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PubMed1989

[A study of IgA.IgG titers for C. trachomatis in serum and prostatic secretion of chronic prostatitis].

In order to study the correlation between chronic prostatitis and C. trachomatis, IgA and IgG titers for C. trachomatis in serum and prostatic secretion were measured using the indirect immunoperoxidase assay (Ipazyme Chlamydia). 1) Positive rate of IgA and IgG titers in serum and prostatic secretion was higher in cases of chronic prostatitis than that in cases of suspected chronic prostatitis or the normal male group. 2) In cases of chronic prostatitis, IgA titers showed a tendency to be high in prostatic secretion, and IgG titers showed the same tendency in serum. This result was considered C. trachomatis infection was appeared local immunization in prostate. 3) After treatments with DOXY for cases of positive IgA titers in prostatic secretion, IgA titers of those cases were decreased and inflammations of prostate were cured. 4) The positive rate of IgA and IgG titers in serum was higher in wives with IgA positive cases than in those with the IgA negative. Those results suggested that chronic prostatitis was correlated by C. trachomatis.

Adult↗
PubMed2002

Significance of vitamin D receptor gene polymorphism for risk and disease severity of prostate cancer and benign prostatic hyperplasia in Japanese.

OBJECTIVE: Recent studies have demonstrated an association between vitamin D receptor (VDR) genotype and prostate cancer. Currently, there is a scarcity of data regarding the association of VDR genotype with benign prostatic hyperplasia (BPH). The purpose of this study was to investigate the TaqI VDR polymorphism in Japanese prostate cancer patients, Japanese BPH patients and Japanese controls in order to determine if an association exists between VDR genotype and the risk of developing prostate cancer and BPH as well as disease severity. METHODS: 110 prostate cancer patients, 83 BPH patients and 90 male age-matched controls were genotyped for a previously described TaqI restriction fragment length polymorphism at codon 352 in exon 9 of the VDR gene. Products were digested into T allele or t allele according to the absence or presence of a TaqI restriction site with individuals being classified as TT, Tt or tt. RESULTS: The frequency of the genotype tt was higher in the control group (6.7%) compared to patients with prostate cancer (1.8%) and BPH (3.6%) but this was not statistically significant. However, the frequency of the genotype TT was significantly higher among prostate cancer patients with locally advanced or metastatic disease (T3/ T4/N1/M1) compared to controls (p = 0.001). In addition, the genotype TT was significantly higher among prostate cancer patients with a high Gleason grade of tumor (grade 5) compared to controls (p = 0.0001). In addition, the genotype TT was statistically higher in BPH patients with high prostate volume (volume >50 cm(3)) compared to controls (p = 0.001). CONCLUSION: These data demonstrate that VDR genotype plays an important role in determining the risk of more advanced and aggressive prostate cancer as well as prostatic enlargement in Japanese men.

Aged↗
PubMed1997

Effects of age and sex hormones on transition and peripheral zone volumes of prostate and benign prostatic hyperplasia in twins.

Benign prostatic hyperplasia has been shown to increase with age and be influenced by sex hormones. The relationship between aging and hormonal influences on growth of zones of the prostate is unresolved. We studied the relationship of age and sex hormones on volume of prostate zones in 214 male twins between 25 and 75 yr old. Volumes of the total prostate (TV), transition zone (TZ), and peripheral zones (PZ) were measured using transrectal ultrasound, and sex steroid concentrations were measured using RIA. Using transformed data corrected for age, TV (r = 0.54, P < 0.00001), TZ (r = 0.58, P < 0.00001), and PZ (r = 0.39, P < 0.00001) volumes increased with age. However, the PZ volume rose more rapidly than the TZ before age 50, and TZ showed a steeper increase after age 50 yr than the PZ volume. The TZ, PZ, and ratio TZ/PZ correlated significantly (r = 0.87, 0.90, and 0.52, respectively; P < 0.00001). After a TV exceeded 30 g, the rise of the PZ became attenuated, and the slope of the TZ became steeper. Age-adjusted sex hormone concentration was not evaluated in men with larger prostate volumes. Men with American Urological Association symptom scores above 10 had significantly (P < 0.001) larger total prostate volume (TV) and TZ volume, but not PZ volumes, than men with scores below 10. Prostate volumes correlated inversely with age-adjusted serum testosterone (T), dihydrotestosterone, sex hormone binding globulin, and sex hormone binding globulin-bound T concentrations. These results demonstrate that before age 50 yr or before a prostate weight exceeds 30 g, prostate growth may be mainly from enlargement of the PZ and after age 50, the TZ. In addition, elevated T and dihydrotestosterone concentrations do not predispose men to prostate enlargement or symptoms of benign prostatic hyperplasia.

