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PubMed1999

Expression of the RNA component of human telomerase (hTR) in prostate cancer, prostatic intraepithelial neoplasia, and normal prostate tissue.

Telomerase is a ribonucleoprotein that synthesizes telomeric DNA on chromosomal ends. While telomerase is undetectable in most normal somatic tissues, telomerase activation has been detected by a polymerase chain reaction (PCR)-based assay (TRAP) in many immortal cell lines and various cancers, including prostate cancers. To investigate the role of telomerase in prostate cancer at the cellular level, the expression of one of the ribonucleoprotein complexes, the RNA component of human telomerase (hTR), was studied in normal, preneoplastic, and cancerous prostate tissues using a non-radioactive in situ hybridization procedure. Nine human prostates resected at the time of radical prostatectomy were studied. In each case, archival paraffin-embedded samples from normal tissue, prostatic intraepithelial neoplasia (PIN) lesions, the putative precancerous lesion, and prostate carcinomas were selected for in situ hybridization. hTR mRNA expression was detected in carcinomatous glands of seven out of the nine cancers (75 per cent). Furthermore, in seven out of the eight cases showing PIN lesions, the epithelial cells of PIN foci also expressed hTR mRNA. By contrast, in normal tissue, epithelial cells were negative, whereas hTR mRNA expression was detected in the basal cells. The detection of hTR mRNA in PIN lesions clearly strengthens the link between PIN and carcinomatous glands and suggests that telomerase expression occurs early in prostate carcinogenesis. Furthermore, this study confirms previous experimental data suggesting that the basal cell layer is the stem cell compartment in prostate.

Aged↗

PubMed1999

Growth factors in expressed prostatic fluid from men with prostate cancer, BPH, and clinically normal prostates.

BACKGROUND: Although growth factors such as epidermal growth factor (EGF), transforming growth factor (TGF)-alpha, and TGF-beta are important regulators of prostate cell growth in vitro and in animal models, evidence to support their role in human prostate cancer development remains sparse. We previously showed that men without prostate cancer have concentrations of EGF and TGF-alpha in expressed prostatic fluid (EPF) that are individually distinct and stable over time. This study addressed whether growth factor levels in EPF are associated with the presence or progression of prostate cancer. METHODS: We measured levels of immunoreactive EGF, TGF-alpha, and TGF-beta1 in stored EPF samples from three age-matched groups: 19 men with untreated, histologically diagnosed prostate cancer (CaP), 38 with benign prostate hyperplasia (BPH), and 19 with normal prostate glands (NPD). RESULTS: Median TGF-alpha was lower in the BPH group (0.45 ng/ml) than in either CaP (0.63 ng/ml) or NPD (0.58 ng/ml) groups (P = 0.03 and 0.12, respectively). For EGF, the median was lowest in the CaP group and highest in the NPD group (92.5 ng/ml vs. 175.5 ng/ml, P = 0.006). For TGF-beta1, the median level in CaP was 2.7 times higher than the median level among all controls (6.65 ng/ml vs. 2.46 ng/ml, P = 0.002). Growth factor levels were not associated with tumor stage or Gleason score. However, the single case with distant metastases had TGF-beta1 levels 23-fold higher than the CaP median. CONCLUSIONS: The results suggest that at the time of CaP diagnosis, EGF levels in EPF are significantly lower, and TGF-beta1 levels significantly higher, than normal. Marked overexpression of TGF-beta1 in advanced CaP might be reflected in extremely high EPF levels.

Aged↗

PubMed1993

Prostate-specific antigen and prostate volume: a meta-analysis of prostate cancer screening criteria.

