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PubMed1996

Accumulation of p53 and expression of CD44 in human prostatic cancer and benign prostatic hyperplasia: an immunohistochemical study.

OBJECTIVE: To investigate the expression of mutant p53 and wild-type CD44 in human benign and neoplastic prostate. PATIENTS AND METHODS: The accumulation of p53 and the expression of CD44 were investigated immunohistochemically in formalin-fixed and paraffin-embedded tissue specimens (obtained by transurethral resection and open prostatectomy) from 16 patients with primary prostatic cancer (median age 65 years, range 54-75) and six patients with benign prostatic hyperplasia (BPH) (median age 67 years, range 58-75). RESULTS: Positive immunoreactivity for p53 and CD44 was detected in six and eight samples of prostatic cancer tissue, respectively. Additionally, all six prostatic cancer samples showing positive immunoreactivity for p53 were also positive for CD44. There were more samples expressing p53 and CD44 in prostatic cancer with a high Gleason grade score than in samples from cancer with a lower score. In samples from six patients with BPH, positive immunoreactivity for p53 and CD44 was observed in one and two, respectively; stained cells were restricted to the secretory cell layer of the gland. CONCLUSIONS: There was an association between prostatic tumour grade and the increasing expression of p53 and CD44, although there were too few samples for statistical significance. The staining pattern of cells expressing p53 and CD44 may be different between prostatic cancer and BPH tissues.

Aged↗
PubMed1998

Influence of free-to-total prostate specific antigen variability on the early diagnosis of prostate cancer: a comparative study of three immunoassays.

OBJECTIVE: To compare three immunoassays for total prostate specific antigen (tPSA), free PSA (fPSA), free-to-total PSA ratio (f/tPSA), and the f/tPSA thresholds for optimal differentiation between benign prostatic hypertrophy (BPH) and prostate cancer in 141 consecutive patients referred for prostatic disease. PATIENTS AND METHODS: The study included 43 patients with prostate cancer and 98 with BPH, all confirmed histologically. PSA levels were assessed using the following assay kits just before histological analysis of the prostate; Hybritech (Tandem-R PSA, normal values, NV, < 4 ng/mL, and Tandem-R free PSA), Cis Bio (PSA-RIACT, NV < 2.5 ng/mL and fPSA-RIACT) and Immunocorp (PSA-IRMA, NV < 4 ng/mL and Free PSA-IRMA). The results were assessed to determine the sensitivity, specificity and threshold values of the different assays to differentiate patients with BPH and cancer. RESULTS: The mean tPSA and f/tPSA ratio were statistically different in assays with different NVs. The mean fPSA values differed significantly between the Hybritech and Cis Bio, between the Hybritech and Immunocorp but not between the Cis Bio and Immunocorp assays. With receiver operator curve analysis, there were no statistically significant differences among the three immunoassays in f/tPSA (0.72 for Hybritech, 0.73 for Cis Bio and 0.64 for Immunocorp) or between the tPSA and fPSA curves for each manufacturer. With the sensitivity fixed at 90%, different f/tPSA thresholds were defined (0.22, 0.34 and 0.25 for Hybritech, Cis Bio and Immunocorp, respectively). The specificities (i.e. the percentage of unnecessary biopsies spared) were 22%, 21% and 31%, respectively (not significantly different). CONCLUSION: Each immunoassay could be used to distinguish prostate cancer and BPH at different f/tPSA thresholds, with 21-30% of unnecessary biopsies spared. There was no difference in overall performance among the different assays. Further studies are needed to better define the exact use of the f/tPSA ratio in the routine diagnosis of prostate cancer.

Aged↗
PubMed2000

Prostatic manipulation has a minimal effect on complexed prostate-specific antigen levels.

