Tumorigenesis is thought to be a multistep process in which genetic alterations accumulate to bring about the neoplastic phenotype. Colorectal tumors appear to arise as a result of the mutational activation of oncogenes coupled with the inactivation of several tumor suppressor genes. We have found f
p53 gene mutations in early colorectal carcinoma. de novo vs. adenoma-carcinoma sequence
β Scribed by Hirotoshi Hasegawa; Masakazu Ueda; Kazuo Furukawa; Masahiko Watanabe; Tatsuo Teramoto; Makio Mukai; Masaki Kitajima
- Publisher
- John Wiley and Sons
- Year
- 1995
- Tongue
- French
- Weight
- 951 KB
- Volume
- 64
- Category
- Article
- ISSN
- 0020-7136
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β¦ Synopsis
p53 gene mutations in early and advanced colorectal cancer were detected by PCR-SSCP analysis. Early colorectal cancer was classified into de novo cancer and polypforming cancer, respectively, according to morphology and presence of adenomatous components. A total of 94 paraffin-embedded tissue specimens from patients with colorectal cancer were analysed. p53 gene mutations were detected in 40.0V0 (12/30) of de novo cancer, 36.7% (I I /30) of polypforming cancer, and 44% (I 5/ 34) of advanced cancer. p53 mutations were detected at a high frequency in both types of early colorectal cancer as well as in advanced cancer. No correlations were found between p53 mutations and clinicopathological data. Our data suggest that the p53 gene mutations occurred in the early colorectal cancer stage of carcinogenesis regardless of the pathway.
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