Abstract
The recent demonstration of a role of Escherichia coli in the development of invasive carcinoma in mice ushers a new era of bacterial involvement in cancer aetiology. It has been shown previously that the colonic mucosa of colorectal carcinoma (CRC) is exclusively colonized by intracellular E. coli instead of extracellular form found in normal colonic mucosa. Surprisingly, the DNA repair gene MUTYH, which is a homologue of the E. coli gene mutY, is responsible for CRC. The current paper discusses the potential role of mutY in CRC aetiology and concludes that research in this area can bring together the diverse threads of the CRC aetiology puzzle.
| Original language | English |
|---|---|
| Pages (from-to) | 127-131 |
| Number of pages | 5 |
| Journal | Cancer Letters |
| Volume | 341 |
| Issue number | 2 |
| Early online date | 7 Aug 2013 |
| DOIs | |
| Publication status | Published - Dec 2013 |
Keywords
- Escherichia coli
- Colon Cancer
- E. coli
- mut Y
- MUTYH
- chronic inflammation
- carcinogenesis
Access to Document
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NOTICE: this is the author’s version of a work that was accepted for publication in Cancer Letters. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in CANCER LETTERS, [VOL 341, ISSUE 2, (2013)] DOI: 10.1016/j.canlet.2013.08.003