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Review
. 2022 Feb 12;14(2):e22156.
doi: 10.7759/cureus.22156. eCollection 2022 Feb.

The Association of Microbiome Dysbiosis With Colorectal Cancer

Affiliations
Review

The Association of Microbiome Dysbiosis With Colorectal Cancer

Artem Artemev et al. Cureus. .

Abstract

Many studies have been conducted to identify the causative organisms in colorectal cancer (CRC) and compare the microbiota of healthy individuals and those with CRC. The pathways by which the microbiota promotes CRC development are not yet fully understood. The hypothesized mechanisms include damage to the DNA, production of carcinogenic metabolites, and promotion of chronic inflammation. In a state of dysbiosis, the gut loses protective bacteria and is enriched with pathogenic and cancer-promoting bacteria, which promotes functions associated with cancer such as angiogenesis, loss of apoptosis, and cell proliferation. We have established a strong link between microbiota dysbiosis and certain species of bacteria and even viruses involved in tumorigenesis. In this review, we look at some of the major identified species and how they are related to CRC. Future research should include and even focus on mycobiome and virome on CRC development. Due to the diversity of the gut microbiome, there is a high possibility that the gain and loss of bacteria and their metabolic functions lead to CRC.

Keywords: bacterial dysbiosis; cancer genomics; colon cancer prevention; colorectal cancer; gut microbiota; microbiome.

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. Pathophysiology of Bacteroides fragilis toxin resulting in colorectal cancer

References

    1. Colorectal cancer prevalence linked to human papillomavirus: a systematic review with meta-analysis. Pelizzer T, Dias CP, Poeta J, Torriani T, Roncada C. Rev Bras Epidemiol. 2016;19:791–802. - PubMed
    1. Clinical significance of signet-ring-cell colorectal cancer as a prognostic factor. Yun SO, Cho YB, Lee WY, Kim HC, Yun SH, Park YA, Huh JW. Ann Coloproctol. 2017;33:232–238. - PMC - PubMed
    1. The gut microbiome and colorectal cancer: a review of bacterial pathogenesis. Dahmus JD, Kotler DL, Kastenberg DM, Kistler CA. J Gastrointest Oncol. 2018;9:769–777. - PMC - PubMed
    1. Colorectal cancer in the young, many questions, few answers. Deen KI, Silva H, Deen R, Chandrasinghe PC. World J Gastrointest Oncol. 2016;8:481–488. - PMC - PubMed
    1. Rising incidence of early-onset colorectal cancer in Australia over two decades: report and review. Young JP, Win AK, Rosty C, et al. J Gastroenterol Hepatol. 2015;30:6–13. - PubMed

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