Purpose: The p53 gene is considered one of the most important in the contro
l of apoptosis, and its mutations have a close relationship with chemosensi
tivity. The aim of this work was to investigate the role of p53 in the apop
tosis of colorectal cancer cells in vitro, induced by 5-fluorouracil (5-FU)
and hydroxy-camptothecin (HCPT). Methods: A total of 39 colorectal cancer
samples from patients were treated in vitro with 5-FU (10 mu g/ml), 5-FU (1
0 mu g/ml) + leucovorin (5 mu g/ml), HCPT (0.1 mu g/ml) and HCPT (0.1 mu g/
ml) + Salvia mitorrhiza (6 mu l), using an in situ terminal deoxynucleotidy
ltransferase assay to detect chemosensitivity. p53 gene mutations from tumo
r DNA were detected, after amplification by the polymerase chain reaction o
f exons 5-8, by non-radioactive single-strand conformation polymorphism. Re
sults: p53 gene mutations were observed in 43.6% (17/39) of colorectal carc
inomas, when the terminal deoxynucleotidyltransferase assay was used to det
ect the tumor apoptotic rate. Cells with mutated p53 had lower chemosensiti
vity than those without (p < 0.01). Conclusion: Routine assessment of p53 s
tatus may be helpful in selecting patients with the wildtype p53 gene, who
have a predictably better response to chemotherapy.