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PubMed1997

Prostate tissue composition and response to finasteride in men with symptomatic benign prostatic hyperplasia.

PURPOSE: We sought to quantify prostate tissue changes induced by finasteride and to identify a predictor of finasteride response in men with symptomatic benign prostatic hyperplasia (BPH) via a randomized, placebo controlled, double-blind clinical trial. MATERIALS AND METHODS: Men with symptomatic BPH (52 to 78 years old) were randomly assigned to 6 months of treatment with finasteride (26) or placebo (15). Outcome measures were clinical (urinary symptom score and flow rate), chemical (serum prostate specific antigen and dihydrotestosterone levels), volumetric (transrectal ultrasound, and magnetic resonance imaging for whole and zonal prostate volumes) and histological (morphometry of prostate sextant biopsies, separated into inner and outer gland segments, to measure the percent epithelium, stroma and glandular lumen). RESULTS: In the finasteride group we found a suggestion of decreasing symptom scores and increasing flow rates (not significant) with significant decreases (p < 0.01) in prostate specific antigen (48%), dihydrotestosterone (74%) and prostate volume (21%). Finasteride treatment induced a 55% decrease in inner gland epithelium (p < 0.01) with little effect on stroma or lumina. We also found a linear correlation between pretreatment inner gland epithelial content and prostate volume decrease induced by the drug (tau = 0.58, p = 0.01). CONCLUSIONS: Finasteride treatment results in a major suppression of prostate epithelium, which is most pronounced in the inner gland. Moreover, a finasteride induced prostate volume decrease was predictable by quantification of epithelial tissues of the inner gland. These data lend additional support to the emerging concept of transition zone primacy in symptomatic BPH.

Aged↗
PubMed1998

Interleukin-6 regulates prostate-specific protein expression in prostate carcinoma cells by activation of the androgen receptor.

Interleukin-6 (IL-6) levels are frequently elevated in sera of patients with metastatic prostate cancer. IL-6 receptors are expressed in prostate cancer cell lines, as well as in benign prostate hyperplasia and prostate cancer tissue specimens. The androgen receptor (AR) is a key transcription factor that is present in all stages of prostate carcinoma, even in therapy-refractory tumors. In an attempt to investigate possible cross-talk between IL-6 and androgen signal transduction cascades, we tested the effects of this cytokine on AR transcriptional activity. The regulation of AR activity by IL-6 was studied in DU-145 cells, which were cotransfected with the androgen-responsive reporter plasmid ARE2TATACAT and the AR expression vector pSG5AR. We show that IL-6 up-regulates AR activity in a ligand-independent manner, as well as synergistically, with very low doses of the synthetic androgen methyltrienolone (5-10 pM). Therefore, AR activation by IL-6 may be operative in prostate cancer patients who have decreased androgen levels because of androgen ablation therapy. The maximal induction of reporter gene activity by IL-6 alone (50 ng/ml) was 67% of that stimulated by 1 nM of methyltrienolone. The nonsteroidal antiandrogen bicalutamide (Casodex) nearly completely inhibited AR activation by IL-6. IL-6 effects on AR activity were also abolished or greatly reduced by inhibitors of protein kinase A and C and mitogen-activated protein kinase pathways. In concordance with the results obtained in DU-145 cells, IL-6 induced AR-regulated prostate-specific antigen mRNA and protein in LNCaP cells. Stimulation of prostate-specific antigen protein secretion by IL-6 was antagonized by bicalutamide and inhibitors of protein kinase A and mitogen-activated protein kinase signaling pathways. Taken together, our data show for the first time that IL-6 is a nonsteroidal activator of the AR and that this activation is implicated in the regulation of prostate-specific proteins. Keeping in mind that IL-6, its receptor, and the AR are expressed in prostate cancers, cross-talk between IL-6 and AR signaling pathways may have clinical significance.

Down-Regulation↗
PubMed2000

Effects of alpha(1)-adrenoceptor (alpha(1)-AR) antagonists on cell proliferation and apoptosis in the prostate: therapeutic implications in prostatic disease.

