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PubMed2006

Immunohistochemical analysis of Omi/HtrA2 expression in prostate cancer and benign prostatic hyperplasia.

The serine protease Omi/HtrA2 is released from mitochondria into the cytosol after apoptotic stimuli, inducing apoptosis in a caspase-independent manner through its protease activity and in a caspase-dependent manner by neutralizing the inhibition of inhibitor of apoptosis proteins (IAPs) on caspases. Alteration of apoptosis is essential for cancer development, and cancer cell death by radiation and chemotherapy is largely dependent upon apoptosis. Thus, analysis of the expression status of Omi/HtrA2, a regulator of apoptosis, in cancer tissues is needed for an understanding of cancer development. In the current study we analyzed the expression of Omi/HtrA2 in 65 prostate cancer, 40 benign prostatic hyperplasia and 10 normal prostate specimens by immunohistochemistry. Omi/HtrA2 mRNA levels of in vivo prostate cancer and benign prostatic hyperplasia samples were also assayed by semiquantitative reverse transcription-polymerase chain reaction. Immunopositivity (defined as > or =30%) was observed for Omi/HtrA2 in most of the prostate cancers, and the positive rate of Omi/HtrA2 was lower in the well-differentiated group than in the poorly and moderately differentiated groups (p<0.005). By contrast, the cells in the normal prostate and benign prostatic hyperplasia groups showed no or only weak expression of Omi/HtrA2. Meanwhile, the Omi/HtrA2 mRNA level of prostate cancer is much higher than that of benign prostatic hyperplasia (p<0.001). Taken together, these results suggest that prostate cancer cells in vivo may need Omi/HtrA2 expression for apoptosis, and that Omi/HtrA2 expression might be involved in prostate cancer development.

Aged↗
PubMed1995

Prospective observational study to assess value of prostate specific antigen as screening test for prostate cancer.

OBJECTIVE: To evaluate measurement of serum prostate specific antigen as a potential screening test for future clinical prostate cancer among healthy men. DESIGN: Nested case-control study with stored serum samples collected from 49,261 men with follow up using national death and cancer registration systems. SUBJECTS: 265 asymptomatic men who subsequently developed clinical prostate cancer and 1055 controls matched for age, study centre, and duration of storage of samples. MAIN OUTCOME MEASURES: Distribution of concentrations of the antigen in men who developed prostate cancer and in controls. RESULTS: Prostate specific antigen concentrations were significantly higher in men who subsequently developed prostate cancer than in controls. In the first three years after blood collection the median concentration was 23 times greater in cases than in controls of the same age at the same centre (that is, 23 multiples of the median). A smaller difference persisted thereafter; 4.0 multiples of the median 3-6 years after blood collection, 3.6 6-10 years, and 1.8 after 10 years. In the first three years the proportion of men who developed prostate cancer and had raised levels of the antigen (> or = 12 multiples of the median) (detection rate or sensitivity) was 81% (95% confidence interval 54% to 96%). The proportion of men who did not develop prostate cancer but had levels this high (false positive rate) was only 0.5%. CONCLUSION: Prostate specific antigen measurement is a highly discriminatory screening test for prostate cancer among healthy men. In the general population, 60-74 year old men who had > or = 12 times the normal median level would have about a 50% chance of developing clinical prostate cancer in the next three years. Measurement of this antigen is a good enough screening test to justify a randomised controlled trial to determine any reduction in mortality from prostate cancer.

Aged↗
PubMed2005

Sex steroid hormones and the androgen receptor gene CAG repeat and subsequent risk of prostate cancer in the prostate-specific antigen era.

