OBJECTIVETo study the relationship between TMPRSS2: ERG gene fusion and the pathological grade of prostate cancer (PCa).

METHODSWe collected fresh prostatic tissue samples from 62 patients with PCa and another 10 with benign prostatic hyperplasia ( BPH) and included 9 cancer cell strains as the control. We examined the TMPRSS2:ERG fusion gene in the PCa samples by nest RT-PCR, compared the Gleason scores between the TMPRSS2:ERG-positive and -negative cases, and analyzed the association of TMPRSS2: ERG fusion with the pathological features of PCa.

RESULTSThe TMPRSS2: ERG fusion gene was detected in 28 (45.16%) of the PCa cases, but in none of the 10 BPH cases or the 9 cancer cell strains. No statistically significant differences were found in the Gleason scores between the TMPRSS2:ERG-positive and -negative cases (Z = -0.609, P = 0.542), but the primary Gleason score was markedly higher in the former than in the latter (Z = -2.600, P = 0.009). Univariate logistic regression analysis showed that TMPRSS2:ERG was associated with the cribriform growth pattern (OR = 6.250, P = 0.002), foamy gland morphology (OR = 6.666, P = 0.023), and signet-ring cells (OR = 3.240, P = 0.035), but multivariate logistic regression analysis manifested that it was associated with the cribriform growth pattern only (OR = 3.750, P = 0.033).

CONCLUSIONTMPRSS2:ERG gene fusion was associated with higher pathological grades of prostate cancer.

Gene Fusion ; Humans ; Male ; Oncogene Proteins, Fusion ; genetics ; Prostatic Hyperplasia ; genetics ; Prostatic Neoplasms ; genetics ; pathology

OBJECTIVETo explore the association of the androgenic receptor (AR) CAG repeats with the risks of benign prostatic hyperplasia (BPH) and prostate cancer (PCa).

METHODSWe searched the major databases at home and abroad for the literature addressing the correlation of the AR gene CAG repeats with BPH and PCa. Based on the results of heterogeneity tests, we used the M-H fixed effect model and random effect model to pool the odds ratio (OR) effect size. We evaluated publication bias by Begg and Egger bias analysis, investigated the association of CAG repeats with the risks of BPH and PCa by systematic review, and stratified their relationship according to the races of the patients.

RESULTSBased on the selection criteria, 4 of the 29 identified studies were included, with 485 cases of BPH, 767 cases of PCa, and 709 controls. There was no heterogeneity between the BPH and control groups, and no correlation between short CAG repeats and BPH after pooling the odds ratio (OR) effect size. Heterogeneity was found among the BPH, PCa and control groups. Random effects model suggested an association of short CAG repeats with the risk of PCa (OR(PCa/control) = 1.45, OR(PCa/BPH) = 1.86, OR(PCa/(BPH + control)) = 1.66), while subgroup analysis with racial stratification indicated inter-ethnic differences between the two. Begg and Egger bias analysis showed no significant publication bias.

CONCLUSIONShorter CAG repeats are positively correlated with the risk of PCa but not with that of BPH.

Humans ; Male ; Polymorphism, Genetic ; Prostatic Hyperplasia ; genetics ; Prostatic Neoplasms ; genetics ; Receptors, Androgen ; genetics ; Trinucleotide Repeats

OBJECTIVETo screen methylations of CpG islands in prostate cancer using restriction landmark genomic scanning (RLGS).

METHODSThe DNA was extracted from homogeneous cells captured by laser capture microdissection in 20 prostate cancer and 18 benign prostatic hyperplasia (BPH) tissues for scanning the CpG islands using RLGS. The methylation status of each CpG island was compared between the cancer and BPH samples to screen the genes involved in prostate cancer development. The screened genes were uploaded to DAVID database for GO analysis, and the genes with the most significant methylation were analyzed by pyrosequencing.

RESULTS AND CONCLUSIONAmong all the tested CpG islands, 10245 (37.2%) in prostate cancer and 8658 (30.3%) in BPH samples were found to be abnormally methylated, and >60% of the methylated CpG islands were in the promoter region. Compared with BPH samples, the prostate cancer samples showed differential methyation in 735 CpG islands, including 458 hepermethyated and 256 hypomethelated ones. Seven genes (DPYS, P16, APC, GSTP1, TMEM122, RARB, and ARHGAP20) in prostate cancer were identified to have distinct methylations. Bioinformatics analysis suggested that these genes were associated with several biomolecular and biological processes, and among them DPYS gene was involved in 13 GO anotated biologic functions, development of 50 diseases and 47 protein interactions. Pyrosequencing of 7 sites of the CPG island in DPYS gene showed a methylation frequency of 32.7%, suggesting the importance of DPYS gene in the carcinogenesis and progression of prostate cancer.