Adult↗
PubMed2005

Selenium/cadmium ratios in human prostates: indicators of prostate cancer risk of smokers and nonsmokers, and relevance to the cancer protective effects of selenium.

Selenium (Se) in a large-scale human supplementation trial has been shown to significantly reduce the incidence of prostate cancer in elderly men. Because Se is known to interact with cadmium (Cd), it has been suggested that its cancer protective action could be attributable in part to its interaction with Cd, a toxic and suspected carcinogenic element, which is found in many foods, in drinking water, and in the environment. Cadmium is considered a significant prostate cancer risk factor as it stimulates the growth of prostate epithelial cells and promotes their malignant transformation. Accordingly, prostate cancer risk is determined not only by Se status, but also the degree of Cd exposure. Determinations of Se and Cd in 129 prostates of deceased men aged 15-99 yr revealed Cd to accumulate in the prostate. Whereas the atomic Se/Cd ratios of the prostates of young men were invariably >1, indicating a stoichiometric excess of Se over Cd, they were found to decline with age, approaching the 1:1 ratio in elderly nonsmokers, a fact suggestive of the formation of a 1:1 Cd-Se complex. The associated physiological inactivation of Se could account for the increase of the prostate cancer risk with advancing age. The Se/Cd ratios dropped more steeply and consistently with age in smokers than in nonsmokers. In the prostates of some smokers, Se/Cd ratios even reached values <1, indicating a stoichiometric excess of Cd over Se. The excessive accumulation of Cd in the prostates of smokers along with sub-optimal Se intakes could explain why smokers develop more aggressive and lethal forms of prostate cancer than nonsmokers.

Adolescent↗
PubMed2002

The convergence of hormone regulation and cell cycle in prostate physiology and prostate tumorigenesis.

Despite the intense research focused on prostate cancer, it remains the most frequently diagnosed malignancy in men over 40-yr-of-age, and the second most frequent cause of cancer-related deaths in men in the United States (1). In 1990, the National Cancer Institute convened 50 experts and leaders from various disciplines in the prostate cancer field to discuss research directions that would help elucidate the molecular basis of this disease and reduce the incidence and mortality of prostate cancer (2). Critical issues identified at this meeting included the role of androgens and the regulation of cell cycle in prostate tumorigenesis and its progression to androgen-independence. Hormones and cell cycle clearly play important roles in normal and cancerous prostate physiology; however, little information has emerged that clearly delineates their function in the etiology of prostate cancer. Some of the mutational events that occur during prostate tumorigenesis and its progression to androgen-independence involve alterations to normal growth, developmental and apoptotic programs regulated by androgen, and the cell cycle. As such, the delineation of events by which prostate cancer cells circumvent these regulatory mechanisms will be central to our understanding of prostate tumorigenesis and to the development of new modalities to treat this disease. This article is then intended to summarize the functional convergence of androgen regulation and cell cycle in normal prostate physiology and prostate tumorigenesis.

Androgens↗
PubMed1998

Significance of measurement of prostate specific antigen (PSA) in familial prostate cancer lines.