OBJECTIVE: Sex steroid hormones are thought to contribute to the growth, differentiation, and progression of prostate cancer. We investigated plasma levels of sex steroid hormones and length of the androgen receptor gene CAG repeat in relation to incident prostate cancer diagnosed in the prostate-specific antigen (PSA) era. METHODS: Using a nested case-control design, we included 460 prostate cancer cases diagnosed after providing a blood specimen in 1993 but before February 1998 among men in the Health Professionals Follow-up Study. Controls were 460 age-matched men without prostate cancer who had a screening PSA test after the date of providing a blood specimen. We measured plasma concentrations of total testosterone, free testosterone, dihydrotestosterone, androstanediol glucuronide, estradiol, and sex hormone binding globulin (SHBG) and determined the length of the androgen receptor gene CAG repeat. Conditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI) of prostate cancer. RESULTS: Mean concentrations of the sex steroids adjusted for SHBG, and mean CAG repeat length did not differ significantly between the prostate cancer cases and controls. No significant associations with total prostate cancer were detected for plasma total testosterone concentration (comparing highest versus lowest quartiles: OR, 0.78; 95% CI, 0.48-1.28; P(trend) = 0.73) or the other sex hormones after adjusting for SHBG. However, plasma total testosterone concentration was positively associated with low-grade disease (Gleason sum < 7: OR, 1.91; 95% CI, 0.89-4.07; P(trend) = 0.02) and inversely associated with high-grade disease (Gleason sum > or = 7: OR, 0.26; 95% CI, 0.10-0.66; P(trend) = 0.01). Similar patterns for grade were observed for free testosterone. Short CAG repeat length was not associated with total prostate cancer (< or = 19 versus > or = 24: OR, 0.84; 95% CI, 0.57-1.23; P(trend) = 0.22) or grade of disease. No clear associations with regionally invasive or metastatic (> or = T3b, N1, or M1) were found for any of the hormones or the CAG repeat, although the number of these cases was small. CONCLUSIONS: The overall lack of association of prostate cancer diagnosed in the PSA era with sex steroid hormones and the androgen receptor gene CAG repeat length is consistent with the hypothesis that these factors do not substantially contribute to the development of early prostate cancer in the PSA era. The influence of plasma total and free testosterone concentrations on prostate cancer grade merits further evaluation.

Age Factors↗
PubMed2000

Serum human glandular kallikrein-2 protease levels predict the presence of prostate cancer among men with elevated prostate-specific antigen.

PURPOSE: We hypothesize that serum human glandular kallikrein-2 (hK2) levels predict the presence of prostate cancer among men prescreened by prostate-specific antigen (PSA). PATIENTS AND METHODS: We conducted a cross-sectional study of 324 men who had no history of prostate cancer and who were referred for prostate biopsy. PSA and hK2 levels were measured using specific nonisotopic immunometric techniques. Cases were patients who were diagnosed with adenocarcinoma of the prostate from biopsy, and controls were patients who had no evidence of cancer from biopsy. The odds ratio for detection of prostate cancer was determined for hK2 measurements, controlling for age, total-PSA level, digital rectal examination, and symptoms of urinary obstruction. RESULTS: Of 324 men, 159 (49.1%) had cancer. Mean hK2 levels and hK2:free-PSA ratios were significantly higher in cases than in controls (1.18 v 0.53 ng/mL, respectively, for hK2, P =.0001; 1.17 v 0.62 for hK2:free-PSA ratio, P =.0001). The crude odds ratio for prostate cancer detection for patients in the highest quartile of hK2 level was 5.83 (95% confidence interval [CI], 2.8 to 12.1; P =.0001) compared with patients in the lowest quartile. The adjusted odds ratio was 6.72 (95% CI, 2.9 to 15.6; P =.0001). Similarly, the crude and adjusted odds ratios for prostate cancer detection using the hK2:free-PSA ratio were 7.36 (95% CI, 3.6 to 15.1; P =.0001) and 8.06 (95% CI, 3. 7 to 17.4; P =.0001), respectively. These odds ratios were higher than that observed for prostate cancer detection by total-PSA level (2.73; P =.03). CONCLUSION: Among men prescreened with PSA for prostate cancer, patients with high hK2 measurements have a five- to eight-fold increase in risk for prostate cancer, adjusting for PSA level and other established risk factors. hK2 measurements may be a useful adjunct to PSA in improving patient selection for prostate biopsy.

Humans↗
PubMed2003

Prostate hyperplasia in a transgenic mouse with prostate-specific expression of prolactin.

