p53 plays an important function as a negative regulator of cell growth and also inhibits transformation. It has been hypothesized that p53, acting as a control gene at a Gl check point, may detect DNA damage, slow the cell devision, and allow
time
for
DNA repair. If damage is irreparable, the cell may be driven down into the apoptotic pathway, thus preventing replication of defective cells. In this retrospective study, we investigated the correlation between p53 protein expression by IHC
staining
and benign breast disease with or without atypical ductal hyperplasia, DCIS and invasive breast cancer. Also We analyzed the association between p53 protein expression and the following prognostic parameter in breast cancer patients; age, tumor
size,
axillary node involvement, stage, histologic grade, estrogen receptor, progesteron receptor, and DNA ploidy. And, we investigated the correlation between p53 protein expression and the proliferative index of S phase fraction in diploid breast
cancer.
@ES The results were as follows;
@EN 1) In histo-pathological classification, none out of ten benign breast disease, none out of seventeen fibrocystic disease with atypical ductal hyperplasia patients were p53 protein positive, 3 out of fifteen DCIS (20%), 29 out of eighty-six
(34%)
invasive breast cancer patients were p53 protien positive.
2) There were no significant differences between p53 positivity and age, tumor size, axillary node involvement, stage, histologic grade, ER and PGR status, and DNA ploidy by Fisher's exact test with chi-squre test for trend, in invasive breast
cancer
(n=86)
3) In diploid tumor (m=35), statistically significant differences were noted such that high S-phase fraction tumor revealed increased p53 positivity (p<0.05).
We have found that immunopositivity for p53 was detected in 20% of in situ carcinoma, suggesting that p53 mutation can be acquired early in malignant progression. We have also found that there is a strong direct correlation between the amount of
mutant
protein and tumor proliferation rate. These results are consistent with the hypothesis that wild-type p53 is involved in suppression of the cell cycle.
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