Objective-This study was designed to investigate DNA damage and/or repair c
apability, non-random chromatid breakage, and p53 expression in patients wi
th colorectal cancer.
Methods-The bleomycin sensitivity assay was used in a case-control study to
compare the DNA damage repair system between colorectal cancer patients an
d controls. G-banding was used to search for non-random chromatid breaks. I
mmunocytochemistry was used to investigate p53 expression in tumour tissues
and adjacent normal tissues.
Results-It 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 lp, 5q, and 14q were susceptib
le to breakage in patients with colorectal cancer.
Conclusion-Patients with colorectal cancer show increased bleomycin induced
chromatid breaks and may have minor DNA repair deficiencies. p53 aberratio
n is an early event in the development of colorectal cancer, but no definit
e correlation is found between p53 overexpression and mutagen sensitivity.