Although ras and p53 gene mutations have been detected in some prostate cancers, the major genetic alterations involved in its carcinogenesis are not well understood.
In conclusion, this study may indicate that either p53 gene mutation or the presence of HPV's oncogenic protein E6 is involved in the development of prostate cancer.
The expression of bcl-2 or accumulation of p53 protein in prostate cancer metastases did not significantly influence patient survival or the extent of metastatic disease.
We assessed the prognostic value of identifying abnormal p53 protein expression in the tumors of patients with locally advanced prostate cancer who were treated with either external-beam radiation therapy alone or total androgen blockade before and during the radiation therapy.
Several ex vivo and in vivo as well as cell culture studies are suggested for the therapy of the human prostate cancer using transfer and expression of genes that might be implicated in prostate carcinogenesis especially of the tumor suppressor p53.
Abnormal p53 expression is rare in clinically localized human prostate cancer: comparison between immunohistochemical and molecular detection of p53 mutations.
To define better the temporal relationship of p53 nuclear reactivity in prostate cancerp53 immunoreactivity was evaluated in all associated prostatic intraepithelial neoplasia lesions.
Mutation of the TP53 tumor suppressor gene (encoding the p53 protein) has been commonly reported as a critical event in human carcinogenesis, but recent findings in prostate cancer research call into question the correlation between TP53 mutation and prognosis for patients with this tumor.
The analysis of p53, bcl-2, Ki-67, and angiogenesis revealed that only increasing p53 expression and positive family history of PCa approached significance (P = 0.057).
These results indicate that p53 abnormalities are associated with lymph node metastases derived from prostate cancer patients that had not undergone hormonal therapy.