High Gleason Score (high + gleason_score)

Distribution by Scientific Domains


Selected Abstracts


RM2 antigen (,1,4-GalNAc-disialyl-Lc4) as a new marker for prostate cancer

INTERNATIONAL JOURNAL OF CANCER, Issue 1 2005
Seiichi Saito
Abstract Although prostate-specific antigen (PSA) has been widely used for early detection of prostate cancer, PSA has problems with specificity and prediction of pathological stage. Therefore, a new marker for prostate cancer is urgently required. We examined expression of a novel carbohydrate antigen, ,1,4-GalNAc-disialyl-Lc4, defined by the monoclonal antibody RM2, in prostate cancer using 75 cases of radical prostatectomy specimens. RM2 immunoreactivity was negative to weak in all benign glands, and weak to moderate in high-grade prostatic intraepithelial neoplasia. In prostatic adenocarcinoma, RM2 immunoreactivity was negative to weak (lower expression) in 20 cases, and moderate to strong (higher expression) in 55 cases. A clear difference of RM2 expression level was observed between Gleason patterns 3 and ,4. Higher expression of RM2 antigen was significantly associated with primary Gleason pattern ,4, high Gleason score (,8), larger tumor volume and advanced tumor stage. Furthermore, 5-year PSA failure-free survival was significantly lower in the higher expression group. However, no significant relationship was observed between RM2 expression level and preoperative serum PSA. Western blot analysis in prostate cancer cell lines PC3 and LNCap revealed that major 49-kDa and minor 39-kDa glycoproteins were common to both cells, but there was an increase of 59- and 125-kDa glycoproteins unique to LNCap and an increase of 88- and 98-kDa glycoproteins unique to PC3. RM2 antigen is a new histological marker for prostate cancer that may reflect the Gleason grading system. Identification of the glycoproteins carrying the RM2 antigen will provide new insights into the properties of prostate cancer. © 2005 Wiley-Liss, Inc. [source]


Tissue expression of IL16 in prostate cancer and its association with recurrence after radical prostatectomy,

THE PROSTATE, Issue 15 2010
Eva Compérat
Abstract BACKGROUND Genetic polymorphism located within the IL16 gene has been reported to be associated with aggressive prostate cancer (PCa). Our aim was to establish whether the tissue expression of IL16 is a prognostic factor of survival in PCa. METHODS The files of patients who underwent radical prostatectomy (RP) between 1995 and 2001 were reviewed. The cases were selected and classified according to the D'Amico classification for risk of recurrence (intermediate or high). The value of IL16 and its receptor CCR5 (chemokine (C-C motif) receptor 5) expression levels were determined as witness of aggressiveness patterns and markers of biological relapse in patients with PCa treated by RP. A tissue microarray of 304 cases was constructed. IL16 and CCR5 expression levels were characterized by immunohistochemistry. RESULTS IL16 expression was correlated with high Gleason score (i.e., >7) (P,<,0.01). It was not significant for CCR5. IL16 and CCR5 were not associated with prostate-specific antigen (PSA) or capsular extension of the disease. The accurate prediction of disease outcome, using stratification of cases, according to negative margins and D'Amico classification was significantly enhanced by status of IL16 expression (P,,,0.01). In univariate analyses, Gleason score, PSA level, stage and loss of IL16 expression were related to better biological-free survival (P,<,0.05) but not CCR5. In a multivariate analysis, IL16 expression, Gleason score, and tumor stage were independent factors for biochemical-free survival (P,=,0.001). CONCLUSIONS IL16 appears to be a useful prognostic factor in PCa. Its expression in PCa tissue was correlated to tumor aggressiveness and biochemical relapse of the disease. Prostate 70: 1622,1627, 2010. © 2010 Wiley-Liss, Inc. [source]


Expression of toll-like receptor-9 is increased in poorly differentiated prostate tumors,