OBJECTIVE: To assess the effect of prostatic manipulation on complexed prostate-specific antigen (cPSA), as various forms of prostatic manipulation are known to increase the serum free and total PSA level. PATIENTS AND METHODS: A series of 92 men (58 after prostatic biopsy, 16 after digital rectal examination and 18 after flexible cystoscopy) were assessed. Blood samples were taken from each patient before and 30 min after manipulation. Total and cPSA levels were measured using appropriate assays, respectively. RESULTS: There was no significant increase in cPSA levels after flexible cystoscopy and digital rectal examination, but prostate biopsy caused a statistically significant although minimal rise in cPSA level. There was no statistically significant increase in cPSA level after prostate biopsy in patients with prostate cancer (P = 0. 35) although there was a statistically significant but minimal rise in cPSA level in patients with benign histology (P < 0.01, mean increase 2.13 ng/mL) compared with that of total PSA, which increased markedly (P < 0.01, mean increase 19.79 ng/mL). CONCLUSION: Prostatic manipulation has minimal effects on cPSA levels.

Aged↗
PubMed2002

Should the diagnosis of benign prostatic hyperplasia be made on prostate needle biopsy?

Pathologists frequently sign out benign prostate needle biopsies as "benign prostatic hyperplasia (BPH)". There are no data indicating that a diagnosis of BPH on biopsy correlates with either gland weight or with the International Prostate Symptom Score (IPSS) used to measure urinary obstructive symptoms. We examined biopsies for average percentage of glands and average percentage of glands with papillary infolding per case, maximum percentage of glands and maximum percentage of glands with papillary infolding per core per case, and presence of any stromal nodules per case. BPH was measured in 2 ways: (1) IPSS grouped into 3 categories (mild, moderate, severe) and (2) prostate weight at radical prostatectomy in men with limited cancer. IPSS was classified as follows: mild (n = 12), moderate (n = 13), and severe (n = 10). There was no correlation with IPSS and any of the histologic features measured. For the 41 radical prostatectomy specimens, the average weight was 65.3 g (median, 56.0 g, range, 22 to 117 g). There was no correlation between gland weight and the average or maximum percentage of glands, or average or maximum percentage of glands with papillary infolding. Stromal nodules on biopsy correlated with gland weight. In the 30 cases without stromal nodules on biopsy, the mean gland weight was 51.4 g. In the 11 cases with stromal nodules on biopsy, the mean gland weight was 77.4 g (P = 0.0125). However, stromal nodules were not specific for a large prostate (i.e., a 15 g prostate had stromal nodules on biopsy). With the exception of stromal nodules found on biopsy, histologic findings on biopsy are not specific for either clinical or pathologic BPH. Thus benign prostate biopsies should be signed out merely as "benign prostate tissue."

Adult↗
PubMed2005

Differentiation of prostate cancer from normal prostate tissue in an animal model: conventional MRI and dynamic contrast-enhanced MRI.

PURPOSE: To differentiate orthotopically implanted prostate cancer from normal prostate tissue using magnetic resonance imaging (MRI) and Gd-DTPA-BMA-enhanced dynamic MRI in the rat model. MATERIAL AND METHODS: Tumors were induced in 15 rats by orthotopic implantation of G subline Dunning rat prostatic tumor cells. MRI was performed 56 to 60 days after tumor cell implantation using T1-weighted spin-echo, T2-weighted turbo SE sequences, and a 2D FLASH sequence for the contrast medium based dynamic study. The interstitial leakage volume, normalized permeability and the permeability surface area product of tumor and healthy prostate were determined quantitatively using a pharmacokinetic model. The results were confirmed by histologic examination. RESULTS: Axial T2-weighted TSE images depicted low-intensity areas suspicious for tumor in all 15 animals. The mean tumor volume was 46.5 mm(3). In the dynamic study, the suspicious areas in all animals displayed faster and more pronounced signal enhancement than surrounding prostate tissue. The interstitial volume and the permeability surface area product of the tumors increased significantly by 420 % (p < 0.001) and 424 % (p < 0.001), respectively, compared to normal prostate tissue, while no significant difference was seen for normalized permeability alone. CONCLUSION: The results of the present study demonstrate that quantitative analysis of contrast-enhanced dynamic MRI data enables differentiation of small, slowly growing orthotopic prostate cancer from normal prostate tissue in the rat model.