Prolactin (PRL) is one of several polypeptide factors known to exert trophic effects on the prostate. We have previously reported a dramatic prostate enlargement with concurrent chronic hyperprolactinemia and elevated serum androgen levels in a PRL transgenic mouse (Mt-PRL) with ubiquitous expression of the transgene. To address the role of local PRL action in the prostate, a new transgenic mouse model (Pb-PRL) was generated using the prostate-specific rat probasin (Pb) minimal promoter to drive expression of the rat PRL gene. Pb-PRL transgenic males developed a significant enlargement of both the dorsolateral and ventral prostate lobes evident from 10 wk of age and increasing with age. Expression of the transgene was restricted to the prostate and detected from 4 wk of age. Low levels of transgenic rat PRL were detectable in the serum of adult Pb-PRL animals. Serum androgen levels were normal. The Pb-PRL prostate displayed significant stromal hyperplasia, ductal dilation, and focal areas of epithelial dysplasia. Quantitative analysis of prostatic tissue cellularity demonstrated a marked increase in the stromal to epithelial ratio in all lobes of Mt-PRL and Pb-PRL transgenic prostates compared with controls. Microdissections demonstrated an increased ductal morphogenesis in dorsolateral and ventral prostate lobes of Mt-PRL prostate vs. Pb-PRL and controls. In conclusion, this study indicates the ability of PRL to promote, directly or indirectly, ductal morphogenesis in the developing prostate and further to induce abnormal growth primarily of the stroma in the adult gland in a setting of normal androgen levels.

Animals↗
PubMed1994

Apparent quiescence of the metallothionein gene in the rat ventral prostate: association with cadmium-induced prostate tumors in rats.

Several chronic studies in rats indicating that cadmium exposure can induce tumors of the ventral prostate have recently been completed in our laboratory. In one such study, a single dose of cadmium, s.c., increased prostatic tumor incidence only at doses below 5.0 mumol/kg, the approximate threshold for cadmium-induced testicular damage. In a further study, prostatic tumors were elevated with higher doses of cadmium (30 mumol/kg, s.c.) if testicular damage was prevented by zinc pretreatment. Most recently, we found that dietary cadmium (25 to 200 micrograms/g) also can increase prostatic neoplastic lesions, but these were reduced by zinc-deficient diets. Thus it appears that cadmium produces prostatic tumors only if testicular function is maintained. Furthermore, we find that metallothionein (MT), a protein associated with cadmium tolerance, may be deficient in the rat prostate, and the prostatic MT gene, at least in the ventral lobe, is unresponsive to metal stimuli. In liver, MT gene expression, as assessed by MT-1 mRNA, was quite apparent in control tissue and was induced in a dose-dependent manner 24 hr following cadmium exposure (1 to 10 mumol/kg, s.c.). However, in the ventral prostate very low constitutive levels of MT-1 mRNA were detected and increases did not occur with cadmium exposure. Cadmium concentrations in the ventral prostate were in excess of those that cause significant induction in the liver. In sharp contrast to the gene in the ventral prostate, in the dorsal prostate the MT gene was quite active. The dorsal prostate is not susceptible to cadmium carcinogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Research into molecular and genetic mechanisms underlying prostate carcinogenesis would be greatly advanced by in vitro prostate cell models.

Prostate cancer is the most commonly diagnosed malignancy in the United States, as well as in the Western world, and the second leading cause of male cancer death in the United States. Despite its high incidence, the molecular and genetic events involved in prostate cancer progression remain poorly understood. A hurdle in understanding the molecular genetic changes in prostate cancer has been the difficulty in establishing premalignant lesions and primary prostate tumors as in vitro cell cultures. Primary epithelial cells grow for a finite life span and then senesce. Immortalization is defined by continuous growth of otherwise senescing cells and is believed to represent an early stage in tumor progression. In order to examine these early stages, we and others have developed in vitro models of prostate epithelial cell immortalization. Because prostate cancer is a multistep, progressive disease with a typical onset later in life and with an usually high number of latent cases that do not develop into clinically manifest cancer, the steps in the progression to malignancy are of particular interest. To understand the many factors that are suspected to contribute to the development of this malignancy, there is a need for an in vitro multistep human prostate epithelial culture system. These models have been extremely important in identifying genetic and molecular changes involved in prostate cancer progression. Recently, novel human cell culture models for the study of prostate cancer have been developed. Successful establishment of primary prostate cancer cell lines from patients' familial and sporadic prostate cancer has been accomplished using telomerase, the gene that prevents cellular senescence. The novel models will be useful for identification and characterization of prostate cancer genes and will provide the new means for testing for chemoprevention and chemotherapeutic agents.

