Analysis of genetic mutation and expression of p63, Hwnt2 and TSG101 in colorectal carcinoma
Colorectal carcinoma (CRC) arises as a result of mutational activation of oncogenes coupled with inactivation of tumour suppressor genes. Mutations in APe, K-ras and p53 have been commonly reported. The p63 gene, a member of the p53 gene family, has been previously reported by others to be mutated i...
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| Format: | Thesis |
| Language: | English |
| Published: |
2007
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| Subjects: | |
| Online Access: | http://ir.unimas.my/id/eprint/24791/2/Ma%20Xiang%20Ru.pdf |
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| Summary: | Colorectal carcinoma (CRC) arises as a result of mutational activation of oncogenes coupled with inactivation of tumour suppressor genes. Mutations in APe, K-ras and p53 have been commonly reported. The p63 gene, a member of the p53 gene family, has been previously reported by others to be mutated in colon cancer cell-lines. This gene plays essential roles in development and its increased expression was reported
in squamous cell carcinoma of lung tumours and bladder carcinomas. Hwnt2 and TSG10l , another two genes of interests in this study, were found to be persistently
upregulated in CRC cases in previous studit>5 by us. Hwnt2 is potentially important in the Wnt/i3-catenin pathway that targets genes regulating cell proliferation and developmental processes as well as tumour progression. TSG10l was reported to closely relate to cancers of the breast, brain and colon, and its overexpression in human papillary thyroid carcinomas had previously been reported by others n this study, we aimed to examine the existence of mutations (if any) and the expression pattern of these genes in local CRC biopsy samples, in an effort to evaluate role(s) of -v
these genes in CRC progression. Our results revealed no mutation in these genes, despite persistent upregulation of Hwnt2 and TSG10l in CRC cases studied. Our findings suggest that the effects of p63, Hwnt2 and TSG10l in cases of colorectal carcinoma may be via an indirect influence. |
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