BACKGROUND: Benign prostate hyperplasia (BPH) and prostate cancer established that disruption of the molecular mechanisms that regulate apoptosis and cell proliferation among the stromal and epithelial cell populations, may underlie the neoplastic development that characterizes the aging gland. This work examined the effects of selected alpha(1)-adrenoceptor (alpha(1)-AR) antagonists (blockers) on cellular dynamics to determine whether induction of apoptosis or inhibition of proliferation could contribute to the overall clinical profile. METHODS: Our efforts were focused on investigating whether alpha(1)-AR antagonists of two different chemical classes affect prostate pathophysiology via mechanisms other than smooth muscle contraction. In in vitro experiments, the two clinically used quinazoline alpha(1)-adrenoceptor antagonists terazosin and doxazosin and the chemically-distinct sulphonamide, tamsulosin, were examined for effects on prostatic tumor growth, by inhibiting cell proliferation and'or inducing apoptosis. RESULTS: Our findings suggest that alpha(1)-AR antagonists, terazosin and doxazosin, suppress prostatic growth by inducing apoptosis in a dose-dependent manner and without affecting cell proliferation. Tamsulosin exerted no effect on prostate cancer cell growth. The apoptotic effect of terazosin and doxazosin appears to be independent of the alpha(1)-adrenoceptor block. CONCLUSIONS: Taken together, our findings demonstrate the ability of the quinazoline alpha-blockers, terazosin and doxazosin, but not the sulphonamide, tamsulosin, to suppress prostate growth by inducing apoptosis among the epithelial cells in the benign and malignant prostate. These studies underwrite the durability of the response seen in long-term studies with terazosin, and suggest the potential of this drug in the treatment of prostate carcinoma.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed1991

Prostate-specific antigen levels from completely sectioned, clinically benign, whole prostates.

Clinically benign whole, untrimmed prostates and pelvic lymph nodes were obtained from 105 patients at autopsy. All 105 patients had premortem serum from which prostate-specific antigen (PSA) levels were obtained. Sixty-eight did not have carcinoma of the prostate (CAP), 28 had CAP less than 1 ml and 9 had CAP larger than 1 ml. Eleven untrimmed prostates weighed 80 g or more and eight had elevated PSA levels (more than 4.0 ng/ml): five of eight without CAP, two of two with CAP less than 1 ml, and one of one with CAP larger than 1 ml. Ninety-four whole untrimmed prostates weighed less than 80 g and 20 had elevated PSA levels: ten of 60 without CAP, two of 26 with CAP less than 1 ml, and eight of eight with CAP larger than 1 ml. This study suggests that PSA levels from patients with untrimmed prostates weighing 80 g or more (equivalent to a 60-g trimmed prostate) are usually elevated regardless whether CAP is present. However, CAP less than 1 ml, in untrimmed prostates less than 80 g, usually does not elevate PSA levels whereas CAP larger than 1 ml usually does (P less than 0.0001). The likelihood that elevated PSA levels, from patients with untrimmed prostates less than 80 g, are due to CAP larger than 1 ml increases as the PSA level increases.

Adult↗
PubMed1990

Prostate-specific antigen and prostate gland volume: correlation and clinical application.

We studied 103 patients seen in our Prostate Cancer Detection Clinic to determine whether a correlation exists between serum prostate-specific antigen (PSA) values and ultrasound-calculated prostate gland volume. Seventy men (68%) had a PSA value less than or equal to 4 ng/ml (our upper limit of normal). The men were subclassified by prostate gland volume at arbitrary break points. Twenty-five men (24%) had a prostate gland volume less than or equal to 25 cm3; in 96%, the PSA value was less than or equal to 4 mg/ml. Further analysis revealed that the percentage of men with a normal serum PSA value decreased as the prostate gland volume increased; 65.6% of the group with a gland volume between 25 and 50 cm3 (40 of 61) and 35.5% of the group whose prostate volume exceeded 50 cm3 (6 of 17) had PSA values less than or equal to 4 ng/ml. Four men had PSA values greater than 20 ng/ml; all had prostate cancer. Cancer was diagnosed in four additional patients, three with PSA values between 5 and 10 ng/ml and one with a PSA value less than 4 ng/ml. There appears to be a direct relationship between prostate gland volume and PSA value, as well as a cancer value threshold. The clinical implications of these findings are discussed.