Cell Line, Tumor↗
PubMed2005

Clinical correlation, ecographic and levels of prostate specific antigen in patients with prostate cancer.

PURPOSE: This report provides information about clinical correlation, ecographic and levels of prostate specific antigen in patients with prostate cancer in the Regional Hospital from Trujillo, Peru. MATERIALS AND METHODS: Retrospective, descriptive observation study of all the clinical histories from patients with histopathology diagnosis of prostate cancer during the period of January 2000 - December 2004. The sample was constituted by 60 patients with clinics histories, study by image based on the prostate ecography and the prostate specific antigen results. The average of age found was of 75.4 years old; the most frequent clinical case reported a 91.6% of patients with obstructive and irritative symptoms. In the levels of prostate antigen the PSA found values between 10-50 ng/ml, in 48.78% of the patients. In the ecography prostate study there where evidence of hypoecogenic images in 56%, hyperecogenics images 12%, heterogenics images 20% and 12% homogenics images. In the TNM classification the higher percentage is located in T stage with an 81.67%, and in smaller proportions in the N1 and M1 stages with 8.33% and 10.0% respectively. According to Gleason it was found levels from 2-4 with 36.67%, in the level 5-7 with 23.33% and in the level 8-10 with 40.0%. CONCLUSIONS: All the patients with prostate cancer showed a clinical symptoms about, obstructive and irritative and in other organs a less percentage of symptoms that shows metastases; in more than a half of the patients, the digital rectal examination showed nodules and irregularities in its surface; in the prostate ecography it is report a higher percentage of hypoecogenics images suggestive of neoplasia. The levels of specific prostate antigen in more than 70% of the patients where over of 10 ng/ml; in the totally of the patients the histological type most frequent is the Adenocarcinoma, with a high grade of percentage of patients who had been bad prognosticated according to the Gleason score. According the NTM, more of the two thirds parts of patients with prostate cancer are in T stage, with a high percentage extending on the prostatic capsule.

Adult↗
PubMed2004

Can a 12 core prostate biopsy increase the detection rate of prostate cancer versus 6 core?: a prospective randomized study in Korea.

Several studies suggest that standard 6 core sextant transrectal ultrasound (TRUS) guided biopsies of the prostate provides insufficient material to adequately detect clinically important prostate cancer, and that a larger biopsy cores may improve the cancer detection rate. We performed a prospective randomized trial by comparing 6 and 12 core prostate biopsies to determine whether doubling the number of cores in a sextant biopsy improves the prostate cancer detection rate. We randomized 240 men with an elevated serum total prostate specific antigen (PSA) level, abnormal digital rectal examination (DRE) and/or TRUS suspicious for prostate cancer into a 6 core biopsy group and 12 core biopsy group from Jan. 2002 to Jan. 2003. We acquired 3 cores from the right and left prostate lobes for the 6 core biopsy group and three additional cores from each side more peripheral than a 6 core for the 12 core biopsy group. The 6 core and 12 core biopsy groups were well matched with no significant differences in age, prostate volume, PSA and PSA density. The overall cancer detection rate by prostate biopsy was 15.8% (38/240) and the cancer detection rate was not significantly different between the 6 core biopsy group (14.4%, 17/118) and 12 core biopsy group (17.2%, 21/122) (p=0.60). Our study demonstrates no statistically significant improvement in prostate cancer detection rate by increasing the number of biopsy cores. In conclusion, we believe that the standard 6 core sextant biopsy of the prostate is as effective at detecting prostate cancer as a 12 core biopsy in Korean men.

