Purpose: To evaluate the effect of an anterograde approach to radical retropubic prostatectomy (RRP) in terms of positive surgical margins (SM+).
Methods: 323 untreated patients underwent anterograde RRP for clinically localized prostate adenocarcinoma. Spearman coefficients, logistic univariate and multivariate analysis were used.
Purpose: To verify whether a significant relationship between the risk of Gleason upgrading and the prostate volume remains when the number of biopsies is increased for larger prostate volumes.
Materials: A total of 281 biopsy-proven prostate adenocarcinoma cases who underwent radical prostatectomy (RRP) formed the cohort for this study. Change in transrectal ultrasound of the prostate (TRUS) biopsies number based on total gland volume was made simply by increasing the number of biopsies from 6 to 10 when prostate volume was >50 cc.
Background/aim: To compare serum chromogranin A (CgA) and insulin-like growth factor 1 (IGF-1) with the classical prostate-specific antigen (PSA) marker in clinically localized prostate adenocarcinomas.
Materials And Methods: This is a prospective single-center study that included 64 consecutive men with newly diagnosed clinically localized prostate adenocarcinoma and 20 consecutive men with histologically confirmed benign prostatic hyperplasia (BPH). A blood sample for the determination of serum total PSA, CgA and IGF-1 levels (RIA) was obtained from all cases.
ATP is abundantly released from stressed or damaged cells in response to mechanical stimulation, bacteria, or noxious agents. In this study, we have investigated the possible involvement of P2 receptors (receptor for extracellular nucleotides) in the expression and release of inflammatory mediators by human keratinocytes. Notably, extracellular ATP displayed a complex regulation of IFN-gamma-stimulated chemokine expression, with upregulation of CC chemokine ligand 2 (CCL2), CCL5 and CXC chemokine ligand 8 (CXCL8), and suppression of the receptor CXC chemokine receptor 3 (CXCR3), CXCL9, CXCL10, and CXCL11.
View Article and Find Full Text PDFIn this review, we will present some of the information that is known about neuroendocrine (NE) cells and differentiation in the prostate. We will then speculate on the potential role that NE differentiation in prostate carcinoma may play and how this differentiation may be clinically analysed and treated. The androgen-independent growth of prostate cancer can be caused by different mechanisms; one of these is receptor-specific paracrine or autocrine growth modulation of human prostatic cancer cells by neuropeptides secreted by NE cells.
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