Adult↗
PubMed2006

Finasteride targets prostate vascularity by inducing apoptosis and inhibiting cell adhesion of benign and malignant prostate cells.

BACKGROUND: This study investigated the effects of finasteride, a 5alpha-reductase inhibitor, clinically used for the treatment of benign prostatic hyperplasia (BPH) on prostate tumor vascularity, apoptosis, and cell adhesion in situ and in vitro. METHODS: Prostate specimens from BPH patients treated with finasteride for 1-12 months (n = 13), or without finasteride treatment (n = 14), were evaluated for apoptosis (TUNEL assay), microvessel density (Factor VIII), and prostate specific antigen (PSA) immunoreactivity. In vitro, the effect of finasteride was investigated in benign prostate cells, BPH-1, and its tumorigenic derivatives, CAFTD-01 and CAFTD-03, using Hoechst staining and cell adhesion assays. RESULTS: A significant increase in the apoptotic index, and reduced microvessel density and PSA expression were detected in prostates from finasteride-treated patients, compared to controls (P < 0.01). In vitro finasteride led to a significant decrease in prostate epithelial cell adhesion (P < 0.05). CONCLUSIONS: Finasteride can induce prostate apoptosis and reduce tissue vascularity by inhibiting epithelial cell adhesion. This evidence supports that finasteride has apoptotic and anti-angiogenic effects against benign and malignant prostate.

Apoptosis↗
PubMed2004

Pilot study to explore effects of low-fat, flaxseed-supplemented diet on proliferation of benign prostatic epithelium and prostate-specific antigen.

OBJECTIVES: Dietary factors may influence the prostate and have an impact on prostatic growth and disease. A small number of studies have suggested that flaxseed-supplemented, fat-restricted diets may thwart prostate cancer growth in both animals and humans. Unknown, however, is the potential effect of such a diet on benign prostatic epithelium. METHODS: We undertook a pilot study to explore whether a flaxseed-supplemented, fat-restricted diet affects the proliferation rates in benign epithelium. We also explored the effects on circulating levels of prostate-specific antigen (PSA), total testosterone, and cholesterol. Fifteen men who were scheduled to undergo repeat prostate biopsy were instructed to follow a low-fat (less than 20% kcal), flaxseed-supplemented (30 g/day) diet and were provided with a supply of flaxseed to last throughout the 6-month intervention period. The PSA, total testosterone, and cholesterol levels were determined at baseline and at 6 months of follow-up. Reports from the original and repeat biopsies were compared, and proliferation (MIB-1) rates were quantified in the benign prostatic epithelium. RESULTS: Statistically significant decreases in PSA (8.47 +/- 3.82 to 5.72 +/- 3.16 ng/mL; P = 0.0002) and cholesterol (241.1 +/- 30.8 to 213.3 +/- 51.2 mg/dL; P = 0.012) were observed. No statistically significant change was seen in total testosterone (434.5 +/- 143.6 to 428.3 +/- 92.5 ng/dL). Although 6-month repeat biopsies were not performed in 2 cases because of PSA normalization, of the 13 men who underwent repeat biopsy, the proliferation rates in the benign epithelium decreased significantly from 0.022 +/- 0.027 at baseline to 0.007 +/- 0.014 at 6 months of follow-up (P = 0.0168). CONCLUSIONS: These pilot data suggest that a flaxseed-supplemented, fat-restricted diet may affect the biology of the prostate and associated biomarkers. A randomized controlled trial is needed to determine whether flaxseed supplementation, a low-fat diet, or a combination of the two regimens may be of use in controlling overall prostatic growth.

Biopsy↗
PubMed1991

The ability of systematic transrectal ultrasound guided biopsy to detect prostate cancer in men with the clinical diagnosis of benign prostatic hyperplasia.