Aged↗
PubMed1999

Molecular detection of prostate cells in ejaculate and urethral washings in men with suspected prostate cancer.

PURPOSE: To determine whether prostatic cells were normally present in ejaculate and if the sensitivity and specificity of the detection of malignant prostate cells in ejaculate and urethral washings from men with suspected prostate cancer could be improved using the more sensitive molecular technique of reverse transcriptase-polymerase chain reaction (RT-PCR). MATERIALS AND METHODS: RT-PCR for prostate-specific antigen (PSA), prostate-specific membrane antigen (PSM) and Apoliprotein D (3 putative prostate-specific and/or cancer-specific markers) was performed on RNA extracts of ejaculate (80) and urethral washings (52) from 77 men with suspected prostate cancer and 12 young controls (<30 years of age) and urines from 5 men who had radical prostatectomies and 10 women. RESULTS: PSA, PSM and Apolipoprotein D expression was detected in ejaculates and urethral washings from both patient and control groups. No differences were observed in the results obtained for 58 men with suspected or 19 men with confirmed prostate cancer or the 18 vasectomized men within the patient group. Urines from the 5 men who had radical prostatectomies and 10 women were all negative for PSA, but PSM was detected in 2 female urines and in 3 radical prostatectomy samples. As few as 10 LNCaP prostate tumor cells could be detected by PSA RT-PCR when added to female urine. CONCLUSION: We have established a sensitive method of detecting prostatic cells in ejaculate and urethral washings and shown that PSA RT-PCR is a reliable indicator of prostate cells in these samples. However, RT-PCR for PSA, PSM and Apoliprotein D were not useful for discriminating malignant from non-malignant prostate cells.

Adult↗
PubMed1999

Prostate-specific antigen (PSA) promoter-driven androgen-inducible expression of sodium iodide symporter in prostate cancer cell lines.

Currently, no curative therapy for metastatic prostate cancer exists. Causing prostate cancer cells to express functionally active sodium iodide symporter (NIS) would enable those cells to concentrate iodide from plasma and might offer the ability to treat prostate cancer with radioiodine. Therefore, the aim of our study was to achieve tissue-specific expression of full-length human NIS (hNIS) cDNA in the androgen-sensitive human prostatic adenocarcinoma cell line LNCaP and in subcell lines C4, C4-2, and C4-2b in vitro. For this purpose, an expression vector was generated in which full-length hNIS cDNA coupled to the prostate-specific antigen (PSA) promoter has been ligated into the pEGFP-1 vector (NIS/PSA-pEGFP-1). The PSA promoter is responsible for androgen-dependent expression of PSA in benign and malignant prostate cells and was therefore used to mediate androgen-dependent prostate-specific expression of NIS. In addition, two control vectors were designed, which consist of the pEGFP-1 vector containing the PSA promoter without NIS cDNA (PSA-pEGFP-1) and NIS cDNA without the PSA promoter (NIS-pEGFP-1). Prostate cancer cells were transiently transfected with each of the above-described expression vectors, incubated with or without androgen (mibolerone) for 48 h, and monitored for iodide uptake activity. In addition, stably transfected LNCaP cell lines were established for each vector. Prostate cells transfected with NIS/PSA-pEGFP-1 showed perchlorate-sensitive, androgen-dependent iodide uptake in a range comparable to that observed in control cell lines transfected with hNIS cDNA. Perchlorate-sensitive iodide uptake was not observed in cells transfected with NIS/PSA-pEGFP-1 and treated without androgen or in cells transfected with the control vectors. In addition, prostate cancer cell lines without PSA expression (PC-3 and DU-145) did not show iodide uptake activity when transfected with NIS/PSA-pEGFP-1. Western blotting of LNCaP and C4-2b cell membranes transfected with NIS/PSA-pEGFP-1 using a monoclonal antibody that recognizes the COOH-terminus of hNIS revealed a band with a molecular weight of 90,000 that was not detected in androgen-deprived cells or in cells transfected with the control vectors, as well as a minor band at Mr 150,000 in transiently transfected LNCaP cell membranes. In conclusion, tissue-specific androgen-dependent iodide uptake activity has been induced in prostate cancer cells by PSA promoter-directed NIS expression. This study represents an initial step toward therapy of prostate cancer with radioiodine.

