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MINI SYMPOSIUM: MOLECULAR ONCOLOGY: ORIGINAL ARTICLE
Year : 2015  |  Volume : 4  |  Issue : 2  |  Page : 88-90

Correlation of p53 immunoexpression with DNA ploidy and apoptotic index in subsets of prostate cancer: A marker reiterated in progression and recurrence of prostate cancer


1 Department of Pathology, Tumour Biology Lab, National Institute of Pathology (ICMR), Safdarjang Hospital Campus, New Delhi, India
2 Department of Urology, Safdarjang Hospital, New Delhi, India

Correspondence Address:
Anju Bansal
Department of Pathology, Tumour Biology Lab, National Institute of Pathology (ICMR), Safdarjang Hospital Campus, New Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2278-330X.155693

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Background: Prediction of biological behavior in patients of prostate cancer (CaP) is a major challenge as current parameters only partially meet the need for prognostication. p53 as a prognostic indicator has been studied in several human cancers, including breast, lung, and colorectal carcinoma. However, its significance as a predictive biomarker for CaP is less well-studied. Materials and Methods: This study included 125 cases of CaP, 27 cases of prostatic intraepithelial neoplasia and 25 cases of benign prostatic hyperplasia. Immunohistochemical assessment for p53 nuclear protein was performed. Assessment for apoptotic index and DNA ploidy status by flow cytometry were also done. Results: p53 immunoreactivity was low in organ confined CaP cases having Gleason score ≤3 (P < 0.003). More hormone resistant cases 37 (83%) were aneuploid when compared with hormone sensitive cases 26 (33%) (P < 0.005). 93% of p53 positive cases and none of the p53 negative patient were aneuploid suggesting a significant relation between p53 immunoreactivity and aneuploidy. p53 positivity and DNA aneuploidy, independently, were also predictors of progression and relapse. Conclusion: DNA ploidy and p53 positivity go hand in hand and together yield additional prognostic information in CaP. p53 positivity is possibly a late event in carcinogenesis in CaP and a marker of change in biological behavior of CaP.


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