Benign Prostatic Hyperplasia and Its Aetiologies

Briganti, Alberto; Capitanio, Umberto; Suardi, Nazareno; Gallina, Andrea; Salonia, Andrea; Bianchi, Marco; Tutolo, Manuela; Girolamo, V. Di; Guazzoni, G.; Rigatti, Patrìzio; Montorsi, Francesco

doi:10.1016/j.eursup.2009.11.002

Cited by 121 publications

(108 citation statements)

References 68 publications

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“…We categorized the up-and Regulation of growth (23) P = 6.86×10 -6 P = 9.59×10 -6 P = 4.61×10 -24 P = 2.98×10 -13 P = 9.56×10 -24 Response to wounding (43) P = 4.59×10 -6 Response to pest, pathogen or parasite (57) P = 1. (82) triacylglyceride synthesis (19) TCA cycle (18) synthesis and degradation of ketone bodies (3) steroid biosynthesis (8) statin pathway (17) prostaglandin synthesis and regulation (31) pentose phosphate pathway (4) nucleotide metabolism (14) nuclear receptors in lipid metabolism and .... mitochondrial LC-fatty acid beta oxidation (19) heme biosythesis (7) glycolysis and gluconeogenesis (33) glycogen metabolism (13) glytathione metabolism (28) glycocorticoid metabolism (8) fatty acid biosynthesis (20) fatty acid beta oxidation 3 (6) fatty acid beta oxidation 2 (6) fatty acid beta oxidation 1 (25) electron transport chain (37) eicosanoid synthesis (16) cholesterol biosynthesis (14) biogenic amine synthesis (13) beta oxidation of unsaturated fatty acid (6) beta oxidation meta MAPP (27) alanine and asparate metabolism (23) acetylcholine synthesis (6) 0…”

Section: Discussionmentioning

confidence: 99%

Molecular classification of benign prostatic hyperplasia: A gene expression profiling study in a rat model

et al. 2016

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Abbreviations & Acronyms BPH = benign prostatic hyperplasia GPCR = G-protein-coupled receptor IL = interleukin RT-PCR = polymerase chain reaction SHR = spontaneously hypertensive rat UGS = urogenital sinus Objectives: To characterize the molecular features of benign prostatic hyperplasia by carrying out a gene expression profiling analysis in a rat model. Methods: Fetal urogenital sinus isolated from 20-day-old male rat embryo was implanted into a pubertal male rat ventral prostate. The implanted urogenital sinus grew time-dependently, and the pathological findings at 3 weeks after implantation showed epithelial hyperplasia as well as stromal hyperplasia. Whole-genome oligonucleotide microarray analysis utilizing approximately 30 000 oligonucleotide probes was carried out using prostate specimens during the prostate growth process (3 weeks after implantation). Results: Microarray analyses showed 926 upregulated (>2-fold change, P < 0.01) and 3217 downregulated genes (<0.5-fold change, P < 0.01) in benign prostatic hyperplasia specimens compared with normal prostate. Gene ontology analyses of upregulated genes showed predominant genetic themes of involvement in development (162 genes, P = 2.01 9 10 À4 ), response to stimulus (163 genes, P = 7.37 9 10 À13 ) and growth (32 genes, P = 1.93 9 10 À5 ). When we used both normal prostate and non-transplanted urogenital sinuses as controls to identify benign prostatic hyperplasia-specific genes, 507 and 406 genes were upregulated and downregulated, respectively. Functional network and pathway analyses showed that genes associated with apoptosis modulation by heat shock protein 70, interleukin-1, interleukin-2 and interleukin-5 signaling pathways, KIT signaling pathway, and secretin-like G-protein-coupled receptors, class B, were relatively activated during the growth process in the benign prostatic hyperplasia specimens. In contrast, genes associated with cholesterol biosynthesis were relatively inactivated. Conclusion: Our microarray analyses of the benign prostatic hyperplasia model rat might aid in clarifying the molecular mechanism of benign prostatic hyperplasia progression, and identifying molecular targets for benign prostatic hyperplasia treatment.

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Section: Discussionmentioning

confidence: 99%

Molecular classification of benign prostatic hyperplasia: A gene expression profiling study in a rat model

et al. 2016

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“…Recent studies strongly suggest that BPH is an immune inflammatory disease [7]. Cytokines produced by inflammatory cells are believed to play essential roles in the development and maintenance of prostate growth by increasing growth factor production and angiogenesis [8,9,10]. Nickel et al demonstrated Citation: Gokkaya CS, Aktas BK, Ozden C, Bulut S, Karabakan M, Erkmen AE, Memis A. Flurbiprofen alone and in combination with alfuzosin for the management of lower urinary tract symptoms.…”

Section: Introductionmentioning

confidence: 99%

Flurbiprofen alone and in combination with alfuzosin for the management of lower urinary tract symptoms

Gökkaya¹,

Aktaş²,

Özden³

et al. 2015

CEJU

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“…Thus, with increasing age there is a tendency of increasing prostatic volume. [3][4][5] Of the diseases which affects the prostate the most frequently encountered in clinical practice are benign prostatic hyperplasia, prostatic cancer and prostatitis. 6 Prostate specific antigen (PSA), a glycoprotein serine protease, was first identified by Wang et al in 1979.…”

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confidence: 99%

Study of prostatic pathology and its correlation with prostate specific antigen level

et al. 2017

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Background: Diseases primarily inflicting prostate gland are inflammation, benign prostatic hyperplasia and cancer. Prostate specific antigen is a protein produced by the cells of prostate gland. It has been widely used in the diagnosis and management of patients with prostatic cancer. The aim this study was to determine the correlation between serum prostate specific antigen level and histological findings in biopsy specimens of men with prostatic disease. Materials and Methods: This study was carried out at Kathmandu Medical College and TeachingHospital, department of Pathology over a period of 2 years. One hundred and twenty eight cases with prostatic lesions were included in this study. Prostate specific antigen values of these cases were recorded before the surgical process. Histology of the tissue samples collected after transurethral resection of prostate was studied and relationship with prostate specific antigen level were analyzed.Results: Benign prostatic hyperplasia was the most common histological lesion encountered (n=95; 74.22%). Prostatic adenocarcinomas were seen a decade older than those with benign lesions. Maximum number of the benign cases had the Prostate specific antigen range of 0-7ng/ml. Most of the prostatic intraepithelial neoplasia lesions were seen within the PSA range of 0-7ng/ml and adenocarcinoma in the range of >20ng/ml. Conclusion:Prostate specific antigen is specific for the prostate but not for prostate cancer. Both benign and malignant lesions in prostate can cause increase in serum prostate specific antigen levels, but the chances of malignancy it rising level.

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Benign Prostatic Hyperplasia and Its Aetiologies

Cited by 121 publications

References 68 publications

Molecular classification of benign prostatic hyperplasia: A gene expression profiling study in a rat model

Molecular classification of benign prostatic hyperplasia: A gene expression profiling study in a rat model

Flurbiprofen alone and in combination with alfuzosin for the management of lower urinary tract symptoms

Study of prostatic pathology and its correlation with prostate specific antigen level

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