The concentration of prostate specific antigen (PSA) in serum was measured in 20 brothers or sons in 10 families in which the father and son or brothers had prostate cancer using the E test TOSOH IIPA. The patients were between 32 and 70 years old with a mean age of 48.2 years. The PSA value was between 0.4 and 19.5 ng/ml with a mean value of 3.4 ng/ml. Five patients (25%) had PSA values exceeding the cut-off value of 4.0 ng/ml. After obtaining their consent, systematic prostate needle biopsy by transrectal ultrasonography was performed on 3 patients (15%). Prostate cancer was detected in all of them. Among them 2 patients were brothers, and since the other two brothers already had prostate cancer, all four brothers were confirmed to have prostate cancer. This is the first report of a familial prostate cancer in four brothers in Japan. In the western countries where the incidence of prostate cancer is higher than that in Japan, studies have been performed on the risk factors. Family history is one of the most important risk factors. In Japan, the incidence of prostate cancer is increasing rapidly. Moreover, patients with a prostate cancer family history are expected to increase. In such cases, prostate cancer screening should be performed aggressively from a young age.

Adult↗
PubMedDate not supplied

Prostatic marker-negative amphicrine carcinoma of the prostate.

It has been shown that prostatic adenocarcinoma differentiation correlates with prostatic-specific marker and neuroendocrine expression; that is, the more undifferentiated the tumor, the less it expresses prostatic markers and the more neuroendocrine cells are found in it. Complete absence of prostatic markers together with marked neuroendocrine expression has been associated with small cell morphology. This report describes a case of a metastatic, prostatic marker-negative, non-small cell prostatic adenocarcinoma with a prominent neuroendocrine component. The architecturally well-organized luminal-exocrine cells appeared ultrastructurally undifferentiated, however, displaying an almost empty cytoplasm. This contrasted with the prostatic marker-positive control cases of prostatic carcinoma, which contained relatively numerous cytoplasmic vacuoles. The neuroendocrine cells could be identified by light microscopy as eosinophilic cells. The number of the latter cells was markedly increased in the metastatic foci compared with the primary tumor. Light microscopically and ultrastructurally, the eosinophilic cells in this case differed from the Paneth-like cells described in prostatic carcinoma in previous reports. This case provides support for the general concept of multidirectional differentiation in human epithelial cancers and in particular for the association of poor tumor differentiation with neuroendocrine expression in prostatic carcinoma. In addition, in contrast with previous reports describing absence of basement membrane in metastatic foci of prostatic carcinoma, in the current case well-formed basal laminae were identified.

Acid Phosphatase↗
PubMed1999

Detection of subclinical cancers by prostate-specific antigen screening in asymptomatic men from high-risk prostate cancer families.

Positive family history is a significant risk factor for prostate cancer. Improved knowledge of the epidemiology and molecular basis of hereditary prostate cancer has led to a need for counseling and clinical follow-up for men with a positive family history of prostate cancer. However, very little information is available on the efficacy of early screening procedures, such as serum prostate-specific antigen (PSA) measurements, in the management of genetically predisposed, high-risk individuals. In a nationwide study, we obtained family histories from 2099 Finnish prostate cancer patients and identified 302 families with two or more affected cases. Here, 209 asymptomatic 45-75-year-old males from these families were included in a study to determine the frequency of serum PSA positivity and the prevalence of subclinical prostate cancers. Serum PSA was elevated in 21 (10.0%) of these high-risk individuals. Seven prostate cancers (3.3%) and two high-grade prostatic intraepithelial neoplasia lesions were diagnosed, with three cancers occurring in men ages < or = 59 years. Men from prostate cancer families with an average age of onset of < 60 years had a significantly higher frequency of PSA positivity (28.6%, P = 0.01) as well as cancers (14.3%, P = 0.02) than those with a later age of onset. The results suggest that prostate cancer development in genetically predisposed individuals is preceded by a subclinical period when PSA detection is possible. Serum PSA screening may be particularly useful in men with a family history of early-onset prostate cancer.

Adenocarcinoma↗
PubMed2000

Susceptibility to prostate cancer: interaction between genotypes at the androgen receptor and prostate-specific antigen loci.

