prostatic hyperplasia/protease

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Protease-activated receptor-1 upregulates fibroblast growth factor 7 in stroma of benign prostatic hyperplasia.

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BACKGROUND Benign prostatic hyperplasia (BPH) is characterized by abnormal epithelial and stromal proliferation causing urinary obstruction. Prostate growth is regulated by a variety of growth factors secreted from the stroma, including fibroblast growth factor 7 (FGF-7), a potent

Caspase 3 expression in benign prostatic hyperplasia and prostate carcinoma.

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BACKGROUND Apoptotic resistance to androgen ablation represents a significant problem in the treatment of prostate cancer. Over expression of antiapoptotic proteins such as Bcl-2 and mutations in p53 contribute to this resistance. The caspase family of proteases are central executioners of the cell

A novel transcript from the KLKP1 gene is androgen regulated, down-regulated during prostate cancer progression and encodes the first non-serine protease identified from the human kallikrein gene locus.

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BACKGROUND The kallikrein-related (KLK) serine protease, prostate specific antigen is the current marker for prostate cancer (PCa). Other members of the KLK family are also emerging as potential adjunct biomarkers for this disease. Our aim was to identify and characterize novel KLK-related genes

Effect of dextran-coated charcoal treatment on 17 beta-estradiol receptor in human benign prostatic hyperplasia.

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Using glycerol density gradient centrifugation technique, single saturation dose assay, and Scatchard plot, the effect of dextran-coated charcoal (DCC) treatment of homogenate or crude cytosol on estradiol binding protein in human benign prostatic hyperplasia was investigated. Receptor binding is

Differential diagnosis of prostate cancer and benign prostate hyperplasia using two-dimensional electrophoresis.

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Prostate specific antigen (PSA) is a protease which is characteristic of the prostate. It is widely used as a serum marker for the early diagnosis of prostate cancer (PCa). Nevertheless, for concentrations between 4 and 10 ng/mL, PSA does not enable PCa to be distinguished from benign diseases, such

Detection of TMPRSS2-ERG fusion gene in benign prostatic hyperplasia.

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The Ets-related gene fusions are among the most common molecular alterations in prostate cancer (PCa) and are detected in more than 50 % of PCas. Transmembrane protease serine 2 and Ets-related gene fusion (TMPRSS2-ERG) is the most frequently identified chimeric gene and has been associated with

Prostate specific antigen in benign prostatic hyperplasia: purification and characterization.

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OBJECTIVE The ratio of free-to-total prostate specific antigen (PSA) in serum is greater in patients with benign prostatic hyperplasia (BPH) than in those with prostate cancer, and it provides a means of partially discriminating these 2 diseases. To understand the molecular mechanism of why the

Insulin-like growth factor I (IGF-I) and IGF-binding protein-3 in benign prostatic hyperplasia and prostate cancer.

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In view of evidence indicating significant involvement of the insulin-like growth factor (IGF) system in the pathogenesis of prostate cancer, we measured serum IGF-I and IGF-binding protein-3 (IGFBP-3) in men with benign prostatic hyperplasia (BPH; n = 75) or prostatic carcinoma (CaP; n = 84). The

Molecular genetic profiling of Gleason grade 4/5 prostate cancers compared to benign prostatic hyperplasia.

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OBJECTIVE Because Gleason grade 4/5 cancer is the primary cause of failure to cure prostate cancer, we examined the molecular profiles of this high grade cancer in search of potentially new therapeutic interventions as well as better serum markers than prostate specific antigen. METHODS We compared

SPINK1 Promoter Variants Are Associated with Prostate Cancer Predisposing Alterations in Benign Prostatic Hyperplasia Patients.

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OBJECTIVE Several studies reported that patients with benign prostatic hyperplasia (BPH) experienced a 10% increased incidence of prostate cancer (PCa) after the first 5 years of diagnosis. We investigated the association between single nucleotide polymorphisms (SNPs) in the promoter of Serine

Expression of the serine protease kallikrein 7 and its inhibitor antileukoprotease is decreased in prostate cancer.

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BACKGROUND Kallikreins are a subgroup of serine proteases with diverse physiologic functions. It has been confirmed that kallikrein 7 (KLK7) is differentially expressed in ovarian and breast cancer. Antileukoprotease (ALP) has been shown to be a specific inhibitor of human kallikrein 7 (hK7).

Characterization and determination of the complex between prostate-specific antigen and alpha 1-protease inhibitor in benign and malignant prostatic diseases.

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Prostate-specific antigen (PSA) is a tissue-specific serine protease which forms complexes with protease inhibitors such as alpha 1-antichymotrypsin and alpha 2-macroglobulin. We have studied the interaction between PSA and alpha 1-protease inhibitor (API) in vitro and found that 15% of the added

The release of free prostate specific antigen into the circulation during transurethral resection of the prostate: kinetics and interaction with serum protease inhibitors.

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OBJECTIVE To determine the nature and extent of the release of prostate specific antigen (PSA) and its interaction with its plasma protein-derived inhibitors after transurethral resection of the prostate (TURP). METHODS Twenty-three consecutive patients undergoing routine TURP for benign prostatic

Regulation of the enzymatic activity of prostate-specific antigen and its reactions with extracellular protease inhibitors in prostate cancer.

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Prostate-specific antigen (PSA) is a tissue-specific serine protease similar in structure to the trypsin-like glandular kallikreins but which is unique inasmuch as the enzyme activity is similar to that of chymotrypsin. The active enzyme is a single chain glycoprotein of 237 amino acids. The major

Ammonium-chloride-induced prostatic hypertrophy in vitro: urinary ammonia as a potential risk factor for benign prostatic hyperplasia.

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To test the possibility that urinary ammonia could be a risk factor for benign prostatic hyperplasia (BPH), we explored the cellular effects of ammonium chloride (NH(4)Cl) on prostatic cancer cells used as an experimental model. Following treatment of human prostatic cancer DU-145 cells with the

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