%0 Journal Article
%T Lack of prognostic significance of p16 and p27 after radical prostatectomy in hormone-na£żve prostate cancer
%A Panagiotis J Vlachostergios
%A Foteini Karasavvidou
%A Grigorios Kakkas
%A Kassiani Kapatou
%A Ioannis Gioulbasanis
%A Danai D Daliani
%A George Moutzouris
%A Christos N Papandreou
%J Journal of Negative Results in BioMedicine
%D 2012
%I BioMed Central
%R 10.1186/1477-5751-11-2
%X Nuclear overexpression of p16 was not associated with time to biochemical failure (BF) (p = 0.572). Same was the case for nuclear p27 overexpression (p = 1.000). Also, no significant correlations were found between either p16 or p27, and pre-operative PSA level, pT stage and Gleason grade. pT stage emerged as the only independent prognostic factor for biochemical recurrence (p = 0.01).These data question previously reported data supporting the prognostic relevance of both p16 and p27 proteins in early PC.There is increasing evidence that cell cycle regulators are disrupted in human cancers [1]. The cell cycle is governed by cyclin-dependent kinases (CDKs), the activities of which are regulated by binding of positive effectors, the cyclins [2]; by negative regulators, the CDK inhibitors [3] and by phosphorylation and dephosphorylation events.p16 protein, encoded by the INK4A gene mapping to the 9p21 region [4,5] acts as a negative cell cycle regulator. Specific mechanisms may contribute to p16 altered expression, overcoming p16-mediated tumor suppressor activities. Unlike other primary tumors, INK4A inactivation, through deletions, mutations, or promoter methylation, seems to be an infrequent event in primary prostate cancer (PC) [6]. In contrast, the more frequent alterations of p16 in metastatic disease suggest that this might be a late event during the progression of some prostate carcinomas. It seems that p16 is overexpressed rather than lost in a large proportion of prostate carcinomas as p16 protein expression was increased in a majority of adenocarcinomas of the prostate and in prostate intra-epithelial neoplasia (PIN) when compared with surrounding benign glands [7]. Loss of transcriptional repression in the presence of inactivating mutations in the retinoblastoma (RB) gene is the most well-defined mechanism of p16INK4A overexpression [8]. p16 expression in premalignant lesions and carcinomas but not in normal or benign tissues implies a role of p16INK4A dete
%U http://www.jnrbm.com/content/11/1/2