The androgen receptor (AR) regulates gene transcription by binding to androgen response elements in target gene promoters. The prostate-specific antigen (PSA) gene has a polymorphic androgen response element sequence with two alleles, A and G. We hypothesize that allelic differences in AR-driven PSA expression may influence prostate cancer risk. To test this hypothesis, we assayed PSA genotype for 57 prostate cancer cases and 156 controls from our previous pilot study in which prostate cancer risk was associated with the AR "CAG-short" genotype. Odds ratios (ORs) were estimated relating prostate cancer risk to AR and PSA genotypes, singly and in combination. Subjects with the PSA GG genotype were at significantly increased risk for advanced, but not for localized, prostate cancer (OR, 2.90; 95% confidence interval, 1.24-6.78). When cross-classifying subjects by AR and PSA genotypes, subjects with either a CAG-short allele (and not PSA GG) or with the PSA GG genotype (and not CAG-short) had a modest, statistically insignificant increase in prostate cancer risk overall. However, subjects with both a short CAG allele and PSA genotype GG had a more than 5-fold increase in prostate cancer risk (OR, 5.08; 95% confidence interval, 1.59-16.25). All of the ORs were substantially greater for advanced prostate cancer. Studies with larger numbers of advanced cases will be needed to confirm these results. These results indicate that polymorphism in the PSA gene promoter influences prostate cancer risk, and that the allelic variation in promoter activity may be androgen-dependent. Furthermore, these results support a multigenic etiology for prostate cancer.

Aged↗
PubMed2002

High prevalence of screening-detected prostate cancer among Afro-Caribbeans: the Tobago Prostate Cancer Survey.

Risk for prostate cancer is high among African Americans. We hypothesized that risk for prostate cancer is also high in other populations of African descent. Our objective was to determine the screening-detected prevalence of prostate cancer in the predominantly Afro-Caribbean population on the island of Tobago. Male residents, ages 40-79 years, were invited to participate in a population-based screening for prostate cancer using serum prostate-specific antigen (PSA) and digital rectal exam (DRE). Men with elevated PSA (>or=4 ng/ml) or abnormal DRE were offered an ultrasound-guided sextant biopsy of the prostate gland. Men (2484), ages 40-79 years, underwent prostate cancer screening between September 1997 and June 2001. Mean age was 55.9, SD was 10.6 years, and median was 54 years. Mean serum PSA was 14.8 ng/ml, SD was 376 [excluding 4 values >or= 2 SD above the mean (1,112, 1,317, 1,818, and 18,330 ng/ml) mean PSA was 5.5 ng/ml and SD was 29.6], and median PSA was 1.2 ng/ml. Elevated PSA and/or abnormal DRE were observed in 31% (759 of 2484) overall, and in age groups 40-49 (87 of 843, 10%), 50-59 (201 of 729, 28%), 60-69 (262 of 584, 45%), and 70-79 (209 of 328, 64%). Of 681 men biopsied, 259 (38%, or 10% of the 2484 screened) were diagnosed with prostate cancer. Age-specific rates of screening detected prostate cancer were: 1%, ages 40-79 years; 7%, ages 50-59 years; 18%, ages 60-69 years; and 28%, ages 70-79 years. These screening results indicate a very high screening-detected prevalence of prostate cancer in this population of West African descent. These data support the hypothesis that populations of African descent share genetic and/or lifestyle factors that contribute to their elevated risk for prostate cancer.

Adult↗
PubMed2002

Fibroblast growth factor 8 isoform B overexpression in prostate epithelium: a new mouse model for prostatic intraepithelial neoplasia.

