ArticleInternational urology and nephrology2009
Expression profile and prognostic importance in prostate lesions of the reverse transcriptase component of human telomerase (hTERT) and of cyclin-dependent kinase inhibitor p57 (p57kip2a).
Article in International urology and nephrology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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2 citing papers in PubMed, 7 citations in OpenAlex.
- Podocytes proliferate: novel mechanism identified in collapsing glomerulopathies.International urology and nephrology · 2013Review
- p57(KIP2) control of actin cytoskeleton dynamics is responsible for its mitochondrial pro-apoptotic effect.Cell death & disease · 2012Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesTo investigate expression of the reverse transcriptase component of human telomerase (hTERT) and of cyclin-dependent kinase inhibitor p57 (p57(kip2a)) in prostate neoplasms and evaluate the relationship between these proteins and the Gleason score.
methodshTERT and p57(kip2a) antibodies were studied by immunohistochemical methods in 70 prostate adenocarcinomas (33 high-grade and 37 low-grade carcinomas), 29 benign prostate hyperplasias, and 19 prostatic intraepithelial neoplasias (PIN). Only nuclear staining was evaluated with p57(kip2a) whereas both nuclear and nucleolar staining were evaluated with hTERT.
resultsImmunohistochemical histologic scores (HSCOREs) of hTERT were significantly higher in the PIN group than in the hyperplasia group (P = 0.03). hTERT HSCOREs were not significantly different between hyperplasias and carcinomas or between low and high-grade carcinomas. p57(kip2a) HSCOREs were significantly higher in hyperplasias than other groups, and in PINS than carcinomas, but did not differ significantly between low and high-grade carcinomas. A significant negative correlation was observed between hTERT and p57(kip2a) (P = 0.007) in the hyperplasia group. No such correlation was found in PINs and carcinomas.
conclusionsThis study suggests that p57(kip2a) is down-regulated in the malignant side of the spectrum of prostate carcinogenesis. Loss of p57(kip2a) control on hTERT might have an important role in the development of prostate cancer.
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