Multiple directed and systematic ultrasound guided biopsies of the prostate were performed in 73 men with the clinical diagnosis of benign prostatic hyperplasia (BPH). Seven men (10%) had prostate cancer. Of the 67 patients with benign biopsies 40 underwent subsequent transurethral prostatectomy and 2 (5%) had prostate cancer. Multiple directed and systematic biopsies of the prostate detected 78% of the nonpalpable prostate cancers diagnosed in the study population. Radical prostatectomy was performed in all 9 men with prostate cancer: there were 3 small organ-confined tumors, 5 large organ-confined tumors and 1 stage C tumor with 1 focus of microscopic capsular penetration. Our results suggest that multiple directed and systematic ultrasound guided biopsies are capable of detecting low volume nonpalpable prostate cancer in men with BPH. However, the exact indication for pre-treatment ultrasound guided biopsy of the prostate in men with symptomatic BPH remains unclear. It may be that use of this modality is most appropriate for patients undergoing pharmacological therapy or balloon dilation of BPH rather than for those undergoing transurethral prostatectomy.

Aged↗
PubMed2003

Immunohistochemical staining of prostate cancer with monoclonal antibodies to the precursor of prostate-specific antigen.

OBJECTIVES: To characterize the immunohistochemical staining (IHS) of precursor forms of prostate-specific antigen (pro-PSA) forms in prostate cancer, high-grade prostatic intraepithelial neoplasia (HGPIN), and benign tissue from the peripheral and transition zones. Pro-PSA have previously been shown to be more concentrated in prostate cancer tissue extracts than in benign tissue. METHODS: Prostate needle biopsies showing HGPIN (22 sections, 11 patients) and adenocarcinoma (30 sections, 21 patients) and 17 radical prostatectomy and 3 open prostatectomy specimens were identified from the surgical pathology files of Johns Hopkins Hospital. IHS was performed on formalin-fixed, paraffin-embedded sections using one monoclonal antibody (mAB) against pro-PSA with a truncated pro-leader peptide containing two amino acids, [-2]pPSA, and a second mAB against native pro-PSA ([-5/-7]pPSA). RESULTS: The mABs were specific for both benign and malignant prostatic glandular tissue and did not stain stromal, vascular, or colonic tissue when present in the specimens. All sections with HGPIN and/or adenocarcinoma showed staining with both mABs. HGPIN was strongly positive in most cases (66.1%). The native pro-PSA mAB showed little differential between cancer and benign glands, and the mAB to the truncated [-2]pPSA stained cancer tissue more strongly than benign tissue. Benign atrophic glands often showed negative or weak/patchy staining. No difference was found in the staining pattern between benign glands in the peripheral zone and transition zone. CONCLUSIONS: This study is the first to demonstrate that mABs to pro-PSA can be used as specific IHS for benign and malignant prostatic tissue. [-2]pPSA appears to be preferentially more concentrated in cancer tissue than in benign glands, correlating with previous tissue extract studies. Unlike previous studies with PSA staining, the IHS for pro-PSA remained uniform among the different tumor grades. Therefore, pro-PSA may be a useful marker in differentiating high-grade prostate adenocarcinoma from other non-prostate carcinomas.

Adenocarcinoma↗
PubMed2003

Effect of subclinical prostatic inflammation on serum PSA levels in men with clinically undetectable prostate cancer.

OBJECTIVES: To examine whether subclinical prostatic inflammation might influence serum prostate-specific antigen (PSA) levels in men with clinically undetectable prostate cancer. METHODS: A total of 461 patients who underwent prostate biopsy at our hospital were studied between January 1996 and December 1999. Of these patients, a total of 125 patients without detectable prostate cancer or a history or symptoms of prostatitis, with serum PSA levels of less than 20.0 ng/mL and other specified exclusion criteria, were included in the study. Inflammation observed at biopsy was scored for inflammation extent and inflammatory aggressiveness, and the effects of these morphologic aspects of inflammation on serum PSA levels were examined. RESULTS: The extent of inflammation tended to increase as the prostate volume increased (P = 0.006). Patients with a PSA greater than 2.5 ng/mL had a greater extent and aggressiveness of inflammation than those with PSA levels of 2.5 ng/mL or less (P = 0.004 and P = 0.050, respectively). However, no statistically significant differences were found in terms of the extent of inflammation or inflammatory aggressiveness between patients with PSA levels greater than 4.0 ng/mL and those with PSA levels of 4.0 ng/mL or less. Furthermore, the extent of inflammation did not account for PSA levels greater than 2.5 or 4.0 ng/mL by multivariate analysis. CONCLUSIONS: Our results indicate that subclinical prostatic inflammation is not the etiology of a serum PSA greater than 4.0 ng/mL in men without clinically detectable prostate cancer.