Adenocarcinoma↗
PubMed2000

Increased risk of prostate cancer and benign prostatic hyperplasia associated with a CYP17 gene polymorphism with a gene dosage effect.

The CYP17 gene (CYP17) codes for the cytochrome P450c17alpha enzyme, which mediates two key steps in the sex steroid synthesis. There is a polymorphism (a T-to-C substitution) in the 5'-untranslated region, which may influence the transcription level of CYP17 mRNA. There is a continuing controversy as to whether the variant allele is associated with a subset of breast cancer or polycystic ovary syndrome. In prostate cancer research, there are contradictory data concerning the CYP17 risk allele. We explored the association between CYP17 polymorphism and a risk of prostate cancer or benign prostatic hyperplasia (BPH) in a Japanese population. This study included 252 prostate cancer patients, 202 BPH patients, and 131 male controls. A 451-bp fragment encompassing the polymorphic site was amplified by PCR, treated with restriction enzyme MspA1, and electrophoresed on an agarose gel. The MspA1-undigested allele with the published sequence and the MspA1-digested variant allele were designated as A1 and A2, respectively. There was a significant difference (P < 0.05) in the genotypes between prostate cancer patients and male controls, and between BPH patients and male controls. Men with the A1/A1 CYP17 genotype had an increased risk of prostate cancer [odds ratio (OR), 2.57; 95% confidence interval (CI) = 1.39-4.78] and BPH (OR, 2.44; 95% CI = 1.26-4.72) compared with those with the A2/A2 genotype. Men with the A1/A2 genotype had an intermediate increased risk of prostate cancer (OR, 1.45; 95% CI = 0.84-2.54) and BPH (OR, 1.60; 95% CI = 0.89-2.87) compared with those with the A2/A2 genotype. The trend of an increasing risk of prostate cancer and BPH with an increasing number of the A1 allele was statistically significant (prostate cancer versus male control, P = 0.003; OR, 1.57; 95% CI = 1.16-2.12; BPH versus male control, P = 0.008; OR, 1.55; 95% CI = 1.12-2.13). There was no significant association between the CYP17 genotype and the tumor status (grade and stage) of prostate cancer. Our results suggest that the A1 allele of the CYP17 polymorphism is associated with an increased risk of prostate cancer and BPH, with a gene dosage effect. However, the CYP17 genotype does not seem to influence the disease status in prostate cancer.

Aged↗
PubMed2001

Human prostate cancer and benign prostatic hyperplasia: molecular dissection by gene expression profiling.

Critical aspects of the biology and molecular basis for prostate malignancy remain poorly understood. To reveal fundamental differences between benign and malignant growth of prostate cells, we performed gene expression profiling of primary human prostate cancer and benign prostatic hyperplasia (BPH) using cDNA microarrays consisting of 6500 human genes. Frozen prostate specimens were processed to facilitate extraction of RNA from regions of tissue enriched in either benign or malignant epithelial cell growth within a given specimen. Gene expression in each of the 16 prostate cancer and nine BPH specimens was compared with a common reference to generate normalized measures for each gene across all of the samples. Using an analysis of complete pairwise comparisons of expression profiles among all of the samples, we observed clearly discernable patterns of overall gene expression that differentiated prostate cancer from BPH. Further analysis of the data identified 210 genes with statistically significant differences in expression between prostate cancer and BPH. These genes include many not recognized previously as differentially expressed in prostate cancer and BPH, including hepsin, which codes for a transmembrane serine protease. This study reveals for the first time that significant and widespread differences in gene expression patterns exist between benign and malignant growth of the prostate gland. Gene expression analysis of prostate tissues should help to disclose the molecular mechanisms underlying prostate malignant growth and identify molecular markers for diagnostic, prognostic, and therapeutic use.

