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 language | English |
---|---|
Pages (from-to) | 119-124 |
Number of pages | 6 |
Journal | Journal of Gastroenterology and Hepatology (Australia) |
Volume | 10 |
Issue number | 2 |
Publication status | Published - 1995 |
Externally published | Yes |
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Keywords
- Amplified created restriction site
- Colorectal tumorigenesis
- Direct sequencing
- P53 gene
- Ras oncogene
ASJC Scopus subject areas
- Gastroenterology
- Hepatology
Cite this
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
}
TY - JOUR
T1 - Ras oncogene and p53 gene hotspot mutations in colorectal cancers
AU - Lin, S. Y.
AU - Chen, P. H.
AU - Yang, M. J.
AU - Chen, T. C.
AU - Chang, C. P.
AU - Chang, J. G.
PY - 1995
Y1 - 1995
N2 - 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.
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.
KW - Amplified created restriction site
KW - Colorectal tumorigenesis
KW - Direct sequencing
KW - P53 gene
KW - Ras oncogene
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UR - http://www.scopus.com/inward/citedby.url?scp=0028931279&partnerID=8YFLogxK
M3 - Article
C2 - 7787154
AN - SCOPUS:0028931279
VL - 10
SP - 119
EP - 124
JO - Journal of Gastroenterology and Hepatology (Australia)
JF - Journal of Gastroenterology and Hepatology (Australia)
SN - 0815-9319
IS - 2
ER -