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Review
. 2018 Apr 3;9(25):17915-17927.
doi: 10.18632/oncotarget.24681.

Microbiota effects on cancer: from risks to therapies

Affiliations
Review

Microbiota effects on cancer: from risks to therapies

Domenica Rea et al. Oncotarget. .

Abstract

Gut microbiota, a group of 1014 bacteria, eukaryotes and virus living in gastrointestinal tract, is crucial for many physiological processes in particular plays an important role in inflammatory and immune reactions. Several internal and external factors can influence this population, and shifts in their composition, have been demonstrated to contribute and affect different diseases. During dysbiosis several bacteria related to inflammation, one of the most necessary factors in carcinogenesis; it has been shown that some bacterial strains through deregulation of different signals/pathways may affect tumor development through the production of many factors. Gut microbiota might be considered as a holistic hub point for cancer development: direct and indirect involvements have been studying in several neoplasms such as colon rectal cancer, hepatocellular carcinoma and breast cancer. This review discuss over the evidence of crosstalk between gut microbiota and cancer, its ability to modulate chemotherapy, radiotherapy and immunotherapy, and the possibility that the intestinal microbial is a new target for therapeutic approaches to improve the prognosis and quality of life of cancer patients.

Keywords: cancer; colon rectal cancer; gut microbiota; inflammation; probiotics.

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Conflict of interest statement

CONFLICTS OF INTEREST The authors have no relevant competing interests.

Figures

Figure 1
Figure 1. Microbiota composition
Representative image of microbiota species in the GI (A), in particular at the level of the duodenum-jejunum-ileum, stomach and colon. (B) Description of the species present in the intestinal lumen and in epithelial surface-mucus layer.
Figure 2
Figure 2. Regulation of intestinal immune system
Regulation of intestinal immune system in pro-inflammatory (A) and anti-inflammatory conditions (B).
Figure 3
Figure 3. Etiology of hepatocellular carcinoma in model for obesity whit Gram Positive dysbiosis
Clostridium Clusters convert bile acid in DCA, which arrive at liver by portal system. Elevated levels of DCA induces SASP in HSCs, which in turn, secretes various inflammatory and tumor-promoting factors in liver, that promote the making of HCC. Abbreviations: SASP: Senescence Associated Secretory Phenotype, DCA: DexyCholic Acid, HSCs: Hepatic Stellate Cells, HCC: HepatoCellular Carcinoma.
Figure 4
Figure 4. Possible mechanisms of gastrointestinal microbiome for the development of breast cancer
Coniugated estrogens take place in liver. They are deconiugate by gut microbiota as free estrogens; these are reabsorbed through enterohepatic circulation. The reabsorption determine the elevated concentration of ‘‘estrogen-like substances’’ that induce the synthesis of ‘‘estrogen-inducible growth factors (estromedins)’’, which are polypeptides with carcinogenic potential with breast tropism.

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