THE PROSTATE, Issue 8 2010
Marja-Riitta Väisänen
Abstract BACKGROUND Toll-like receptor-9 (TLR9) is a cellular receptor for bacterial and vertebrate DNA. In addition to cells of the immune system, it is also expressed in various human cancer cell lines, including prostate cancer. We demonstrated previously that synthetic TLR9 ligands induce matrix metalloproteinase-13-mediated invasion in TLR9-expressing prostate cancer cells in vitro. Other studies have suggested possible sex steroid regulation of the function of the various TLRs. The role of TLR9 in the pathophysiology of prostate or any cancer is, however, unknown. METHODS Expression of TLR9, androgen receptor (AR), or the estrogen receptors , (ER,) and , (ER,) were studied with immunohistochemistry in prostate cancer (n,=,62) and benign prostatic hyperplasia (n,=,45) specimens. TLR9 staining scores were compared with tumor stage, Gleason score, prostate-specific antigen (PSA) concentrations before tissue sampling and with the staining scores of AR, ER,, and ER,. RESULTS TLR9 expression was statistically significantly increased in prostate cancer epithelium and stroma, as compared with the same cellular compartments in benign hyperplasia. Significantly increased (P,=,0.04) TLR9 expression was detected in cancers with high Gleason score (>7, n,=,23), as compared with lower Gleason scores (,7, n,=,39). No statistically significant associations were detected between TLR9 expression scores and PSA concentrations or tumor staging. Prostate adenocarcinoma cells were all positive for TLR9, AR, and ER, but negative for ER, expression. In cancer stroma cells, increased TLR9 expression was associated with increased ER, expression. CONCLUSIONS Expression of TLR9 is increased in prostate cancer specimens, especially in the most poorly differentiated forms. Prostate 70: 817,824, 2010. © 2010 Wiley-Liss, Inc. [source]


Cytochrome P450 2B6 is a growth-inhibitory and prognostic factor for prostate cancer

THE PROSTATE, Issue 10 2007
Jinpei Kumagai
Abstract BACKGROUND Cytochrome P450s (CYPs) influence the biological effects of carcinogens, drugs and hormones including testosterones. Among them, Cytochrome P450 2B6 (CYP2B6) plays a critical role in the deactivation of testosterone. In the present study, we examined CYP2B6 expression in human prostate tissues and prostate cancer. METHODS Immunohistochemical analysis was performed in 98 benign and 106 malignant prostate tissues and patients' charts were reviewed for clinical, pathologic and survival data. We also investigated whether stable expression of CYP2B6 in LNCaP (human prostate cancer cell line) influences cellular proliferation. RESULTS CYP2B6 was abundantly expressed in the normal epithelial cells compared to the prostate cancer cells. Significant immunostaining of CYP2B6 was found in 75 of 106 samples (71%), in the cytoplasm of cancerous tissue samples. CYP2B6 immunoreactivity was inversely correlated with high Gleason score (P,<,0.001). Decreased immunoreactivity of CYP2B6 significantly correlated with poor prognosis (P,<,0.0001). Univariate and multivariate hazard analyses revealed a significant correlation of decreased CYP2B6 expression with poor cancer-specific survival (P,=,0.0028 and 0.0142, respectively). Furthermore, overexpression of CYP2B6 in LNCaP cells significantly decreased testosterone-induced proliferation. CONCLUSIONS These results demonstrated that decreased expression of CYP2B6 might play a role in the development of prostate cancer, and be useful as the prognostic predictor for human prostate cancer. Prostate 67: 1029,1037, 2007. © 2007 Wiley-Liss, Inc. [source]


Stanniocalcin 2 overexpression in castration-resistant prostate cancer and aggressive prostate cancer

CANCER SCIENCE, Issue 5 2009
Kenji Tamura
Prostate cancer is usually androgen-dependent and responds well to androgen ablation therapy based on castration. However, at a certain stage some prostate cancers eventually acquire a castration-resistant phenotype where they progress aggressively and show very poor response to any anticancer therapies. To characterize the molecular features of these clinical castration-resistant prostate cancers, we previously analyzed gene expression profiles by genome-wide cDNA microarrays combined with microdissection and found dozens of trans -activated genes in clinical castration-resistant prostate cancers. Among them, we report the identification of a new biomarker, stanniocalcin 2, as an overexpressed gene in castration-resistant prostate cancer cells. Real-time polymerase chain reaction and immunohistochemical analysis confirmed overexpression of stanniocalcin 2, a 302-amino-acid glycoprotein hormone, specifically in castration-resistant prostate cancer cells and aggressive castration-naïve prostate cancers with high Gleason scores (8,10). The gene was not expressed in normal prostate, nor in most indolent castration-naïve prostate cancers. Knockdown of stanniocalcin 2 expression by short interfering RNA in a prostate cancer cell line resulted in drastic attenuation of prostate cancer cell growth. Concordantly, stanniocalcin 2 overexpression in a prostate cancer cell line promoted prostate cancer cell growth, indicating its oncogenic property. These findings suggest that stanniocalcin 2 could be involved in aggressive phenotyping of prostate cancers, including castration-resistant prostate cancers, and that it should be a potential molecular target for development of new therapeutics and a diagnostic biomarker for aggressive prostate cancers. (Cancer Sci 2009; 100: 914,919) [source]