Animals↗
PubMed2002

Vitamin E succinate inhibits the function of androgen receptor and the expression of prostate-specific antigen in prostate cancer cells.

Although epidemiological evidence indicates that a daily supplement of vitamin E may reduce the risk of prostate cancer, the detailed mechanism underlying this effect remains unclear. Here we demonstrate that alpha-tocopheryl succinate (VES) can suppress the expression of prostate-specific antigen (PSA), a marker for the progression of prostate cancer. VES can also suppress androgen receptor (AR) expression by means of transcriptional and posttranscriptional modulation, but not ligand binding, nuclear translocation, or AR dimerization. This VES-mediated inhibition of AR is selective because VES does not repress the expression of other nuclear receptors. Cell growth studies further show that VES inhibits the growth of prostate cancer LNCaP cells. In contrast, hydroxyflutamide (HF), an antiandrogen currently used to treat prostate cancer patients, only slightly inhibits LNCaP cell growth. Interestingly, simultaneous addition of HF and VES results in a more significant inhibition of LNCaP cell growth. Moreover, selenomethionine (SM), a prostate cancer treatment adjuvant, shows an inhibitory effect on LNCaP cell growth, yet has no effect on the AR/PSA pathway. Together, our data indicate that VES may suppress androgen/AR-mediated cell growth and PSA expression by inhibiting AR expression at both the transcription and translation levels. This previously undescribed mechanism may explain how VES inhibits the growth of prostate cancer cells and help us to establish new therapeutic concepts for the prevention and treatment of prostate cancer.

Androgen Receptor Antagonists↗
PubMed2002

POTE, a highly homologous gene family located on numerous chromosomes and expressed in prostate, ovary, testis, placenta, and prostate cancer.

We have identified a gene located on chromosomes 21 that is expressed in normal and neoplastic prostate, and in normal testis, ovary, and placenta. We name this gene POTE (expressed in prostate, ovary, testis, and placenta). The POTE gene has 11 exons and 10 introns and spans approximately equal 32 kb of chromosome 21q11.2 region. The 1.83-kb mRNA of POTE encodes a protein of 66 kDa. Ten paralogs of the gene have been found dispersed among eight different chromosomes (2, 8, 13, 14, 15, 18, 21, and 22) with preservation of ORFs and splice junctions. The synonymous:nonsynonymous ratio indicates that the genes were duplicated rather recently but are diverging at a rate faster than the average for other paralogous genes. In prostate and in testis, at least five different paralogs are expressed. In situ hybridization shows that POTE is expressed in basal and terminal cells of normal prostate epithelium. It is also expressed in some prostate cancers and in the LnCAP prostate cancer cell line. The POTE protein contains seven ankyrin repeats between amino acids 140 and 380. Expression of POTE in prostate cancer and its undetectable expression in normal essential tissues make POTE a candidate for the immunotherapy of prostate cancer. The existence of a large number of closely related but rapidly diverging members, their location on multiple chromosomes and their limited expression pattern suggest an important role for the POTE gene family in reproductive processes.

Amino Acid Sequence↗
PubMed1997

Estradiol activates the prostate androgen receptor and prostate-specific antigen secretion through the intermediacy of sex hormone-binding globulin.

