2013
DOI: 10.1016/j.tim.2013.08.004
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Fusobacterium spp. and colorectal cancer: cause or consequence?

Abstract: Although increasing evidence suggests a relationship between bacterial dysbiosis and colorectal cancer (CRC), few studies have identified specific microbes as etiologic factors. Recent studies have implicated overabundance of Fusobacterium species in association with colorectal adenomas and cancer. Two articles published in the current issue of Cell Host and Microbe provide insights into the mechanisms for this Fusobacterium-CRC relationship.

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Cited by 65 publications
(45 citation statements)
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“…pylori , E . coli , Fusobacterium , and Enterobacteriaceae have been implicated in colorectal carcinoma [38, 39]. Among microaerophilic bacteria, members of the genus Helicobacter are the most interesting, because they have been implicated in a variety of GI diseases including peptic ulcer, gastric cancer, and inflammatory bowel disease in humans and animals [32, 35, 37, 40].…”
Section: Discussionmentioning
confidence: 99%
“…pylori , E . coli , Fusobacterium , and Enterobacteriaceae have been implicated in colorectal carcinoma [38, 39]. Among microaerophilic bacteria, members of the genus Helicobacter are the most interesting, because they have been implicated in a variety of GI diseases including peptic ulcer, gastric cancer, and inflammatory bowel disease in humans and animals [32, 35, 37, 40].…”
Section: Discussionmentioning
confidence: 99%
“…␤-Catenin then translocates into the nucleus and stimulates the lymphocyte enhancer factor (LEF), T-cell factor (TCF), and NF-B oncogenes. This bacterium invades the cell via internalization of E-cadherin by clathrin; stimulates the interleukin-10 (IL-10), IL-8, IL-6, IL-1␤, tumor necrosis factor alpha (TNF-␣), and COX-2 inflammatory genes; and ultimately induces tumorigenesis (40,41). Prevotella can adhere to epithelial cell lamellipodia and construct bacterial biofilm via its special affinity (42).…”
Section: Discussionmentioning
confidence: 99%
“…As in APO, F. nucleatum is often detected in conjunction with other oral species, suggesting an oral source of infection [71]. The question arises whether F. nucleatum is a passenger or a driver of colorectal tumorigenesis [72,73]. Rubinstein et al demonstrate that F. nucleatum stimulates CRC cancer growth by modulating the E-cadherin/β catenin signaling via its unique FadA adheisn (see below).…”
Section: Diseases Implicating F Nucleatummentioning
confidence: 99%