Gene Expression Profiling↗
PubMed2001

Alterations in gap junction protein expression in human benign prostatic hyperplasia and prostate cancer.

PURPOSE: Gap junctions composed of connexin proteins have an essential role in intercellular communication and differentiation. Dysregulation of connexin expression is believed to have a role in carcinogenesis. The human prostate has been reported to express connexin 32 and 43. However, the expression pattern in prostate cancer is controversial, while to our knowledge connexin expression has not been reported in benign prostatic hyperplasia (BPH). To understand the potential involvement in prostate disease connexin 32 and 43 expression was evaluated in a series of normal prostate, BPH and prostate cancer specimens that were surgically removed due to bladder outlet obstruction. MATERIALS AND METHODS: Frozen sections of 23 normal, 43 BPH and 40 cancer involved prostates were evaluated for the presence, staining intensity and pattern of connexin 32 and 43 by immunocytochemical testing. RESULTS: In all specimens examined connexin 43 stain was punctate along the borders of the basal epithelial cells, whereas connexin 32 immunolocalized to luminal epithelial cells. In normal prostate connexin 43 and 32 were present in 87% and 65% of specimens, respectively, at low to moderate stain intensity. Importantly none of the normal samples were negative foreach connexin. In BPH specimens there was a marked increase in the incidence and intensity of connexin 43 and 32 immunostaining within epithelial cells. In addition, 23% of BPH samples showed strong connexin 43 expression in stromal cells. In contrast, connexin was decreased in prostate cancer specimens, of which 65% and 38% were negative for connexin 43 and 32, respectively, and 28% were negative for each type. In poorly differentiated tumors connexin 43 and 32 were present in only 10% and 40% of tumors, respectively, at low immunostaining intensity. CONCLUSIONS: In normal human prostate basal cells communicate via connexin 43 gap junctions, whereas luminal cells communicate via connexin 32 gap junctions. In BPH gap junctional intercellular communication is increased in epithelial and stromal cells, which may have a role in BPH pathogenesis. In prostate cancer gap junctional intercellular communication is decreased, is as indicated by decreased expression of connexin 43 and 32 with severe loss in poorly differentiated prostate cancer. These alterations in connexin expression may have a role in dedifferentiation and tumor progression.

Adenocarcinoma↗
PubMed2002

Expression, localization and activity of neutral endopeptidase in cultured cells of benign prostatic hyperplasia and prostate cancer.

PURPOSE: Neutral endopeptidase is a cell surface enzyme that cleaves and inactivates neuropeptides. Neutral endopeptidase is expressed by prostatic epithelial cells and is thought to have a key role in the growth of androgen independent prostate cancer. In contrast to the encouraging data dealing with neutral endopeptidase and prostate cancer progression, only few studies are available of the significance of neutral endopeptidase in prostatic stromal cells and benign prostatic hyperplasia (BPH). We report the expression and activity of neutral endopeptidase in human prostatic stromal cells. MATERIALS AND METHODS: We recently established and characterized human prostatic stromal cells from BPH tissue. Reverse transcriptase-polymerase chain reaction, Western blot experiments and immunohistochemistry were performed to investigate the expression levels of neutral endopeptidase and show the cellular localization of the enzyme in these cells. Enzymatic neutral endopeptidase activity was evaluated using a colorimetric assay in nonstimulated cells, and after androgen and estrogen application. RESULTS: Stromal BPH cells showed strong expression of the neutral endopeptidase messenger RNA and protein, equaling the neutral endopeptidase expression level in prostate cancer cells. The neutral endopeptidase protein located in the plasma membrane of the cells showed a mean enzymatic activity plus or minus standard deviation of 75% +/- 2.5% compared with LNCaP prostate cancer cells. Interestingly enzymatic activity of the membrane bound neutral endopeptidase in stromal cells was not regulated by androgen and estrogen. CONCLUSIONS: These data suggest that neutral endopeptidase is expressed by prostatic stromal cells. In addition to its role in the progression of prostate cancer, it may also be involved in regulatory processes in the stroma, namely the degradation of neuropeptides released from prostatic neuroendocrine cells.

