented dendritic cell function leading to enhanced CD8(+) T cell priming and accumulation in the tumor microenvironment mediated the effect. Our data suggest that manipulating the microbiota may modulate cancer immunotherapy.
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              Formation of propionate and butyrate by the human colonic microbiota

              Petra Louis, Harry J. Flint (2017)
              The human gut microbiota ferments dietary non-digestible carbohydrates into short-chain fatty acids (SCFA). These microbial products are utilized by the host and propionate and butyrate in particular exert a range of health-promoting functions. Here an overview of the metabolic pathways utilized by gut microbes to produce these two SCFA from dietary carbohydrates and from amino acids resulting from protein breakdown is provided. This overview emphasizes the important role played by cross-feeding of intermediary metabolites (in particular lactate, succinate and 1,2-propanediol) between different gut bacteria. The ecophysiology, including growth requirements and responses to environmental factors, of major propionate and butyrate producing bacteria are discussed in relation to dietary modulation of these metabolites. A detailed understanding of SCFA metabolism by the gut microbiota is necessary to underpin effective strategies to optimize SCFA supply to the host.
              Article 0 comments Cited 948 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Indranil Chattopadhyay:
                ORCID: https://orcid.org/0000-0002-0191-2621
                indranil@cutn.ac.in , indranil_ch@yahoo.com
                Journal
                Journal ID (nlm-ta): Cancer Rep (Hoboken)
                Journal ID (iso-abbrev): Cancer Rep (Hoboken)
                Journal ID (doi): 10.1002/(ISSN)2573-8348
                Journal ID (publisher-id): CNR2
                Title: Cancer Reports
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Electronic): 2573-8348
                Publication date (Electronic): 02 August 2023
                Publication date Collection: November 2023
                Volume: 6
                Issue: 11 ( doiID: 10.1002/cnr2.v6.11 )
                Electronic Location Identifier: e1878
                Affiliations
                [ 1 ] Department of Biotechnology Central University of Tamil Nadu Thiruvarur India
                [ 2 ] ER stress and Mucosal Immunology Team School of Health Sciences, University of Tasmania Launceston Tasmania Australia
                Author notes
                [*] [* ] Correspondence

                Indranil Chattopadhyay, Department of Biotechnology, Central University of Tamil Nadu, Thiruvarur 610005, India.

                Email: indranil@ 123456cutn.ac.in ; indranil_ch@ 123456yahoo.com

                Author information
                https://orcid.org/0000-0002-0191-2621
                Article
                Publisher ID: CNR21878
                DOI: 10.1002/cnr2.1878
                PMC ID: 10644335
                PubMed ID: 37530125
                SO-VID: 4b9bfa4a-54e3-422d-b5b4-830107dd6b47
                Copyright © © 2023 The Authors. Cancer Reports published by Wiley Periodicals LLC.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date revision received : 20 June 2023
                Date received : 07 March 2023
                Date accepted : 22 July 2023
                Page count
                Figures: 2, Tables: 0, Pages: 10, Words: 8914
                Categories
                Subject: Review
                Subject: Reviews
                Custom metadata
                source-schema-version-number 2.0
                cover-date November 2023
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:6.3.4 mode:remove_FC converted:14.11.2023

                Keywords: bacterial metabolites,gastric cancer,gut microbiome,helicobacter pylori
                Data availability:
                Keywords: bacterial metabolites, gastric cancer, gut microbiome, helicobacter pylori

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