Abstract
Colorectal carcinoma (CRC) is a common disease, the incidence of which is increasing according to Western lifestyle; it remains to have a poor prognosis. Western nutriments are presumed to induce mild inflammation within the colonic mucosa, resulting in the accumulation of DNA alterations in colonocytes through a multistage carcinogenesis process. This suggests that most CRCs are related to the environment. Of interest, fecal microbiota composition has been shown yielding a novel approach regarding how environment changes may impact health and disease. Here, we compare whole shotgun metagenomic gut microbiota of two monozygotic twin sisters, one of whom is suffering from an advance colorectal tumor with a profound disequilibrium of the composition of the gut microbiota due to the overexpression of virulent bacteria such as E. coli, Shigella, and Clostridium species in the colon cancer patient’s feces contrasting with low levels of bacterial species such as Faecalibacterium and Akkermansia usually enriched in the healthy adults’ microbial flora. The disequilibrium in microbiota of the CRC patient’s feces as compared to her monozygotic twin sister is linked to inflammatory and immune cell infiltrates in the patient’s colonic tissue. We speculate on the role of microbiota disequilibrium on the immune-tolerant cell infiltrate within CRCs.
Highlights
Colorectal carcinoma (CRC) is one of the three most common cancers
With regard to the main bacteria genera usually associated with CRCs (for meta-analysis, see Ref. (Liu et al, 2019)), various species of Bacteroides, Escherichia, Fusobacteria, Clostridia, and Proteobacteria were enriched in the stool CRC compared with the control twin case
This establishes that gut microbiota dysbiosis in colorectal cancer conditions leads to an enrichment of pathogenic bacteria encompassing Shigella, Escherichia, Clostridia, and Streptococcus species
Summary
Colorectal carcinoma (CRC) is one of the three most common cancers. There are more than 1.2 million new cases per year worldwide, accounting for about 600,000 deaths (Jemal et al, 2011). The disease is due to a multistep process involving gene- and environment-related factors (Vogelstein et al, 1988; Jass, 2007; Cancer Genome Atlas Network, 2012). Accumulation of DNA alterations (e.g., punctual DNA mutation, hypo or hypermethylation of anti-oncogene or oncogene promotors, respectively) corrupts key signaling pathways in the colonic mucosa in various carcinogenesis processes that involve hyperproliferation, the development of aberrant crypt foci (ACF), a transition from adenoma to carcinoma, tumor invasion, and metastasis (Vogelstein et al, 1988; Jass, 2007; Cancer Genome Atlas Network, 2012). We analyzed gut microbiota as a boost for carcinogenesis in two monozygotic sisters and examined findings associated with tumor characteristics including inflammatory and immune patterns
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