Mutagen sensitivity and p53 expression in colorectal cancer in China
L Shao, M Lai, Q Huang
Zhejiang
University, School of Medicine, Department of Pathology, Hangzhou,
310031, Peoples Republic of China
Correspondence to: Dr Lai lmd{at}sun.zju.edu.cn
Submitted 20 November
2000;
Accepted 15 May 2001
OBJECTIVE
This study was designed
to investigate DNA damage and/or repair capability, non-random
chromatid breakage, and p53 expression in patients with colorectal cancer.
METHODSThe bleomycin sensitivity
assay was used in a case-control study to compare the DNA damage repair
system between colorectal cancer patients and controls. G-banding was
used to search for non-random chromatid breaks. Immunocytochemistry was
used to investigate p53 expression in tumour tissues and adjacent
normal tissues.
RESULTSIt was found that cases
typically had a higher number of chromosome breaks than controls (0.84 v 0.69 breaks/cell, p<0.01). After
correction by sex and age, the difference was still significant (F=4.38, p<0.05). The correlation coefficient between mutagen sensitivity and age was 0.31(p<0.05) in controls and 0.18 (p>0.05) in
cases. The ratio of odds ratios among bleomycin resistant, sensitive,
and hypersensitive classes was 1:2.31:3.85. Overexpression of p53 was
detected in 25 of 47 tumour tissues independent of tumour stage. Cases
who had a family history of cancer were susceptible to the p53
aberration (p<0.05). Chromosomes 1p, 5q, and 14q were susceptible to
breakage in patients with colorectal cancer.
CONCLUSIONPatients with colorectal
cancer show increased bleomycin induced chromatid breaks and may have
minor DNA repair deficiencies. p53 aberration is an early event in the
development of colorectal cancer, but no definite correlation is found
between p53 overexpression and mutagen sensitivity.
Keywords: bleomycin induced chromatid break; p53 tumour suppressor gene; colorectal cancer
© 2001 by The Fellowship of Postgraduate Medicine
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