These experiments were designed to examine the relationship between the effects of steroid hormones mediated by classic intracellular steroid hormone receptors and those mediated by a signaling system subserved at the plasma membrane by a receptor for sex hormone-binding globulin. It is known that unliganded sex hormone-binding globulin (SHBG) binds to a receptor (RSHBG) on prostate membranes. The RSHBG.SHBG complex is rapidly activated by estradiol to stimulate adenylate cyclase, with a resultant increase in intracellular cAMP. In this paper we examine the effect of this system on a prostate gene product known to be activated by androgens, prostate-specific antigen. In serum-free organ culture of human prostates, dihydrotestosterone caused an increase in prostate specific antigen secretion. This event was blocked by the anti-androgens cyproterone acetate and hydroxyflutamide. In the absence of androgens, estradiol added to prostate tissue, whose RSHBG was occupied by SHBG, reproduced the results seen with dihydrotestosterone. Neither estradiol alone nor SHBG alone duplicated these effects. The estradiol.SHBG-induced increase in prostate-specific antigen was not blocked by anti-estrogens, but was blocked both by anti-androgens and a steroid (2-methoxyestradiol) that prevents the binding of estradiol to SHBG. Furthermore, an inhibitor of protein kinase A prevented the estradiol.SHBG-induced increase in prostate-specific antigen but not that which followed dihydrotestosterone. These data indicate that there is a signaling system that amalgamates steroid-initiated intracellular events with steroid-dependent occurrences generated at the cell membrane and that the latter signaling system proceeds by a pathway that involves protein kinase A.

Culture Techniques↗
PubMed1998

Expression of human prostatic acid phosphatase correlates with androgen-stimulated cell proliferation in prostate cancer cell lines.

Androgen plays a critical role in regulating the growth and differentiation of normal prostate epithelia, as well as the initial growth of prostate cancer cells. Nevertheless, prostate carcinomas eventually become androgen-unresponsive, and the cancer is refractory to hormonal therapy. To gain insight into the mechanism involved in this hormone-refractory phenomenon, we have examined the potential role of the androgen receptor (AR) in that process. We have investigated the expression of AR and two prostate-specific androgen-responsive antigens, prostatic acid phosphatase (PAcP) and prostate-specific antigen (PSA), for the functional activity of AR in LNCaP and PC-3 human prostate carcinoma cells. Our results are as follows. (i) Clone 33 LNCaP cells express AR, PAcP, and PSA, and cell growth is stimulated by 5alpha-dihydrotestosterone (DHT). Stimulation of cell growth correlates with decreased cellular PAcP activity. (ii) In clone 81 LNCaP cells, the expression of PAcP decreases with a concurrent decrease in the degree of androgen stimulation of cell growth, whereas the expression of PSA mRNA level is up-regulated by DHT, as in clone 33 cells. Conversely, in PAcP cDNA-transfected clone 81 cells, an additional expression of cellular PAcP correlates with an increased stimulation by androgen, higher than the corresponding control cells. (iii) PC-3 cells express a low level of functional AR with no detectable PAcP or PSA, and the growth of PC-3 cells is not affected by DHT treatment. Nevertheless, in two PAcP cDNA-transfected PC-3 sublines, the expression of exogenous cellular PAcP correlates with androgen stimulation. This androgen stimulation of cell growth concurs with an increased tyrosine phosphorylation of a phosphoprotein of 185 kDa. In summary, the data indicate that the expression of AR alone is not sufficient for androgen stimulation of cell growth. Furthermore, in AR-expressing prostate cancer cells, the expression of cellular PAcP correlates with androgen stimulation of cell proliferation.

Acid Phosphatase↗
PubMed1985

Clinical utility of serum prostatic acid phosphatase measurements for detection (screening), diagnosis, and therapeutic monitoring of prostatic carcinoma; assessment of monoclonal and polyclonal enzymes and radioimmunoassays.

Serum prostatic acid phosphatase (PAP), measured by three different technics, was used to screen 560 men over 50 years of age for prostatic cancer. All three PAP procedures failed to detect the one subject found to have prostatic cancer on physical examination and confirmed by biopsy, and all assays had a significant number of "falsely" elevated PAP levels. Four PAP assays were assessed in 80 men undergoing prostatic biopsy/removal in whom histologic examination of prostatic tissue was made. Clinical sensitivity and specificity for detecting those patients with and without prostatic cancer ranged from 20-57% and 54-95%, respectively, with the monoclonal enzyme immunoassay being the most sensitive but the least specific, and the traditional enzyme assay being the most specific but insensitive. In men with diagnosed prostatic cancer undergoing radiation or chemotherapy, the assays were useful in distinguishing between those with active and inactive disease. The authors conclude that serum PAP assays, irrespective of the type of procedure used, has no place in screening for prostatic cancer, a minimal role in establishing a definitive diagnosis, but a useful role in monitoring therapy.