OBJECTIVE: To establish the value of serum prostate-specific antigen (PSA) and prostate-specific antigen per unit volume of prostate gland (PSAD) in detecting prostate carcinoma (CaP) in a hypothetical screening algorithm, a meta-analysis of the sensitivities, specificities, predictive values and likelihood ratios were combined from the published data. DATA SOURCES: Journal articles identified by a MEDLINE database search from 1988 to October 1992, using prostate-specific antigen as a key word were used to calculate the distribution of PSA in healthy men, men with benign prostatic hyperplasia (BPH) and men with prostate carcinoma (CaP). STUDY SELECTION: Only studies that contained the specified serum PSA values and patient outcomes were included. DATA EXTRACTION: The distributions of the serum PSA were plotted versus serum PSA for healthy men (2567), men with BPH (798) and men with CaP (835) from the abstracted data. Prostate volume distributions were estimated from the published transrectal ultrasound (TRUS) calculations. DATA SYNTHESIS: Hypothetical cohorts of 1,000 men between the ages of 60 and 70 years were screened using three different screening decision algorithms. Using a serum PSA cutoff of 3.0 ng/ml for referral for transrectal biopsy, 59 of 80 (74%) CaP would be detected and 21 (26%) would be missed. 209 transrectal biopsies would be performed, and 150 (72%) of them would be negative for CaP. Using a serum PSA cutoff of 4.0 ng/ml, 52 of 80 (65%) CaP would be detected and 28 (35%) would be missed. 146 transrectal biopsies would be performed, and 94 (64%) of them would be unnecessary. Using a cutoff of 2.0 ng/ml for serum PSA and 0.1 ng/ml/cc for PSAD, 55 of 80 (69%) of the cancers would be detected and 25 (31%) would be missed. Only 84 transrectal biopsies would be performed, and 29 (35%) of them would be negative for cancer. CONCLUSION: This algorithm maximizes the number of cancers detected (true-positive cases) and at the same time reduces the number of false-positive cases, minimizing the number of patients who would have to receive an unnecessary transrectal biopsy, compared to using a serum PSA cutoff of 3.0 or 4.0 ng/ml.

Adult↗

PubMed1992

Prostate specific antigen and prostatitis. I. Effect of prostatitis on serum PSA in the human and nonhuman primate.

Prostate specific antigen (PSA) has become a mainstay in the diagnosis and management of patients with prostate cancer. We have found, as have others, that it may be elevated in patients with prostatic inflammation. Ten patients had clinical evidence of prostatitis and elevated PSA levels. Six of these had persistently elevated levels after antibiotic treatment. After transrectal ultrasonography and biopsy, two had findings of adenocarcinoma, and the rest had a pathologic diagnosis of acute or chronic prostatitis. We studied this process in an experimental model of prostatitis using a nonhuman primate. We infected six cynomolgus monkeys and followed their PSA levels until resolution of the infection. The PSA peaked between 5 and 7 days after inoculation and gradually returned to baseline in 8 weeks. The dramatically elevated serum PSA levels in bacterial prostatitis can cause confusion in the diagnosis of prostatic carcinoma.

Adult↗

PubMed1994

Differential expression of transforming growth factor-beta 1 and beta 3 as well as c-fos mRNA in normal human prostate, benign prostatic hyperplasia and prostatic cancer.

The discrepancy between the incidence of latent prostate cancer and that of clinically overt carcinoma suggests that there can be different courses in the biological progression of prostate cancer. As this cancer is detected increasingly at an infraclinical stage, markers are needed to indicate which lesions will progress and lead to the patient's death. To investigate the possibility that specific growth factors and/or proto-oncogenes are expressed differentially, we measured mRNA levels of transforming growth factors beta 1 (TGF-beta 1), TGF-beta 2 and TGF-beta 3 and of the c-fos and c-jun oncogenes by Northern blotting in normal prostate, benign prostatic hyperplasia (BPH) and prostate cancer. Our data demonstrate that expression of TGF-beta 1 increased, whereas that of TGF-beta 3 fell to an almost undetectable level in carcinoma. Expression of c-fos followed the TGF-beta 1 pattern, whereas no difference could be seen in c-jun expression in cancer as compared with BPH and normal prostate. The differential expression of TGF-beta 1, TGF-beta 3 and c-fos could possibly be used to improve the characterisation of prostate cancer. Long-term follow-up of patients may indicate whether mRNA levels of these growth factors and oncogenes correlate clinically and whether they can be used as markers for progression in human prostate cancer.

Adult↗

PubMed1993

An algorithm for prostate cancer detection in a patient population using prostate-specific antigen and prostate-specific antigen density.