Adenocarcinoma↗
PubMed2001

Prostatic MR imaging. Accuracy in differentiating cancer from other prostatic disorders.

PURPOSE: We assessed the accuracy of MR imaging in differentiating between cancer and other prostatic disorders, and evaluated the diagnostic criteria for various prostatic diseases. MATERIAL AND METHODS: A total of 74 endorectal coil MR studies were performed on 72 patients. Twenty patients had prostatic cancer, 20 benign prostatic hyperplasia (BPH), 4 acute bacterial prostatitis, 5 chronic bacterial prostatitis (2 also belonging to the previous category), 19 chronic non-bacterial prostatitis/chronic pelvic pain syndrome, and 6 were symptomless voluntary controls. All studies were interpreted by two experienced radiologists in random order. Radiologists were blinded to all clinical data including the age of the patients. Based on MR findings, both radiologists filled in a form covering diagnostic criteria and diagnosis. RESULTS: Accuracy in diagnosing prostate cancer was 74%. Sensitivity was 50% and specificity 83%, and positive and negative predictive values were 53 and 82%, respectively. Bacterial prostatitis showed some features similar to carcinoma. Abundant BPH rendered cancer detection more difficult. No diagnostic criterion was clearly better than the others. Interobserver agreement on the MR diagnosis ranged from moderate to good. CONCLUSION: Without knowledge of accurate clinical data, MR seems to be too insensitive in detecting prostate cancer to be used as a primary diagnostic tool.

Aged↗
PubMed1988

The usefulness of prostate-specific antigen and prostatic acid phosphatase in clinical practice.

A comparative study was performed on the usefulness of prostate-specific antigen (PSA) and prostatic acid phosphatase (PAP) in control subjects (69), benign prostatic hypertrophy (BPH) patients (150), and patients with prostatic carcinoma (113) in a urology department. We establish, as others, the greater clinical sensitivity of PSA and its effectiveness as a prognostic tool in the evaluation of prostatic cancer therapy and in the early detection of residual tumor following radical prostatectomy. However, patients are admitted to our department with more severe and complicated benign prostatic pathology and urinary dysfunctions, which decreases the specificity of the PSA test to 30% (N = 2.7 ng/ml). A cutoff threshold of 50 ng/ml becomes necessary to maintain a 90% positive predictive value. The combination of PSA sensitivity (96%) and PAP specificity (95%) enabled a better definition of the high-risk subpopulation among noncancer patients and, in addition, was a help for differential diagnosis, confirmation of advanced stages of prostatic cancer, and selection of low-stage prostatic cancer candidates undergoing radical prostatectomy. Routine serum PSA measurements in the population of patients consulting a urology department will no doubt bring about a new approach to the management of prostate cancer.

Acid Phosphatase↗
PubMed2003

Increased prostate-specific antigen in subclinical prostatitis: the role of aggressiveness and extension of inflammation.

OBJECTIVES: Subclinical prostatitis is a very frequent histologic finding in pathological examinations of prostate biopsy and prostate surgery material. In this study, we tried to investigate the correlation between the morphological parameters of histological prostatitis and total serum prostate-specific antigen (PSA)-PSA density (PSAD) to determine if either the extent or aggressiveness of inflammation might affect serum PSA. METHODS: 269 patients who had undergone TURP or transvesical prostatectomy with pathological diagnosis of BPH and prostatitis were included in the study. We retrospectively reviewed and scored the extent and aggressiveness of inflammation in prostate specimens of BPH, according to the scale that has been reported by Irani et al. and then correlated those scores with PSA and PSAD. RESULTS: When the inflammation grades correlated with PSA and PSAD, the extent of the inflammation did not show a significant correlation with total PSA and PSAD (p > 0.05). However, there was a statistically significant correlation between aggressiveness grades and total PSA and PSAD (p < 0.001). Median PSA levels in grades 0, 1 and 2 of aggressiveness of inflammation were 3.2, 4.2 and 5.8 respectively. CONCLUSION: Aggressiveness grade of the inflammation in subclinical prostatitis is the most important morphological factor that is responsible for PSA elevation. We believe that it should be a more accurate guide for the clinician if pathologists report on the aggressiveness grades of the inflammation, especially on initial prostate biopsies, in order to help for timing of the further biopsy.