Fibroblast growth factor 8 isoform b (FGF8b), a mitogenic and transforming polypeptide, was demonstrated to be naturally up-regulated in prostatic premalignant and malignant lesions in men. We generated four independent lines of transgenic mice with targeted overexpression of FGF8b in the prostatic epithelium using an improved rat probasin promoter, ARR(2)PB. Transgene expression in the prostate tissue was readily demonstrated by reverse transcription-PCR and localized to the prostatic epithelium by in situ hybridization. The histopathology of the prostate tissues was followed in different age groups of the various lines but most extensively in one line (line 3), starting from 1 month of age up to 24 months. Prostatic hyperplasia appeared in the lateral and ventral prostates in some animals as early as 2-3 months and in other lobes between 6 and 16 months. Beginning at 5-7 months, dysplasia, akin to what may be considered low-grade prostatic intraepithelial neoplasia (LGPIN) in humans, was detected. During the first 14 months, 100% of animals exhibited multifocal epithelial hyperplasia; 35% also had areas of LGPIN. This profile changed in subsequent months (15-24 months) to a higher incidence of LGPIN (66%) along with high-grade PIN (HGPIN) lesions (51%). Similar to HGPIN, stromal proliferation and appearance of papillary hyperplasia with atypia displayed a delayed pattern. The affected stroma consisted primarily of the smooth muscle cell component. The incidence of chronic inflammation, mostly involving T cells, was higher in the prostate of the transgenic mice relative to controls; however, the presence of a direct correlation between inflammation and hyperplasia or preneoplastic lesions was not identified. These transgenic mice represent a "natural" animal model for investigating the mechanism of development and progression of prostatic diseases, such as prostatic hyperplasia and preneoplastic lesions.

Animals↗
PubMed2003

[Comparison of serum prostate specific antigen levels and bone scintigraphy in patients with prostate carcinoma].

The aim of this study was to analyze the levels of serum prostate specific antigen in patients with and without bone metastases detected by means of bone scintigraphy and to determine the highest prostate specific antigen level in patients without bone metastases. The 50 patients consecutively diagnosed of prostate cancer between 1999 and 2001 in our institution made up the study population. Prostate specific antigen plasmatic levels were determined and bone scintigraphy was performed (whole body study after 99mTc-methyl-diphosphonate administration) in all the patients. In patients with positive bone scans (n=23), the mean prostate specific antigen level was 71.4+/-35.2 ng/ml and was significantly (p<0.00005) higher than in 14 patients with negative bone scans (mean prostate specific antigen level was 10.1+/-10.5 ng/ml). Suspicious lesions were found in 13 patients and their mean prostate specific antigen level was 8.5+/-7.7 ng/ml. Regarding prostate specific antigen levels, no statistically significant differences were found between patients with suspicious lessons and normal bone scans. The highest determined prostate specific antigen level in patients without bone metastases was 18 ng/ml. The bone scintigraphy should be performed in all patients with prostate specific antigen level above 18 ng/ml, but it is of limited value in patients with prostate specific antigen level below 18 ng/ml.

Adult↗
PubMed2004

Signal transducer and activator of transcription 3 (STAT3) activation in prostate cancer: Direct STAT3 inhibition induces apoptosis in prostate cancer lines.

Signal transducers and activators of transcription (STAT) were originally discovered as components of cytokine signal transduction pathways. Persistent activation of one STAT, STAT3, is a common feature of prostate cancer. Activated STAT3 was found in pathology specimens obtained from prostatectomy in the cancerous areas but not in the normal margins. Because the activation of STAT3 is mediated by the action of an upstream Janus kinase (JAK) kinase, usually JAK1 or JAK2, the activation step for STAT3 might itself be a target for therapy in prostate cancer. However, the redundancy of upstream kinases may make this strategy unreliable for therapy. To develop molecular targets for prostate cancer treatment, JAK kinase and STAT3 inhibition of two prostate cancer lines were compared. DU145 and NRP-154 cells were treated with JAK kinase inhibitors, analyzed for onset of apoptosis, and measured by annexin V binding and propidium iodide uptake. Activation of caspases in the cells was determined by measuring cleaved caspase-3 following treatment. For determining the effect on mitochondrial membrane depolarization that accompanies apoptosis, the fluorescent dye JC-1 was used. STAT3 was specifically inhibited by transfecting either a dominant-negative (DN) STAT3 plasmid or antisense STAT3 oligonucleotides into the cells. To look for reduction in STAT3 levels within cells, fixed and permeabilized prostate cancer cells were stained with antibody to STAT3. We found that more than one JAK kinase is involved in STAT3 activation in prostate cancer lines. AG490 (JAK2 specific) induced apoptosis in DU145 but not in NRP-154 prostate cancer lines, whereas piceatannol (JAK1 specific) induced apoptosis in NRP-154 but not in DU145 cells. Next, we demonstrated efficacy of specific STAT3 inhibitors in prostate cancer lines. Both induction of apoptosis and reduction in intracellular STAT3 protein were observed following treatment with antisense STAT3 oligonucleotides, while transfection of a DN-STAT3 plasmid into both prostate cancer cell lines resulted in loss of viability and onset of apoptosis. We conclude that STAT3-specific inhibitors, rather than JAK kinase-specific inhibitors, should be more useful therapeutically in treating androgen-resistant prostate cancer and that STAT3 is an appropriate target in the treatment of prostate cancer.