Acid Phosphatase↗
PubMed2002

Catechol estrogen metabolites and conjugates in different regions of the prostate of Noble rats treated with 4-hydroxyestradiol: implications for estrogen-induced initiation of prostate cancer.

Prostate carcinomas arise in 100% of Noble rats treated with estradiol and testosterone. We hypothesize that estrogens initiate prostate cancer mainly by formation of 4-catechol estrogens (CE), followed by their oxidation to catechol estrogen-3,4-quinones (CE-3,4-Q), which can react with DNA. To avoid cancer initiation, CE can be detoxified by catechol-O-methyltransferase (COMT), and CE-3,4-Q by conjugation with glutathione (GSH) or by reduction to CE, catalyzed by quinone reductase and/or cytochrome P450 reductase. To investigate the prostatic metabolism of estrogens, Noble rats were treated with the CE 4-hydroxyestradiol (4-OHE2) or estradiol-3,4-quinone (E2-3,4-Q), and CE metabolites and conjugates were analyzed in the four regions of the prostate, which differ in susceptibility to carcinoma formation. Following treatment of rats with 4-OHE2 (6 micromol/100 g body weight in 200 microl of trioctanoin/dimethylsulfoxide (4:1) by intraperitoneal injection) for 90 min, the non-susceptible ventral (VP) and anterior (AP) prostate had higher levels of 4-methoxyCE and GSH conjugates than the susceptible dorsolateral prostate (DLP) and periurethral prostate (PUP). After treatment with the same molar amount of E2-3,4-Q, the VP and AP contained more GSH conjugates, 4-CE and 4-methoxyCE than the susceptible DLP and PUP. These results suggest that prostate areas susceptible to carcinoma induction have less protection by COMT, GSH, and quinone reductase and/or cytochrome P450 reductase, favoring reaction of CE-3,4-Q with DNA, presumably to initiate cancer.

Animals↗
PubMed1994

Expression of p160erbB-3 and p185erbB-2 in prostatic intraepithelial neoplasia and prostatic adenocarcinoma.

BACKGROUND: Although prostatic adenocarcinoma is the most frequent malignancy among American men, little is known concerning the roles of growth factors, growth factor receptors, or proto-oncogene products in the development and progression of this malignancy. PURPOSE: We examined and compared the expression and cellular distribution of the erbB-3 protein (p160erbB-3) and the erbB-2 protein (p185erbB-2) in various stages of development and progression of prostatic adenocarcinoma. METHODS: Immunoperoxidase staining was used to determine the expression of p160erbB-3 and p185erbB-2 in benign prostatic epithelium, prostatic intraepithelial neoplasia, localized adenocarcinomas (pathologic stages B and C) as well as matching primary and lymph node lesions from patients with stage D adenocarcinoma. In order to test antibody specificity, we used Western blot analysis to examine the expression of p160erbB-3 and p185erbB-2 in selected prostatic adenocarcinomas. RESULTS: Within benign glands, immunostaining for p160erbB-3 or p185erbB-2 was strongest in the basal cells and was typically absent or weak in the luminal (secretory) cells. Expression of both proteins within luminal cells was localized to cell membranes. We examined the expression of p160erbB-3 and p185erbB-2 in the prostatic intraepithelial neoplastic lesions of 22 radical prostatectomy specimens. Like benign glands, the basal cells of these neoplastic lesions typically demonstrated strong to moderate immunostaining when stained with either antibody. In contrast to benign glands, moderate to strong immunostaining for p160erbB-3 and p185erbB-2 was frequently observed within the cytoplasm and cell membranes of the prostatic intraepithelial neoplastic luminal cells. p160erbB-3 and p185erbB-2 were detected within the malignant cells in 28 and 29 of 29 localized adenocarcinomas, respectively. Immunostaining with either antibody was typically moderate to strong in the malignant cells. Both proteins were expressed on the cellular membranes as well as in the cytoplasm of malignant cells. Immunostaining for p160erbB-3 was detected in the matching primary and metastatic lesions (lymph nodes) in 10 of 11 patients with stage D adenocarcinoma. Immunostaining for p185erbB-2 was detected in matching primary and metastatic lesions (lymph nodes) obtained from 16 patients with stage D adenocarcinoma. Western blot analysis confirmed the specificity of the antibodies. CONCLUSIONS: These results suggest that increased expression and changes in the subcellular distribution of both p160erbB-3 and p185erbB-2 represent early events in the development and progression of prostatic adenocarcinomas. The high expression and distribution of both p160erbB-3 and p185erbB-2 are retained both in advanced-stage primary and metastatic tumors.