Aged↗
PubMedDate not supplied

Prostate-specific antigen (PSA) and cancer-associated serum antigen (CASA) in distinguishing benign and malignant prostate disease.

The Prostate-Specific Antigen (PSA) and the Cancer-Associated Serum Antigen (CASA) assay for the MUC1 mucin were compared in the serum of 303 patients with malignant or benign prostatic disease. Using cutpoints of 4, 10, and 20 micrograms/l, PSA was elevated in 93%, 81%, and 64% of patients with prostate cancer (n = 113), with corresponding specificities of 55%, 84%, and 96% in benign prostate disease (prostatic hyperplasia or prostatitis, n = 190). Using the recommended cutpoint of 4 Units/ml, CASA was elevated in 38% of patients with prostate cancer, with a specificity of 91% in benign disease. PSA and CASA showed a poor correlation in prostate cancer (r = 0.367) and benign disease (r = 0.158), and CASA was elevated in some PSA negative samples. Used together, PSA > or = 20 micrograms/l and CASA > or = 4 kU/l gave perfect specificity in benign disease, with a corresponding sensitivity of 29% (positive and negative predictive values of 100% and 70%, respectively). However, this combination gave no improvement over the use of PSA alone, with sensitivity 47% when the cutpoint was raised to give perfect specificity. These data suggest that CASA is of little use as an adjunct to PSA in the differentiation of benign and malignant prostate disease.

Aged↗
PubMed1999

[The incidence of lesions associated with prostatic biopsy and its effect on the serum concentration of the prostate-specific antigen].

OBJECTIVE: To analyze the incidence of pathoanatomical lesions seen in systematic prostate biopsies and to evaluate their influence on PSA serum levels. MATERIAL AND METHODS: 495 consecutive prostate biopsies, indicated by a suspicion digital rectal examination in 194 patients (39.2%) and raised serum PSA in 301 (60.8%), were evaluated. Biopsy was performed by sextant and hypoechoic nodes, and PSA serum measurements by dual monoclonal antibody radioimmunoassay, Tandem PSA. RESULTS: Cancer was diagnosed in 42.6% biopsies and BPH in 67.4%; additionally, other associated lesions were detected in 74.6% cases, the most frequent ones being chronic prostatitis (47.3%), glandular atrophy (35.9%) and acute prostatitis (23%). All lesions were significantly related to the primary BPH diagnosis in 74.2% to 85% cases. High grade PIN (14.1%) was related to primary cancer diagnosis in 87.1% cases. The multivariate analysis showed that the main diagnosis (BPH vs cancer) was the only variable that had a significant influence on PSA serum levels. When BPH patients were considered separately, the only variable with significant influence on PSA serum levels was the prostatic volume. The univariate analysis showed a nonsignificant increase in association with acute prostatitis and high grade PIN, and a decrease in association with chronic prostatitis. CONCLUSIONS: BPH or cancer associated damage is very frequent in prostatic biopsies. However, the only factors showing a significant contribution to PSA serum levels appear to be the presence or absence of cancer, or the prostatic volume when the main diagnosis is BPH.

Adult↗
PubMed2000

Molecular forms of prostate-specific antigen in malignant and benign prostatic tissue: biochemical and diagnostic implications.