Animals↗
PubMed2005

Detection of prostate cancer: the impact of the European Randomized Study of Screening for Prostate Cancer (ERSPC).

The European Randomized Study of Screening for Prostate Cancer (ERSPC) is a large, randomized controlled trial of screening versus control, conducted in eight European countries (Belgium, Finland, France, Italy, the Netherlands, Spain, Sweden, and Switzerland). This article focuses on important aspects relating to recent findings from the ERSPC about two topics: first, leadtime and overdiagnosis, and second, prostate-specific antigen (PSA) as a test for repeated screening. The ERSPC together with the prostate cancer arm of the Prostate, Lung, Colon and Ovary (PLCO) screening trial of the National Cancer Institute in the United States are set to show or exclude an effect of screening on prostate cancer mortality. Both studies are progressing according to plan. Definitive endpoint-related data can be expected between 2005 and 2010 depending on the difference in prostate cancer mortality that may be shown between the screening and control arms. The ERSPC will allow a risk-to-benefit analysis including parameters of quality of life and cost. Overdiagnosis with present prostate cancer screening regimens is high. This amount of overdiagnosis is likely to be unacceptable for most healthcare policy makers and providers. Addressing overdiagnosis will be a major research task for urologists for the years to come. Present screening needs to be more "selective" for cases that have aggressive patterns and are likely to lead to clinical diagnosis of prostate cancer and/or death. The test characteristics of prostate-specific antigen (PSA) change after one use. The positive relation between PSA levels and positive predictive value (PPV) and detection rates in first screening rounds are lost. This may be compatible with the observation that tumor volumes in second round screening are smaller, and larger tumors are harvested. Tumor volume becomes a negative predictor in round 2, indicating that a large proportion of elevated PSA values are caused by benign prostatic hyperplasia (BPH) rather than by prostate cancer. While the outcome of the ongoing randomized studies is uncertain, screening tests cannot be refused to men who are well-informed and accept to take the risk of experiencing more harm than benefit as a result of a positive screening test result.

Age Distribution↗
PubMed2006

Relationship between the prostatic tissue components and natural history of benign prostatic hyperplasia.

OBJECTIVE: Few reports have been published on the relationship between prostatic tissue components and the natural history of benign prostatic hyperplasia (BPH). The present study was undertaken to evaluate this relationship. STUDY DESIGN: Forty-nine patients with BPH who underwent suprapubic prostatectomy were studied. Six infant prostates and 10 non-BPH specimens were obtained from autopsy. Specimens were stained with antibodies to alpha-smooth muscle actin, and the mean ratio of the stroma was determined with computer image analysis. Stromal ratios were evaluated according to resected prostate weight and age. RESULTS: The stroma comprised 82.6 +/- 8.4% of the prostate area at 0-1 year of age and 43.7 +/- 5.1% at 15-28 years of age. In BPH, the stromal proportion increased to 55.9 +/- 10.2%, but decreased with increases in prostate weight and/or age. CONCLUSION: The stromal component increased in patients with BPH and decreased with increased prostate weight and/or age, comprising approximately 42-47% of the prostate area, as in the non-BPH prostate, indicating a balance in prostatic tissue components in both patients with BPH and the non-BPH prostate.

Actins↗
PubMed2006

[Indication of repeat prostate biopsy for the diagnosis of prostate cancer].