Prostate-specific antigen (PSA) is the most accurate serum marker for cancer of the prostate (CaP). However, its sensitivity and specificity are suboptimal, especially at values ranging between 4.1 and 10.0 ng/ml (monoclonal), because benign prostatic hypertrophy and hyperplasia (BPH) and CaP frequently coexist in this range. This study was undertaken to determine the value of incorporating prostate volume measurements with serum PSA levels in a quotient (PSA/volume) entitled PSA density (PSAD). A total of 3140 patients were analyzed and stratified by serum PSA, digital rectal examination (DRE), transrectal prostate ultrasound (TRUS), TRUS volume determination and PSAD. All patients were referred for evaluation and therefore do not represent a screened population. Patients underwent prostate biopsies when abnormalities in TRUS or DRE were detected. Although both PSA and PSAD have statistical significance when the serum PSA value is < or = 4.0 ng/ml, neither has clinical significance in differentiating BPH from CaP. At serum levels ranging between 4.1 and 10.0 ng/ml, PSA has no ability to differentiate BPH from CaP, whereas PSAD does so with statistical and clinical significance. When the PSA value is between 10.1 and 20.0 ng/ml, only PSAD is statistically significant. When PSA exceeds 20 ng/ml, PSAD is redundant. We conclude that all patients with an abnormality on DRE or TRUS should undergo prostate biopsy. If the PSA value is < or = 4.0 ng/ml, TRUS and PSAD are not warranted and routine biopsy is not recommended. For intermediate PSA levels, 4.1-10.0 ng/ml, TRUS, TRUS prostate volume, and PSAD are important.2_

Aged↗

PubMed1993

Effect of cystoscopy, prostate biopsy, and transurethral resection of prostate on serum prostate-specific antigen concentration.

To assess the effect of cystoscopy, prostate biopsy, and transurethral resection of the prostate (TURP) on the serum prostate-specific antigen (PSA) concentration, 101 patients were evaluated. For cystoscopic examination, 69 men were randomized in a prospective manner to one of three groups: flexible cystoscopy, rigid cystoscopy, and a control cohort. The median change in serum PSA was 0.1 ng/mL following flexible cystoscopy, 0.05 ng/mL after rigid cystoscopy, and 0.05 ng/mL for the control group, in which two serum PSA determinations were obtained without an intervening cystoscopy. The differences between the three groups were not statistically significant. The effect of prostate biopsy and TURP was examined in 32 men. Prostate biopsy caused an immediate elevation in the serum PSA level, with a median increase of 7.9 ng/mL (p < 0.0001). Similarly, TURP produced an elevation in the serum PSA concentration, with a median change of 5.9 ng/mL (p < 0.001). The median time required for the serum PSA value to return to a stable level after prostate biopsy was fifteen days (range: 5-21 days) for men with prostate cancer and seventeen days (range: 3-30+ days) for men without cancer, and eighteen days (range: 12-30+ days) for men who underwent TURP. These findings indicate that a serum PSA determination after either a flexible or a rigid cystoscopy is accurate and reliable. Both biopsy and TURP cause an immediate increase in the serum PSA level, which usually returns to a stable, baseline level within three weeks. However, because in some patients the serum PSA still remained elevated after four weeks, it is recommended that a serum PSA determination not be obtained for at least six weeks after either a prostate biopsy or TURP.

Aged↗

PubMed2002

Anti-thrombin is expressed in the benign prostatic epithelium and in prostate cancer and is capable of forming complexes with prostate-specific antigen and human glandular kallikrein 2.

Anti-thrombin, a member of the serpin family and an inhibitor of thrombin and blood coagulation factor Xa, was recently shown to inhibit angiogenesis and tumor growth. In the present study, we examined the expression of anti-thrombin in benign and malignant prostate gland. Using immunohistochemistry, anti-thrombin was found in prostate epithelium and stroma cells. Tissue microarrays of tumors (n = 112) and three different prostate cancer cell lines (PC-3, LNCaP, and DU-145) were all positive for anti-thrombin. Abundant expression in a population of prostatic tumor cells was further evidenced by in situ hybridization experiments. The immunostaining for anti-thrombin was confined to the cytoplasm, was most intense in Gleason grade 3 tumors, and in part overlapped with that of prostate-specific antigen. Western blotting of benign and malignant tissue homogenates revealed a predominant 58-kd anti-thrombin immunoreactive component. In vitro, anti-thrombin formed complexes more readily with human kallikrein 2, particularly in the presence of heparin, and less efficiently with prostate-specific antigen. Both complexes could be recognized by polyclonal and monoclonal IgGs against anti-thrombin. We conclude that anti-thrombin is widely expressed in prostate cancer but is gradually lost in tumors of high Gleason grade. Anti-thrombin may act as a local anti-angiogenic factor, the effect of which is partially lost in poorly differentiated prostatic tumors.

