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• W2068789516 abstract "Dear Sir, The recent correspondence by Biyani et al. [1] is a thorough discussion of the recent hypothesis that carcinogenesis can occur in hyperplastic colonic polyps. However, the ‘Deleted in Colorectal Carcinoma’ (DCC) gene, which they refer, has not been definitively proved to be involved in the initiation of colorectal carcinogenesis. Mutations in the DCC gene were thought to be involved in this process [2], because 18q allelic loss was very frequently seen in colorectal carcinoma. Later studies identified this gene as being located at 18q21.3. Further analysis showed the DCC gene actually coded for a component of the receptor complex that mediated the effects of netrin-1, a molecule involved in axon guidance [3], which seemed an unlikely function for this role. In a study of 57 colorectal cancers, it was found that there were almost never any mutations in the DCC gene in human colorectal tumours showing 18q allelic loss [4]. Mouse knockout models of adenomatous polyposis coli (APC) ⁄ DCC have shown that loss of the DCC gene in mice that have adenomas initiated by APC loss causes a bias towards highly dysplastic adenomas [5]. The DCC gene possesses pro-apoptotic activity, thought to be because of cleavage by a capsase (cysteine protease) exposing a pro-apoptotic domain on the DCC receptor, which is inhibited by netrin-1. Over-expression of netrin-1 in mouse models, coupled with loss of the APC gene has been shown to suppress pro-apoptotic activity and is postulated to promote carcinogenesis [5]. However, studies of human colorectal cancers [5] have shown that only 7% of colorectal cancers have overexpression of netrin-1, implying that loss of the DCC receptor complex by 18q allelic loss or direct mutation may not confer the same selective advantage towards human colorectal cancer cells. Characterization and identification of other tumour suppressor genes in the region of 18q21 revealed two candidate genes, namely SMAD2 and SMAD4. The protein product of the SMAD4 gene encodes for intracellular mediators of the transforming growth factor (TGF)-b pathway [6,7]. The TGF-b pathway acts as a tumour suppressor pathway in normal colonic epithelium, as proved by inactivation studies in knock-out mice [8] and the SMAD2 and SMAD4 genes have been found to be mutated in colorectal cancer [9]. In conclusion, the DCC gene may play a role in the development and metastasis of colorectal cancer, although its role in initiation is still unclear." @default.
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• W2068789516 date "2008-07-01" @default.
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• W2068789516 title "The DCC gene and colorectal cancer: the story is more complex" @default.
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• W2068789516 doi "https://doi.org/10.1111/j.1463-1318.2008.01474.x" @default.
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