There is no standard criterion for repeat prostate biopsy in cases with a negative initial biopsy. We retrospectively analyzed our experience of repeat prostate biopsy to establish its indication for the diagnosis of prostate cancer. From April 1997 to March 2005, 35 consecutive patients underwent repeat prostate biopsy at the department of Urology, Asahikawa Medical College Hospital because of clinically suspicious prostate cancer despite a negative initial biopsy. We compared patients' age, number of cores obtained during repeat biopsy, digital rectal examination findings, total prostate volume, the time from the first to the last biopsy, total prostate specific antigen (PSA) value, free PSA/total PSA ratio, PSA density and PSA velocity between cancer-positive and cancer-negative groups. Prostate cancer was detected in 17 of 35 patients (49%). Fifteen patients with prostate cancer were diagnosed by the first repeat biopsy and other 2 patients were diagnosed by the second repeat biopsy. A statistically significant difference was only noted in age and PSA density. Persistently elevated total PSA and a higher PSA density in cases with a negative initial biopsy might be a good indication of repeat prostate biopsy for the diagnosis of prostate cancer.

Age Factors↗
PubMed1991

[Immunohistochemistry of the prostate and prostate carcinomas].

1. The immature multilayered epithelium of the prostate glands and ducts reacts positively throughout the fetal period up to puberty for the following antigens: Acid prostate phosphatase (PAP), the prostate-specific antigen (PSA), keratins demonstrated by the broadly reacting keratin antibody "AE1 + AE3", keratins from stratum corneum, the keratins 7, 8, 18 and 19, binding sites for the peanut agglutinin (PNA) and carcinoembryonic antigen (CEA). The expression of PAP and PSA varies and can in individual cases even be nonexistent. Alpha-1-antichymotrypsin (ACT) is not demonstrable until birth. It is found only focally in two thirds of the cases. The prostate stroma proves positive for vimentin as well as desmin. In the prostate glands, vimentin may occur focally. Squamous cell metaplasias in the fetal prostate show positive for all antikeratin antisera as well as PNA and CEA. The epithelium of the ejaculatory ducts and seminal vesicles proves positive for all keratins investigated. Vimentin as well as PNA-binding sites are found on a general basis. The urothelium of the prostate urethra also contains all keratins and, in addition, PNA and CEA. Endocrine cells, positive for serotonin, are sparse in the prostate glands, in the prostatic ducts and in the urothelium. 2. The onset of the androgen effect during puberty leads very probably to the morphological differentiation of the immature glandular epithelium into the two cell types, basal cell and secretory cylindric epithelium which differ with regard to their immunohistochemical behavior. The glands of benign nodular hyperplasia, including special forms, as well as epithelial alterations with nuclear atypia behave immunohistochemically exactly like normal prostate glands. The markers PAP, PSA, CEA, ACT, the keratins 8 and 18 and focally occurring vimentin are expressed exclusively in the secretory epithelium of the prostate glands and ducts, and not in the basal cells. In contrast, antisera against the following antigens stain only the basal cells and basal cell hyperplasia: Keratins from stratum corneum, a common epitope of the keratins 4, 5 and 6 (antibody KA1) and both the estrogen and progesterone receptor. Squamous cell metaplasias behave immunohistochemically like the basal cells. The keratins 7 and 19, desmoplakin, PNA as well as the patients' own blood group antigens are found in both the basal cells and the secretory epithelium. Keratin 7 and the blood group antigens are always only found focally. PNA-binding sites are secreted by the cylindric epithelium. Atrophic glands and the glands in postatrophic hyperplasia share immunohistochemical features with both the basal cells and the secretory epithelium.(ABSTRACT TRUNCATED AT 400 WORDS)

Humans↗
PubMed1991

[Prostatic venous plexus: ultrasonic guidance for prostatic inflammation?].

The Ultrasonic features of the normal prostate, benign prostatic hyperplasia and prostatic carcinoma are well known, but ultrasonic diagnosis of prostatitis is still questionable. We studied 190 cases of transrectal sonogram for prostatic disease; 89 of them had prominent prostatic plexus. When compared with clinical and pathological results, prostatic venous plexus should be considered as a normal anatomical features in only 28.5 percent of them with prostatic inflammation. When prostatic venous plexus is associated with periurethral halo zone and/or prostatic calculi, the diagnosis of prostatic inflammation can be made.

Aged↗