Animals↗

PubMed1995

Sensitive detection of prostatic hematogenous tumor cell dissemination using prostate specific antigen and prostate specific membrane-derived primers in the polymerase chain reaction.

We developed a polymerase chain reaction based assay enabling sensitive detection of hematogenous tumor cell dissemination in patients with prostate cancer. We performed "nested polymerase chain reaction," amplifying messenger ribonucleic acid sequences unique to prostate specific antigen (PSA) and to the prostate specific membrane antigen, and compared the respective results. Prostatic tumor cells were detected in 2 of 30 patients (6.7%) by polymerase chain reaction with PSA derived primers, while prostate specific membrane primers detected tumor cells in 19 (63.3%). All 16 negative controls had negative PSA and prostate specific membrane polymerase chain reaction. Assays were repeated to confirm results, and polymerase chain reaction products were verified by deoxyribonucleic acid sequencing and Southern analysis. Patients harboring circulating prostatic tumor cells as detected by prostate specific membrane and not by PSA polymerase chain reaction included 7 of 13 previously treated by radical prostatectomy who had nonmeasurable serum PSA levels at the time of this assay. The significance of these findings with respect to future disease recurrence and progression will be investigated.

Base Sequence↗

PubMed1994

The use of prostate specific antigen and prostate specific antigen density in the diagnosis of prostate cancer in a community based urology practice.

Since 1989 we have used serum prostate specific antigen (PSA) levels as an indication for ultrasound guided systematic biopsies of the prostate. Realizing that the PSA level in part reflects prostatic glandular epithelial volume, we reviewed the accumulated data on our last 2,340 biopsies to determine if the quotient of PSA and prostatic volume, prostate specific antigen density, provided any further diagnostic information. There were evaluable data for 2,020 patients. Prostate specific antigen density levels are shown to have a strong correlation with the diagnosis of prostate cancer and provide a more reliable indication for ultrasound guided biopsy of the prostate than PSA alone.

Adult↗

PubMed1991

Effect of the addition of estrogen to medical castration on prostatic size, symptoms, histology and serum prostate specific antigen in 4 men with benign prostatic hypertrophy.

A total of 4 men with benign prostatic hypertrophy who underwent medical castration therapy with a long-acting gonadotropin-releasing hormone agonist (leuprolide) for more than 6 months elected to add an estrogen transdermal patch (0.05 mg. to the skin biweekly) to the leuprolide regimen. The average prostatic size (transrectal ultrasound), serum prostate specific antigen (PSA) levels and symptoms of prostatism were dramatically decreased with leuprolide alone. The addition of estrogen for 6 months did not result in any change in prostate size, symptoms or serum PSA levels over that seen with leuprolide alone. The development of squamous metaplasia was noted in 1 man with leuprolide alone and in 1 man after the addition of estrogen. Immunohistochemical staining with anticytokeratin 903 antibodies reveals that squamous metaplasia appears to arise from prostatic basal cells. We postulate that the target cell for estrogen action in the prostate is the prostatic basal cell. In the absence of androgen the only direct effect of estrogens is the induction of squamous metaplasia.

Aged↗

PubMed1999

Assessing the risk of unsuspected prostate cancer in patients with benign prostatic hypertrophy: a 13-year retrospective study of the incidence and natural history of T1a-T1b prostate cancers.

