Immune profiling of human prostate epithelial cells determined by expression of p38/TRAF-6/ERK MAP kinases pathways.

The aim of the present work was to study the immune profiling of prostate epithelial cells by the expression of ASK-1/p38 and Raf-1/ERK MAP Kinases signaling pathways mediated by TRAF-6. Immunohistochemical and Western blot analyses for TRAF-6, ASK-1, MEK-6, p38, Raf-1, MEK-1, ERK-1, ERK-2 and PSA were carried out in 5 samples of normal prostate gland, 24 samples of BPH and 19 samples of PC. Immunoreaction to TRAF-6 was found in the cytoplasm of epithelial cells of BPH and tumor cells of PC samples.

Cytokine profiling identifies an interaction of IL-6 and IL-1α to drive PSMA-PSA prostate clones.

Background: Several PSMA-PSA prostate clones have been identified during prostate cancer progression; however, until now, their in situ inflammatory characteristics have remained unclear.

Aim: We therefore investigated the interplay between proinflammatory cytokines and (PSMA,PSA) sub-groups.

Materials And Methods: 27 benign prostate hyperplasia (BPH) and 18 prostate cancers (PC) were enrolled in this study.

PSMA-PSA clones controlled by full Akt phosphorylation (T308+,S473+) recapitulate molecular features of human prostate cancer.

Background: (PSMA+,PSA+) and (PSMA+,PSA-) are the two most individual clones that we have previously identified during prostate cancer (PC) progression. However, molecular signatures associated with these distinct PSMA-PSA prostate clones and their specific correlation with disease outcome is yet to be defined.

Aim: Since Akt is a major pathway involved in the critical activating events that leads to malignant form of the disease, we studied the involvement of full Akt activation (T308+,S473+) connected with serum PSA levels, tissue PSMA expression and angiogenic activity on the emergence of (PSMA+,PSA+) and (PSMA+,PSA-) PC clones.

Insight into the heterogeneity of prostate cancer through PSA-PSMA prostate clones: mechanisms and consequences.

A major clinical challenge is posed by the current inability to readily distinguish indolent from aggressive tumors in prostate cancer patients. Research efforts are dedicated to overcome this problem by understanding the molecular basis of the transition from normal, benign cells to prostatic intraepithelial neoplasia (PIN), localized carcinoma, and metastatic cancer. Combined with the evidence of the phenotypic heterogeneity of benign prostate hyperplasia, primary tumors and metastases, it is conceivable that several prostate clones emerge progressively during tumor progression.

PSMA/PSA ratio evaluated by immunohistochemistry may improve diagnosis of prostate cancer.

Prostate-specific antigen (PSA) and prostate-specific membrane antigen (PSMA) measured in serum are not fully satisfactory as biomarkers of prostate cancer (PC). Results obtained in this article indicated that PSMA/PSA ratio evaluated by immunohistochemistry in normal prostate (NP), benign prostatic hyperplasia (BPH), and PC at the individual level could be a useful tool for diagnosis and prognosis of PC. PSMA and PSA were equally expressed in NP and the PSMA/PSA ratio was 1.

Cellular distribution and heterogeneity of Psa and Psma expression in normal, hyperplasia and human prostate cancer.

Background: As promising targets for in vivo diagnostic,prognostic and therapeutic approaches, the distribution and staining pattern of prostate specific antigen (PSA) and prostate specific membrane antigen (PSMA) in tumors are of significant interest.

Aims: To compare the cellular distribution and heterogeneity of PSA and PSMA expression in normal prostate (NP), benign prostatic hyperplasia (BPH) and primary prostatic tumors and to analyze their relation with the angiogenic activity according to Gleason grade (low, medium and high) in primary PC.

Methods: The study was carried out in 6 NP, 44 BPH and 39 PC.

A comparison of the biological features of prostate cancer with (PSA+, PSMA+) profile according to RKIP.

Purpose: To investigate differences in the biological features of the most immunoexpressed prostate cancer (PC) profiles (PSA+, PSMA+) according to the RKIP.

Methods: 19 PC with dominant Gleason grade ≥ 8 were studied. Expression of PSA, PSMA, RKIP, Raf-1, MEK-1, ERK-1, ERK-2, p-Akt (T308), p-Akt (S473), NF- κ B p50, and NF- κ Bp65 were detected immunohistochemically.

Involvement of interleukin-1β mediated nuclear factor κB signalling pathways to down-regulate prostate-specific antigen and cell proliferation in LNCaP prostate cancer cells.

Involvement of NF-κB (nuclear factor κB) mediated by IL-1β (interleukin-1β) on cell proliferation and PSA (prostate-specific antigen) production of LNCaP prostate cell lines and the possible cross-talk with Akt (also known as protein kinase B) signalling pathway has been investigated. NF-κB and Akt were analysed by Western blotting from LNCaP cells treated by IL-1β before proliferation and PSA production were measured. IL-1β inhibited proliferation and decreased PSA production.

Co-expression and impact of prostate specific membrane antigen and prostate specific antigen in prostatic pathologies.

Background: The present study was undertaken to relate the co-expression of prostate-associated antigens, PSMA and PSA, with the degree of vascularization in normal and pathologic (hyperplasia and cancer) prostate tissues to elucidate their possible role in tumor progression.

Methods: The study was carried out in 6 normal, 44 benign prostatic hyperplastic and 39 cancerous human prostates. Immunohistochemical analysis were performed using the monoclonal antibody CD34 to determine the angiogenic activity, and the monoclonal antibodies 3E6 and ER-PR8 to assess PSMA and PSA expression, respectively.

Relationship between IL-6/ERK and NF-κB: a study in normal and pathological human prostate gland.

Background: There is growing evidence that inflammation is a causal factor in cancer, where pro-inflammatory cytokines such as IL-6, IL-1 or TNF-α could induce cellular proliferation by activation of NF-κB. This study focuses on the IL-6/ERK transduction pathway, its relationship with NF-κB, and the consequences of dysregulation in the development of prostate pathologies such as benign prostate hyperplasia (BPH), prostate intraepithelial neoplasia (PIN) and prostate cancer (PC).

Methods: Immunohistochemical and Western blot analyses for IL-6, gp-130, Raf-1, MEK-1, ERK-1, p-MEK, ERK-2, p-ERK, NF-κB/p-50 and NF-κB/p-65 were carried out in 20 samples of normal prostate glands, 35 samples of BPH, 27 samples with a diagnosis of PIN (low-grade PIN or high-grade PIN), and 95 samples of PC (23 with low, 51 with medium and 21 with high Gleason scores).

[Prostatic specific antigen (PS), pro-inflammatory cytokines, and prostatic pathology (benign prostatic hyperplasia and cancer). Relationship with malignancy].

Objectives: Cancer is a complex process in which cytokines play an important role. Cytokines are low-molecular weight soluble proteins involved in cellular transmission signals and several disorders. Pro-inflammatory cytokines (IL-1, TNF-alpha and IL-6) are involved in prostate cancer development.

Pro-inflammatory cytokines and prostate-specific antigen in hyperplasia and human prostate cancer.

Background: The aim of this study was to relate the expression, analyzed by Western blot and immunohistochemistry, of several pro-inflammatory cytokines, including IL-1, IL-6 and TNF-alpha, with serum levels of prostate-specific antigen (PSA) in normal and pathologic (hyperplasia and cancer) prostate tissues to elucidate their possible role in tumor progression. We are also discussing the possible use of these cytokines as a potential therapeutic target.

Methods: The study was carried out in 5 normal, 25 benign prostatic hyperplastic (BPH) and 17 cancerous human prostates (PC).