Cells, Cultured↗
PubMed2003

[Cases of bacillus Calmette-Guerin-induced granulomatous prostatitis and prostatic stromal invasion of the bladder carcinoma in situ, showing similar clinical findings].

Intravesical instillation of bacillus Calmette-Guerin (BCG) is the first-line therapeutic option for flat carcinoma in situ (CIS) of the bladder. Intravesical BCG instillation has been demonstrated to cause granulomatous prostatitis. Bladder CIS often also is known to show prostatic stromal invasion. We report a case of BCG-induced granulomatous prostatitis and a case of prostatic stromal invasion of bladder CIS accompanied by locally advanced prostate cancer, which showed similar clinical findings after the intravesical BCG therapy. In these 2 patients, urinary symptoms such as dysuria were prolonged regardless of anti-tuberculous medication, hard nodules were palpable at the prostate, and hypoechoic lesions were visualized by transrectal ultrasound. Both patients were treated by transurethral resection of the prostate, and the diagnoses were made by histopathological examination. Urinary symptoms were resolved in both patients after surgery, but the prostatic stromal tumor showed recurrence of growth. We report the usefulness of transurethral resection of the prostate for medication-resistant BCG-induced granulomatous prostatitis, and the importance of the correct diagnosis of prostatic stromal invasion of bladder CIS especially in the cases with concurrent prostate cancer.

Administration, Intravesical↗
PubMed2004

[Clinical evaluation of IL-1beta and TNF-alpha in prostatic secretions for chronic prostatitis].

OBJECTIVE: To determine the clinical significance of interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha( TNF-alpha) in expressed prostatic secretions(EPS) for chronic prostatitis. METHODS: Prostatic secretions IL-1beta and TNF-alpha were evaluated for 34 patients with chronic prostatitis, 10 with asymptomatic inflammatory prostatitis, 12 with benign prostatic hyperplasia (BPH) and 8 health controls by enzyme-linked immunosorbent assay (ELISA). RESULTS: IL-1beta and TNF-alpha levels in EPS in the patients of chronic prostatitis with WBC > or = 10/HP and asymptomatic inflammatory prostatitis were obviously higher than those of chronic prostatitis with WBC < 10/HP, BPH and health controls, (P < 0.05 and P < 0.02). There was a correlation between IL-1beta and TNF-alpha (P < 0.003) but none between WBC and IL-1beta or TNF-alpha. CONCLUSION: Cytokines are frequently elevated in EPS in men of chronic prostatitis with high WBC and asymptomatic inflammatory prostatitis, which provides a novel means different from traditional methods based on WBC for the identification of men with chronic prostatitis.

Aged↗
PubMed1988

[Clinical studies against chronic prostatitis and prostatitis-like syndrome (2). Evaluation of therapeutic effect].

We treated 229 cases of chronic prostatitis (bacterial in 29, non-bacterial in 200) and 238 cases of prostatitis-like syndrome and evaluated the clinical efficacy. Clinical efficacy was seen in 77.3% of the chronic prostatitis cases (82.8% bacterial, 76.5% non-bacterial) and 53.8% of the prostatitis-like syndrome cases, with a statistical difference between these two types of disease (p less than 0.01). Treatment included chemotherapy, anti-inflammation agents and minor tranquilizers. None of them were effective against the prostatitis-like syndrome. On the other hand, combination usage (chemotherapies and anti-inflammation agent) was satisfactory on chronic bacterial prostatitis. Also on chronic non-bacterial prostatitis, chemotherapy was significantly effective (p less than 0.05%). Chemotherapeutic effectiveness against chronic prostatitis (both bacterial and non-bacterial) was high with sulfamethoxazole-trimethoprim, tetracyclines, cephalosporins, nalidixic acid and penicillins in this order. There was no difference among these drugs. Prostatic massage was generally effective especially for chronic non-bacterial prostatitis (p less than 0.05) and prostatitis-like syndrome (p less than 0.01). Light psychological treatment was significantly effective toward some cases of prostatitis-like syndrome with strong psychosomatic factors (p less than 0.01).

Adolescent↗