OBJECTIVE: To determine the incidence and natural history of stage T1a-T1b prostate cancer in patients undergoing surgery for benign prostatic hypertrophy (BPH), and thus evaluate the effect that recent medical and 'minimally invasive' treatments (which provide no prostate sample for pathological examination) might have on the percentage of patients with unsuspected prostate cancer. PATIENTS AND METHODS: A series of 1648 patients undergoing surgery for BPH over a 13-year period were reviewed retrospectively; the period overlapped the introduction of serum prostate specific antigen (PSA) as a detection method. RESULTS: Stage T1 prostate cancer was found in 182 patients (11%), comprising 126 (11%) of 1199 transurethral resections and 56 (12%) of 449 open enucleations. The introduction of systematic PSA assays gradually reduced the mean incidence of T1 cancer from 23% to 7%, with a greater effect on T1b (from 15% to 2%), while the incidence of T1a remained nearly constant (+/-5%). The pathological features of surgical specimens from 43 radical prostatectomies undertaken for T1 tumours were reviewed. Locally advanced disease (stage >/=pT3) was apparent in 13% of T1a and 28% of T1b tumours. Amongst the patients electing for surveillance, only 8% of those with T1a progressed within 30-97 months of follow-up (mean progression time 73 months), whereas 29% of those with stage T1b progressed within 36 months of follow-up (mean progression time 17 months). CONCLUSION: These results show that the use of the PSA assay has decreased but not suppressed the incidence of pT1 prostate cancer, with a greater effect on those tumours at higher risk of progression (T1b). This suggests that the detection of prostate cancer based on PSA and transrectal ultrasonography is appropriate for screening patients and is sufficiently accurate that treatments for BPH that provide no pathological materials can be applied safely.

Aged↗

PubMed2001

Inducible nitric oxide synthase expression in benign prostatic hyperplasia, low- and high-grade prostatic intraepithelial neoplasia and prostatic carcinoma.

OBJECTIVE: To elucidate the incidence of inducible nitric oxide synthase (iNOS) expression in benign prostatic hyperplasia (BPH), low- and high-grade prostatic intraepithelial neoplasia (PIN) and prostatic carcinoma lesions, and to explore the role of iNOS in prostate tumorigenesis. MATERIALS AND METHODS: Immunoreactivity for iNOS was examined in 20 samples each of BPH, high-grade PIN, low-grade PIN and prostatic carcinoma. RESULTS: Positive iNOS immunostaining was detected in all samples from all patients; iNOS was detected in both basal epithelial cells and secretory cells of the glandular epithelium. High-grade PIN and prostatic carcinoma samples had more intense iNOS immunostaining than low-grade PIN and BPH samples. In all samples, smooth muscle cells showed weak or moderate iNOS immunoreactivity and endothelial cells showed moderate immunostaining. CONCLUSIONS: Nitric oxide generated by iNOS may be involved in prostate tumorigenesis and further studies with immunohistochemical and molecular biology are needed to determine the exact role of iNOS in the pathogenesis of prostatic carcinoma.

Adenocarcinoma↗

PubMed1995

Prostate tissue specificity of the prostate-specific antigen promoter isolated from a patient with prostate cancer.

We have cloned and characterized a 620-bp fragment of DNA that flanks 5' of the prostate-specific antigen (PSA) gene from a prostate cancer patient. Using DNA transfection, the efficacy of this putative promoter in regulating gene expression was quantitated in several prostate and nonprostate tissue cell lines. Our results demonstrated that the 620-dp DNA fragment actively drives gene expression in LNCaP, a PSA-producing prostate tumor cell line. No promoter activity was detected in the non-PSA-producing prostate tumor lines, DU145 and PC-3, nor in a renal (R11) or breast (MCF-7) cancer cell line. Furthermore, the promoter activity could be regulated in vitro by androgen stimulation. Dihydrotestosterone (DHT) concentrations between 3 and 30 nM induced the highest promoter activity in the transfected LNCaP cells, which parallels the expression profile of the androgen receptor in LNCaP cells. In addition, our PSA promoter exhibited competitive inhibition of the endogenous genomic PSA promoter in transfected LNCaP cells, suggesting that prostate cell-specific DNA-binding proteins are required to activate the PSA promoter. increased its potency four- to five-fold while retaining tissue specificity. Our data suggest that a strong tissue-specific negative regulatory element capable of overriding the nonspecific CMV promoter is present in the PSA promoter and confers its tissue specificity. The use of a highly specific promoter-driven gene vector will allow selective expression of therapeutic genes within PSA-producing prostate cancer cells, providing a unique strategy for prostate cancer gene therapy.

Antigens, Neoplasm↗

PubMed1998

Kinetic analysis of prostatic volume and prostate specific antigen (PSA) in patients with advanced prostatic cancer treated by castration.