CpG Islands ; DNA Methylation ; DNA, Neoplasm ; genetics ; Genomics ; Humans ; Male ; Polymerase Chain Reaction ; Prostatic Hyperplasia ; genetics ; Prostatic Neoplasms ; diagnosis ; genetics

The etiology and pathogenesis of benign prostatic hyperplasia are very complicated, about which a variety of theories have been developed, so it is of utmost importance to decide upon the target of research. Focusing on the pathogenesis of benign prostatic hy-perplasia, the author outlines the candidate targets for the experimental studies of the disease in such approaches as morphology, hormones, growth factors and genes.
Androgens ; metabolism ; Estrogens ; metabolism ; Humans ; Male ; Prostatic Hyperplasia ; etiology ; genetics ; metabolism

Prostaglandin synthase (PGS) can catalyze the production of various types of prostaglandins and regulate the expression levels of related substances. The regulation mechanisms of the PGS gene are closely related with the occurrence and development of prostate diseases. However, few studies are reported on the regulation mechanisms of PGS in prostatic diseases, such as benign prostatic hyperplasia (BPH) and prostate cancer (PCa), or on the relationship between PGS gene regulation and prostate diseases. This review aims to analyze their correlation and provide some ideas for the prevention and control of BPH and PCa by intervention of the prostaglandin synthase regulatory pathway.
Gene Expression Regulation ; Humans ; Male ; Prostaglandin-Endoperoxide Synthases ; genetics ; physiology ; Prostatic Hyperplasia ; enzymology ; genetics ; prevention & control ; Prostatic Neoplasms ; enzymology ; genetics ; prevention & control

The B-cell lymphoma/leukemia-2 (Bcl-2) gene is an important member of the Bcl-2 family, a type of protein that plays an important role in the process of cell apoptosis. Bcl-2 does not change the rate of cell proliferation, but prolongs the life and increases the number of cells by counteracting a series of apoptosis. In the recent years, more and more evidence has shown a close correlation of the Bcl-2 gene with the development and progression of benign prostatic hyperplasia (BPH), a disease whose mechanism is not yet fully understood but is drawing more and more attention towards the role of cell apoptosis.
Animals ; Apoptosis ; Humans ; Male ; Mice ; Prostatic Hyperplasia ; genetics ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; genetics ; Rats

OBJECTIVETo identify the differential expressions of serum cytokines between prostate cancer (PCa) and benign prostatic hyperplasia (BPH), and provide proteomic evidence for the early diagnosis of PCa.

METHODSWe used human cytokine array to determine the profiles of the serum cytokines obtained from 6 PCa and 6 BPH patients with the PSA level within the grey scale of 4 - 10 ng/ml.

RESULTSWe identified 19 differentially expressed cytokines in the PCa patients, 16 obviously up-regulated, including IL-3, IL-6 and IL-16, and 3 markedly down-regulated, which were Fas/TNFRSF6, TRALR-3 and IGFBP-6. Most of them were involved in such cellular bioprocesses as transcription, proliferation, signal transduction, and apoptosis.

CONCLUSIONThe cytokine antibody assay permits simultaneous measurement of multiple markers in a small volume of serum, and can identify a panel of key cytokines related to the malignant biological behavior of cancer cells. And it helps to find the biomarkers for the early diagnosis, efficacy assessment and prognosis of prostate cancer.

Aged ; Humans ; Interleukin-16 ; blood ; Interleukin-3 ; blood ; Interleukin-6 ; blood ; Male ; Middle Aged ; Prostatic Hyperplasia ; blood ; genetics ; metabolism ; Prostatic Neoplasms ; blood ; genetics ; metabolism ; Proteomics

OBJECTIVETo detect and analyze the differentially expressed genes in prostate cancer (PCa) and benign prostatic hyperplasia (BPH).

METHODSOligonucleotide microarray containing 465 genes was used to investigate the differentially expressed genes in PCa and BPH.

RESULTSThere were 35 differentially expressed genes between PCa and BPH, of which 17 were up-regulated and 18 down-regulated in PCa.

CONCLUSIONThe study of the differentially expressed genes in PCa and BPH should help to understand the molecular mechanism of PCa and identify the markers for diagnostic and therapeutic use.

Down-Regulation ; Gene Expression Profiling ; Humans ; Male ; Oligonucleotide Array Sequence Analysis ; Prostatic Hyperplasia ; genetics ; metabolism ; Prostatic Neoplasms ; genetics ; metabolism ; Up-Regulation

To study the expression of matrix metalloproteinase-2 and -9 in human prostate cancer, matrix metalloproteinase-2 and -9 were immunohistochemically detected in tissues of prostate cancer and benign prostatic hyperplasia (BPH). Our results showed that matrix metalloproteinase-2 and -9 levels in prostate cancer were much higher than those in tissues of BPH, with the cancer invasion being positively correlated with the expression of the metalloproteinases. It is concluded that matrix metalloproteinase-2 and -9 are better molecular markers, which are of help in the diagnosis and prediction of prognosis of prostate cancer.
Humans ; Immunohistochemistry ; Male ; Matrix Metalloproteinase 2 ; biosynthesis ; genetics ; Matrix Metalloproteinase 9 ; biosynthesis ; genetics ; Neoplasm Invasiveness ; Prostatic Hyperplasia ; metabolism ; pathology ; Prostatic Neoplasms ; metabolism ; pathology

Carcinoma ; genetics ; metabolism ; pathology ; surgery ; China ; Humans ; Male ; Oncogene Proteins, Fusion ; genetics ; Prostatic Hyperplasia ; genetics ; metabolism ; pathology ; surgery ; Prostatic Neoplasms ; genetics ; metabolism ; pathology ; surgery ; Proto-Oncogene Proteins c-ets ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Serine Endopeptidases ; genetics ; metabolism