Adenocarcinoma↗
PubMed1999

Cancer surveillance series: interpreting trends in prostate cancer--part II: Cause of death misclassification and the recent rise and fall in prostate cancer mortality.

BACKGROUND: The rise and fall of prostate cancer mortality correspond closely to the rise and fall of newly diagnosed cases. To understand this phenomenon, we explored the role that screening, treatment, iatrogenic (i.e., treatment-induced) deaths, and attribution bias (incorrect labeling of death from other causes as death from prostate cancer) have played in recent mortality trends. METHODS: Join point regression is utilized to assess the recent rise and fall in mortality and the relationship of total U.S. trends to those areas served by the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) Cancer Registry Program. Incidence-based mortality (IBM) is estimated with the use of prostate cancer data from the SEER Program to partition (from overall prostate cancer mortality trends) the contribution of cases diagnosed since the widespread use of prostate-specific antigen (PSA) testing starting in 1987. IBM is also used to examine the contribution of stage at diagnosis to the recent prostate cancer mortality trends. RESULTS: IBM for cases diagnosed since 1987 rose above the pre-1987 secular (i.e., background) trend, peaked in the early 1990s, and almost returned to the secular trend by 1994. This rise and fall of IBM track with the pool of prevalent cases diagnosed within the prior 2 years. IBM for cases diagnosed with metastatic disease fell starting in 1991, while IBM for those diagnosed with localized/regional disease was relatively flat. CONCLUSIONS: The rise and fall in prostate cancer mortality observed since the introduction of PSA testing in the general population are consistent with a hypothesis that a fixed percent of the rising and falling pool of recently diagnosed patients who die of other causes may be mislabeled as dying of prostate cancer. The decline in IBM for distant stage disease and flat IBM trends for localized/regional disease provide some evidence of improved prognosis for screen-detected cases, although alternative interpretations are possible.

Age Distribution↗
PubMed2003

Multiplex biomarker approach for determining risk of prostate-specific antigen-defined recurrence of prostate cancer.

BACKGROUND: Molecular signatures in cancer tissue may be useful for diagnosis and are associated with survival. We used results from high-density tissue microarrays (TMAs) to define combinations of candidate biomarkers associated with the rate of prostate cancer progression after radical prostatectomy that could identify patients at high risk for recurrence. METHODS: Fourteen candidate biomarkers for prostate cancer for which antibodies are available included hepsin, pim-1 kinase, E-cadherin (ECAD; cell adhesion molecule), alpha-methylacyl-coenzyme A racemase, and EZH2 (enhancer of zeste homolog 2, a transcriptional repressor). TMAs containing more than 2000 tumor samples from 259 patients who underwent radical prostatectomy for localized prostate cancer were studied with these antibodies. Immunohistochemistry results were evaluated in conjunction with clinical parameters associated with prostate cancer progression, including tumor stage, Gleason score, and prostate-specific antigen (PSA) level. Recurrence was defined as a postsurgery PSA level of more than 0.2 ng/mL. All statistical tests were two-sided. RESULTS: Moderate or strong expression of EZH2 coupled with at most moderate expression of ECAD (i.e., a positive EZH2:ECAD status) was the biomarker combination that was most strongly associated with the recurrence of prostate cancer. EZH2:ECAD status was statistically significantly associated with prostate cancer recurrence in a training set of 103 patients (relative risk [RR] = 2.52, 95% confidence interval [CI] = 1.09 to 5.81; P =.021), in a validation set of 80 patients (RR = 3.72, 95% CI = 1.27 to 10.91; P =.009), and in the combined set of 183 patients (RR = 2.96, 95% CI = 1.56 to 5.61; P<.001). EZH2:ECAD status was statistically significantly associated with disease recurrence even after adjusting for clinical parameters, such as tumor stage, Gleason score, and PSA level (hazard ratio = 3.19, 95% CI = 1.50 to 6.77; P =.003). CONCLUSION: EZH2:ECAD status was statistically significantly associated with prostate cancer recurrence after radical prostatectomy and may be useful in defining a cohort of high-risk patients.