The clinical usefulness of the kinetic analysis of prostate specific antigen (PSA) in patients with advanced prostatic cancer treated by castration has not yet been evaluated. The reduction of both prostatic volume and PSA was monitored in 37 patients with Stage C and Stage D prostatic cancer. The change of prostatic volume was measured frequently by transrectal ultrasonography (TRS) after castration, as was the change of PSA. A kinetic analysis of both prostatic volume and PSA was made by comparing the reduction time tau(PSA) (speed of the reduction of PSA) and tau prostatic volume (PV). There was a statistically significant correlation between tau(PSA) and tau(PV) in patients with a tau(PV) of less than 30 days. However, no correlation was observed in patients with a tau(PV) of more than 30 days, because the tau(PSA) in this group fell into a relatively low range similar to the group with a tau(PV) of less than 30 days. It was assumed that the change of PSA after castration reflected mainly the response of the hormone dependent portion of the total cancer volume. However, all data of tau(PV) with a tau(PSA) less than 10 days were within 30 days. In conclusion, tau(PSA) might be promising as a prognostic factor after castration in patient with advanced prostatic cancer, although tau(PSA) was not a direct substitute for tau(PV).

Adenocarcinoma↗

PubMedDate not supplied

Serum sialic acid and prostate-specific antigen in differential diagnosis of benign prostate hyperplasia and prostate cancer.

In order to improve the diagnostic accuracy of the serum total and free prostate-specific antigen (PSA) in differential diagnosis between benign prostate hyperplasia (BPH) and prostate cancer, the serum total sialic acid (TSA) was measured and logistic regression (LR) models were built. Significantly higher serum PSA (p<0.001) concentrations were observed in patients with prostate cancer compared to control subjects, but no statistically significant differences were found in serum TSA concentrations between these groups. Serum PSA reliably discriminated patients with prostate cancer from control subjects, the area under the ROC curve (AUC) being 0.991 (0.010). When serum PSA was in the gray zone, from 4 to 10 microg/l, the diagnostic accuracy of PSA in discriminating patients with prostate cancer from BPH patients was very poor, AUC being 0.563 (0.132). However, using the same set of patients the LR model combining serum PSA, free to total PSA ratio and TSA values, as well as digital rectal examination results, had good diagnostic accuracy in discriminating the prostate cancer patients from patients with BPH, the area under the ROC curve being 0.895 (0.054). The present data suggest that the logistic regression model combining laboratory measurements and results of the clinical examination may be a useful adjunct in the differential diagnosis of benign and malignant prostate disease.

Biomarkers, Tumor↗

PubMed1997

Induction of tissue-specific autoimmune prostatitis with prostatic acid phosphatase immunization: implications for immunotherapy of prostate cancer.

Prostatic acid phosphatase (PAP) is uniquely expressed in prostatic tissue and prostate cancer. In this study, the immunogenicity of PAP was investigated in a male rat model. We show that immunization with recombinant rat or human PAP in CFA leads to a significant Ab response, but does not generate CTL or result in autoimmune prostatitis. In contrast, immunization with recombinant vaccinia expressing human PAP, but not rat PAP, generates a CTL response and tissue-specific prostatitis in the absence of detectable PAP-specific Abs. These findings suggest that a cellular immune response to PAP, rather than Abs, mediates destructive autoimmune prostatitis. Thus, xenogeneic forms of PAP are a new tool for the induction of prostate-specific immunity and may prove useful for the immunotherapy of prostate cancer.

Acid Phosphatase↗

PubMed1985

Argyrophilic prostatic carcinoma. Case report with literature review on prostatic carcinoid and "carcinoid-like" prostatic carcinoma.

An unusual prostatic neoplasm characterized by a carcinoid-like light microscopic pattern together with argyrophilia of tumor cells is described. Immunoperoxidase stain for prostatic specific antigen, however, was positive, indicating that this neoplasm was an argyrophilic prostatic carcinoma. Although the clinical significance of a carcinoid-like pattern and/or argyrophilia in prostatic carcinoma is currently unknown, pathologic recognition of these features is of paramount importance because prostatic carcinoma with these features has to be distinguished from true primary prostatic carcinoid tumor or, in areas of metastasis, from metastatic carcinoid originating from other sites such as the gastrointestinal or respiratory tracts. The value of the immunoperoxidase technique for prostatic specific antigen as well as prostatic acid phosphatase in this differentiation is stressed.

Adenocarcinoma↗