BACKGROUND: Patients with prostate cancer (PCa) show a lower ratio of free prostate-specific antigen (fPSA) to total PSA (tPSA) in serum than patients with benign prostatic hyperplasia (BPH). The patterns of the intracellular PSA isoforms in malignant and benign prostatic tissue have been studied as potential molecular reasons for this phenomenon. METHODS: Prostatic tissue samples were obtained after cystoprostatectomy from patients with bladder cancer (n = 10), from BPH patients (transurethral resection of the prostate, n = 10; adenomectomy, n = 10), and from the cancerous and noncancerous parts of the same prostates removed surgically by prostatectomy because of PCa (n = 20). PSA pattern was characterized by gel filtration, immunoblotting, and immunoassays for tPSA, fPSA, alpha(1)-antichymotrypsin-PSA (ACT-PSA), and complexed PSA (Bayer Immuno 1 assay). Comparisons were made with the PSA concentrations in serum. RESULTS: The major portion of tPSA in all tissue samples was fPSA; complexed PSA forms were <2%. Samples from cystoprostatectomy patients had the lowest and those from adenomectomy patients the highest values of tPSA and fPSA. PSA concentrations were lower in cancerous than in the noncancerous parts of the prostate. No significant correlations were found between tumor stage or grade and the amounts of tPSA, fPSA, and ACT-PSA in tissue. Tissue PSA values were not correlated with the serum PSA concentrations nor with the ratios fPSA/tPSA and ACT-PSA/tPSA in sera. CONCLUSIONS: The amounts of tPSA and the PSA isoforms in prostatic tissue explain neither the concentrations of tPSA and PSA isoforms in serum nor the behavior of the ratio fPSA/tPSA in patients with BPH and PCa.

Adult↗
PubMed1987

[Clinical evaluation of a prostate-specific antigen as a serum marker of prostatic cancer].

Combined measurement of serum prostate-specific antigen (PA) and prostatic acid phosphatase (PAP) was performed in 235 patients with various urologic diseases including 55 patients with prostatic cancer. A PA level of over 24.7 ng/ml and a PAP level of over 3.1 ng/ml were considered to be positive. The positive rate of PA was 57% in the patients with untreated prostatic cancer and 3% in the patients without prostatic cancer. The positive rate of PAP was 52% in the patients with untreated prostatic cancer and 1% in the patients without prostatic cancer. PA and PAP were considered to be equally sensitive and specific serum markers of prostatic cancer. However, the positive rate increased to 65% without increasing the false positive rate when the PA and PAP were both measured simultaneously. The combined assay of PA and PAP is recommended for screening prostatic cancer. The cross-over titer of PA and gamma-Sm using standard samples in each kit revealed linearity, which suggested that PA and gamma-Sm possess the same antigenicity.

Acid Phosphatase↗
PubMed2003

Gene transfer of alpha1,3-fucosyltransferase increases tumor growth of the PC-3 human prostate cancer cell line through enhanced adhesion to prostatic stromal cells.

Elevated expression of sialyl Lewis X has been postulated to be a prognostic indicator of prostate cancer. However, direct evidence for the relationship between increased expression of sialyl Lewis X and malignancy of prostate cancer is still lacking. To determine whether increased levels of sialyl Lewis X leads to malignancy in prostate tumor, we transfected the human prostate cancer cell line PC-3 with alpha1,3-fucosyltransferase III (FTIII) to obtain stable transfectants, PC-3-FTIII lines, that highly express sialyl Lewis X. When inoculated in the prostate of nude mice, PC-3-FTIII cells produced large prostate tumors, while mock-transfected PC-3 cells, which are negative for sialyl Lewis X antigen, produced small prostate tumors. The aggressive tumor formation by PC-3-FTIII cells was inhibited by preincubation of the tumor cells with anti-sialyl Lewis X antibody, by the presence of sialyl Lewis X oligosaccharide or by selectin ligand mimic peptide but not by control peptide. PC-3-FTIII cells and mock-transfected PC-3 cells exhibited no significant difference in cell numbers when cultured in vitro. Remarkably, PC-3-FTIII adhered to prostatic stromal cells in vitro with higher affinity than mock-transfected PC-3. Such adhesion was inhibited by preincubation of PC-3-FTIII cells with antisialyl Lewis X antibody, by the addition of sialyl Lewis X oligosaccharide or by selectin ligand mimic peptide. However, anti-E-selectin, anti-P-selectin or anti-L-selectin antibodies did not inhibit the adhesion of PC-3-FTIII cells to the stromal cells. These results suggest that prostate cancer cells gain aggressiveness through adhesive interaction with prostatic stromal cells by a novel mechanism involving sialyl Lewis X.

Adenocarcinoma↗