Adult↗
PubMed1991

Effect of combination endocrine therapy (LHRH agonist and flutamide) on normal prostate and prostatic adenocarcinoma. A histopathologic and immunohistochemical study.

The histopathology of 23 radical prostatectomies from patients with prostatic adenocarcinoma pretreated for 3-6 months with combination therapy including a luteinizing hormone-releasing hormone agonist and the antiandrogen drug flutamide was reviewed and compared with the pretreatment biopsies or transurethral resection material. After combination therapy, benign prostatic glands showed marked atrophy with prominent basal-cell layers, basal-cell hyperplasia, and epithelial-cell vacuolization. Immature squamous-cell metaplasia was present in seven cases. Residual carcinoma, on the other hand, was found in 19 of the 23 cases, and in 8 of these, tumor cells were either vacuolated or had scanty cytoplasm. Residual tumor was present as only one focus in 13 cases, and in 3 of these it was composed of single cells with a "hemangiopericytoma-like" pattern. An immunohistochemical study for prostatic acid phosphatase and prostatic-specific antigen could be carried out on paraffin blocks from 19 biopsies and 18 prostatectomies. After combination therapy, a reduction in staining (intensity and number of positive cells) was observed for the two markers in both normal prostate and carcinoma but with more pronounced effects on the latter. The present data show that temporary combination therapy before radical prostatectomy causes marked and very characteristic changes in normal prostatic tissue as well as in the prostatic tumor. These histologic patterns enter the differential diagnosis of a variety of atrophic, metaplastic, and proliferative lesions of the prostate gland. The pathologist must be aware of these histologic changes when looking at biopsy or resection material of treated patients.

Adenocarcinoma↗
PubMed2001

Ratio of free-to-total prostate specific antigen correlates with tumor volume in patients with increased prostate specific antigen.

PURPOSE: We evaluated the relationship between the ratio of free-to-total prostate specific antigen (PSA) and prostate pathology, including grade, stage and tumor volume, among patients with prostate cancer who underwent radical prostatectomy. MATERIALS AND METHODS: We prospectively analyzed 54 consecutive patients with prostate cancer who underwent radical prostatectomy and in whom frozen serum was available for assessment of free-to-total PSA ratio. Pathological review was done with whole mount sections, and total tumor volume was determined by planimetry. Comparison between free-to-total PSA ratio and pathological parameters was performed using the Pearson correlation coefficient. RESULTS: Among the 54 patients mean total and free-to-total PSA ratio were 5.81 and 14.2 ng./ml., respectively, and free-to-total PSA ratio directly correlated with prostate volume (p = 0.037), and inversely correlated with Gleason score (p = 0.012) and extracapsular disease (p = 0.0074). Furthermore, there was a significant relationship between free-to-total PSA ratio and pathological stage pT2a/b in 39 cases versus pT3a/b in 15 (p = 0.005). Overall, there was no correlation between free-to-total PSA ratio and tumor volume. However, among 37 patients with an increased PSA, defined as greater than 4.0 ng./ml., a significant inverse relationship between free-to-total PSA ratio and tumor volume was identified (p = 0.01). Among this subset there was only a weak correlation with prostate volume (p = 0.049). CONCLUSIONS: Our findings suggest that free-to-total PSA ratio may be predictive of tumor biology among those patients with a total PSA of greater than 4 ng./ml. as evidenced by good correlation with tumor grade and volume. This finding appears to be independent of prostate volume. These preliminary results suggest the need for additional studies among patients with an increased PSA designed to evaluate the potential role of free-to-total PSA ratio in combination with traditional clinical variables in the prediction of prostate cancer pathology.

