Carcinogenesis, Vol 18, 473-478, Copyright © 1997 by Oxford University Press
HG Gao, JK Chen, J Stewart, B Song, C Rayappa, WZ Whong and T Ong
Studies were performed to examine the mutational pattern of K-ras exons 1
and 2 and p53 exons 5-8 in lung cancer tissues from 27 Chinese patients (10
smokers, 17 non-smokers) using single-stranded conformational polymorphism
and DNA sequencing. K-ras mutations were found in 13/27 tumors (48%); all
mutations were clustered in exon 1 and distributed between codons 9 and 32.
The frequency and number of patients with K-ras mutations between smokers
and non-smokers were not different, except that a high frequency of G
--> A transitions (11/11) was found in non-smokers. Among cell types,
K-ras mutations were found in 7/13 (54%) squamous cell carcinoma (SC) and
5/12 (42%) adenocarcinoma (AC) patients. A --> T transversions (all six
transversions) were present only in SC. In p53, 18/27 (67%) tumors
contained mutations in exons 7 and 8, frequently at codons 226, 270, 275
and 281. The number of tumors with p53 mutations in smokers (70%) and in
non-smokers (65%) was similar, and the mutation frequency did not differ
except for a higher number of G --> A (6/7) and T --> C (5/6)
transitions in non-smokers. Among cell types, the number of tumors with p53
mutations was 9/13 (69%) in SC and 8/12 (67%) in AC. The A --> G (11/16)
transitions and A --> C (4/4) transversions in p53 were more frequent in
SC than in AC (P < 0.04 for A --> G; P < 0.02 for A --> C). The
varying mutation patterns in both the K-ras and p53 genes between smokers
and non-smokers and among cell types suggest that other than cigarette
smoke, environmental and dietary factors may also be involved in the
genesis of lung cancer among these patients.
ARTICLES
Distribution of p53 and K-ras mutations in human lung cancer tissues
Division of Respiratory Disease Studies, National Institute for Occupational Safety and Health, Morgantown, WV 26505-2845, USA.
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