Ras oncogene and p53 gene hotspot mutations in colorectal cancers

S. Y. Lin, P. H. Chen, M. J. Yang, T. C. Chen, C. P. Chang, J. G. Chang

Research output: Contribution to journal › Article

3 Citations (Scopus)

Abstract

Ras oncogene and p53 gene mutations are frequently observed in colorectal cancers. The role of co-operation between these two genes in the tumorigenesis of colorectal cancer was evaluated. Point mutations in K-ras oncogene and hotspot codons of p53 gene of colorectal cancers were evaluated by naturally created or amplified created restriction site method. Nine of 42 cases (21.4%) of colorectal cancer showed K-ras oncogene mutations. Six of 42 cases (14.3%) of colorectal cancer showed p53 gene hotspot point mutations. The low frequency of p53 gene mutation in this series may be due to racial difference or different hotspot codons. When six cases with mutated p53 gene were examined, only one (16.7%) showed concurrent K-ras oncogene codon 12 and p53 gene codon 248 mutations. We concluded that the co-operation between ras oncogene and p53 gene hotspot point mutations in the tumorigenesis of colorectal cancer in Chinese was not common. Other factors such as adenomatous polyposis coli gene mutations, oncogene activation or tumour suppression gene inactivation may be involved.

Original languageEnglish
Pages (from-to)119-124
Number of pages6
JournalJournal of Gastroenterology and Hepatology (Australia)
Volume10
Issue number2
Publication statusPublished - 1995
Externally publishedYes

Fingerprint

ras Genes
p53 Genes
Colorectal Neoplasms
Mutation
Codon
Point Mutation
Carcinogenesis
APC Genes
Gene Silencing
Oncogenes
Genes
Neoplasms

Keywords

  • Amplified created restriction site
  • Colorectal tumorigenesis
  • Direct sequencing
  • P53 gene
  • Ras oncogene

ASJC Scopus subject areas

  • Gastroenterology
  • Hepatology

Cite this

Lin, S. Y., Chen, P. H., Yang, M. J., Chen, T. C., Chang, C. P., & Chang, J. G. (1995). Ras oncogene and p53 gene hotspot mutations in colorectal cancers. Journal of Gastroenterology and Hepatology (Australia), 10(2), 119-124.

Ras oncogene and p53 gene hotspot mutations in colorectal cancers. / Lin, S. Y.; Chen, P. H.; Yang, M. J.; Chen, T. C.; Chang, C. P.; Chang, J. G.

In: Journal of Gastroenterology and Hepatology (Australia), Vol. 10, No. 2, 1995, p. 119-124.

Research output: Contribution to journal › Article

Lin, SY, Chen, PH, Yang, MJ, Chen, TC, Chang, CP & Chang, JG 1995, 'Ras oncogene and p53 gene hotspot mutations in colorectal cancers', Journal of Gastroenterology and Hepatology (Australia), vol. 10, no. 2, pp. 119-124.
Lin SY, Chen PH, Yang MJ, Chen TC, Chang CP, Chang JG. Ras oncogene and p53 gene hotspot mutations in colorectal cancers. Journal of Gastroenterology and Hepatology (Australia). 1995;10(2):119-124.
Lin, S. Y. ; Chen, P. H. ; Yang, M. J. ; Chen, T. C. ; Chang, C. P. ; Chang, J. G. / Ras oncogene and p53 gene hotspot mutations in colorectal cancers. In: Journal of Gastroenterology and Hepatology (Australia). 1995 ; Vol. 10, No. 2. pp. 119-124.
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AU - Chang, J. G.

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AB - Ras oncogene and p53 gene mutations are frequently observed in colorectal cancers. The role of co-operation between these two genes in the tumorigenesis of colorectal cancer was evaluated. Point mutations in K-ras oncogene and hotspot codons of p53 gene of colorectal cancers were evaluated by naturally created or amplified created restriction site method. Nine of 42 cases (21.4%) of colorectal cancer showed K-ras oncogene mutations. Six of 42 cases (14.3%) of colorectal cancer showed p53 gene hotspot point mutations. The low frequency of p53 gene mutation in this series may be due to racial difference or different hotspot codons. When six cases with mutated p53 gene were examined, only one (16.7%) showed concurrent K-ras oncogene codon 12 and p53 gene codon 248 mutations. We concluded that the co-operation between ras oncogene and p53 gene hotspot point mutations in the tumorigenesis of colorectal cancer in Chinese was not common. Other factors such as adenomatous polyposis coli gene mutations, oncogene activation or tumour suppression gene inactivation may be involved.

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