Aged↗
PubMed2002

Prostate-specific antigen screening coverage and prostate cancer incidence rates in the Belgian province of Limburg in 1996-1998.

According to the 1996-1998 cancer incidence report of the cancer registry of the Belgian province of Limburg (LIKAR), prostate cancer is the most common cancer in men with a crude invasive cancer incidence rate of 123.7 per 100000 person-years (125.4 and 81.8 after standardization for the European and the world standard population). In a study on geographical differences between the occurrence of cancers in municipalities, prostate cancer standardized incidence rates (SIRs) were significantly higher in a number of municipalities, with mean relative risks of 1.2 and 1.3 after full Bayesian smoothing. We hypothesized that prostate cancer incidence rates are largely influenced by the prostate-specific antigen (PSA) screening policy of local physicians and that differences between municipalities are more informative about local screening habits then about real differences in cancer occurrence. The aim of this study was to test this hypothesis by relating local prostate cancer SIRs to the PSA screening coverage of the population of men in each municipality. The SIRs of prostate cancer in 1996-1998 for each municipality were provided by LIKAR. They related to all histologically or cytologically proven new invasive prostate cancers during these years. For each municipality, PSA coverage data were provided by the largest sick fund of the region. Coverage was defined as the proportion of men above the age of 40 that was tested at least once within the registration period. The SIR of each municipality (dependent variable) was related to the age-standardized corresponding coverage (independent variable) by linear regression and was adjusted for the number of inhabitants per municipality: log (standardized incidence rate) = 164 + 602 * (standardized PSA coverage), = 0.12. The model explained 6% of the variance in incidence. In conclusion, in this study no statistically significant relationship was identified between PSA coverage and prostate cancer incidence rate per municipality. This could result from no such relationship existing or from low statistical power.

Adult↗
PubMed2003

High prevalence of human cytomegalovirus in prostatic intraepithelial neoplasia and prostatic carcinoma.

PURPOSE: Recent epidemiological data indicate that a history of increased exposure to sexually transmitted diseases is associated with an increased risk of prostate cancer. Human cytomegalovirus (HCMV) is a member of the herpesvirus family, is sexually transmitted in adults and can persistently infect prostatic epithelium in non-immunocompromised hosts. Based on increased awareness of the oncogenic potential of this virus, we decided to reexplore the issue of whether HCMV might be involved in prostate cancer pathogenesis. MATERIALS AND METHODS: Paraffin embedded biopsy specimens from 22 randomly selected patients with prostatic intraepithelial neoplasia (PIN) lesions and prostatic carcinoma were analyzed by immunohistochemistry, in situ hybridization, polymerase chain reaction and DNA sequencing to detect HCMV nucleic acids and determine whether HCMV gene products were specifically associated with neoplastic cells. RESULTS: We detected HCMV proteins and/or nucleic acids in all 22 of the 22 preneoplastic and neoplastic prostate lesions evaluated. HCMV proteins were specifically and often highly expressed in basal cell hyperplasia and PIN lesions, and to a lesser degree in carcinoma cells. RESULTS: To our knowledge these data demonstrate for the first time the specific localization of HCMV nucleic acids and proteins in a high percent of PIN and prostate carcinoma lesions, and raise the possibility that HCMV might contribute to the natural history of prostatic cancer.

Antibodies, Monoclonal↗