Molecular mechanisms through which pathogenic E. coli can contribute to colorectal cancer development.

Post, Jesper (2023) Molecular mechanisms through which pathogenic E. coli can contribute to colorectal cancer development. Bachelor's Thesis, Biology.

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Abstract

In this review the current knowledge is shown on multiple aspects of colorectal cancer (CRC). The incidence of CRC is on the rise. This predicts a significant increase in the healthcare burden of the disease. CRC is predominantly a disease with a spontaneous genetic onset, in which genes like apc and TP53 are mutated. Often these mutations increase proliferative signalling of the colonic epithelial cells. Evidence amounts for the involvement of pathogenic strains of E. coli which have a pathogenic pks+ virulence island. This codes for a bacterial toxin called colibactin, which has a genotoxic effect because it can form crosslinks between DNA strands. In attempts by the host cell to repair this damage, mutations occur which can induce the onset of colorectal cancer. Furthermore, DNA repair systems are also undermined by an E. coli effector protein, EspF, which makes this a two-hit system. Research has also challenged healthy benefits of Nissle E. coli strains and oligosaccharide probiotics by connecting these to colorectal carcinogenesis. This knowledge can be applied to diagnostics, prognostics, and therapeutics. By combining standard screening with new molecular diagnostics, we can look for oncobacteria in samples of both at-risk (a)symptomatic individuals and patients. The genotoxin colibactin could be a target, by either blocking its active site or reducing its transcription. Finally, by combining early detection with therapeutics, disease outcome can be improved.

Item Type:	Thesis (Bachelor's Thesis)
Supervisor name:	Harmsen, H.J.M.
Degree programme:	Biology
Thesis type:	Bachelor's Thesis
Language:	English
Date Deposited:	06 Jul 2023 14:01
Last Modified:	06 Jul 2023 14:01
URI:	https://fse.studenttheses.ub.rug.nl/id/eprint/30372

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