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At least 19 recordsLinked to original sources

Immunohistochemical study of the expression of epidermal growth factor receptor in benign prostatic hypertrophy, prostatic intraepithelial neoplasia and prostatic carcinoma.

The present study provides an analysis of immunohistochemical expression and localization of epidermal growth factor receptor (EGFR) in formalin fixed paraffin embedded specimens of prostate. Thirty-five cases each of benign prostatic hypertrophy (BPH) and prostatic carcinoma and 30 cases of prostatic intraepithelial neoplasia (PIN) were taken up for study. Streptavidin biotin peroxidase method was employed for immunohistochemical staining. EGFR positivity was observed in all the cases (100%) of BPH and PIN and in only 10 cases (28.5%) of prostatic carcinoma. In both BPH and PIN the basal cells revealed significantly higher intensity and percentage cell positivity than the luminal cells. Intensity and percentage of positively stained basal cells in BPH was higher than PIN basal cells but the difference was not statistically significant. The intensity and percentage cell positivity of BPH basal cells and PIN basal and luminal cells were significantly greater than the epithelial cells of prostatic carcinoma. Presently, the significance of variable expression of EGFR in various types of prostatic lesions is unknown.

Aged↗

Ratio of serum tartrate-inhibitable acid phosphatase to total serum protein in benign prostatic hypertrophy and prostatic carcinoma.

The activity concentration and the specific activity (the ratio of enzyme activity to total serum protein) of the tartrate-inhibitable fraction of acid phosphatase [orthophosphoric monoester phosphohydrolase (acid optimum), EC 3.1.3.2; TIAP] were related to benign prostatic hypertrophy and to prostatic carcinoma. As expected, the TIAP activity concentrations assayed in the sera of patients with benign prostatic hypertrophy were within the range of those assayed in normal human sera. In contrast, the specific activities of TIAP determined in the sera of patients with benign prostatic hypertrophy were significantly higher than those determined in the control group. In the sera of prostatic carcinoma patients, both the TIAP activity concentrations and the TIAP specific activities differed significantly (F = 730) from the normal values.

Acid Phosphatase↗

[Quantitative analyses of alpha-adrenoceptors in human prostatic capsule, adenoma and urethra--a comparison between normal prostate and hypertrophied prostate].

The adrenergic alpha-1 and -2 receptors in the three layers of the prostate (capsule, adenoma and urethra) were measured in humans with or without benign prostatic hypertrophy to examine the differences between the hypertrophied and non-hypertrophied (normal) prostate. Both alpha-1 and -2 receptors were found to exist in similar amounts in prostatic adenoma of both hypertrophied and normal prostate groups. In the prostatic capsule and urethra of both groups alpha-1 receptors were more abundant than alpha-2 receptors. Both alpha-1 and -2 receptors in all three prostatic layers were found to be increased significantly in hypertrophied group compared to normal group. Further more the increases in alpha-1 and -2 receptors of hypertrophied group were most remarkable in prostatic adenoma. These results seems to demonstrate that not only alpha-1 but also alpha-2 receptors play some important roles in benign prostatic hypertrophy.

Adenoma↗

[Expression and significance of PCNA and p27 in benign prostate hypertrophy and prostate carcinoma].

OBJECTIVE: To investigate the expression of PCNA and p27 in human benign prostate hypertrophy (BPH) and prostate carcinoma (PCa) and their effect on the genesis and progression of the tumor. METHODS: The paraffin-embedded sections of 30 cases with BPH and 37 cases with PCa were collected. The expression of p27 and PCNA protein were examined by S-P immunohistochemical method. Comparative analysis for BPH and pathological grade and clinical stage of PCa was performed. RESULTS: The expression of PCNA in BPH (3.3%) was significantly lower than that in Pca (83.8%, P < 0.01). The expression of p27 in BPH (70.0%) was significantly higher than that in Pca (27.0%, P < 0.05). The expression of p27 was not correlated with histological grade and clinical stage in Pca (P > 0.05). An inverse correlation was found between p27 and PCNA expression in BPH (P < 0.01), while no correlation was found in Pca (P > 0.05). CONCLUSION: The loss or decreased expression of p27 protein may be related to the genesis of benign prostate hypertrophy, but not to the development of prostate carcinoma; the overexpression of PCNA may play an important role in the malignant behavior and progression of prostate carcinoma.

Adenocarcinoma↗

Androgen-binding proteins in human benign prostatic hypertrophy.

Prostatic samples were surgically removed from 7 patients suffering from benign prostatic hypertrophy. High-speed supernatants (cytosol) containing 20-25 mg of protein/ml were prepared. Glycerol gradient ultracentrifugations were performed, using cytosol labeled at 0 C with 2-5 nM 3H-17beta-hydroxy-androstan-3-one (androstanolone or dihydrotestosterone) alone, or in the presence of 50-250-fold excess of androstanolone, estradiol, or androstane-3alpha, 17beta-diol (androstanediol). Two high-affinity saturable binding components were observed. One binding component was the androgen receptor. Its sedimentation coefficient was 8 S in low-salt medium. It had a high affinity for androstanolone. The binding of 3H-androstanolone was strongly completed by androstanolone itself, less by estradiol, and not by androstanediol. In one case, endogenous androstanolone found in the 8 S region of glycerol gradients was measured by radioimmunoassay, and it was calculated that more than 90% of the cytosol receptor binding sites might be occupied by this steroid while the total binding capacity of the 8 S receptor was estimated to approximate 2.6 pmol of androstanolone/g of prostate. No testosterone was found in the receptor fraction. The second binding component was attributable, at least in part, to the sex steroid-binding plasma protein (SBP), as indicated by its sedimentation coefficient (congruent to 4 S in low salt medium), its high affinity for androstanolone and androstanediol and its lower affinity for estradiol, and finally, its migration on polyacrylamide gel electrophoresis. In one instance, the concentration of the SBP-like protein in prostate cytosol was measured by equilibrium dialysis, and it was calculated that the binding capacity of the prostate SBP-like component corresponded to 4 pmol of androstanolone/g of prostate, a small (less than 5%) value with regard to SBP concentration in the plasma of the same patient. The blood contamination of the cytosol, as obtained from the measurement of hemoglobin, did not account for the amount of SBP found in the prostate sample. Since SBP-like protein is probably of plasma origin, to determine whether SBP was located in the extracellular space or inside the prostate cells, BPH slices from another patient were incubated in the presence of 3H-testosterone, the cytosol was prepared, and was fractionated by Sephadex G-150 column chromatography. The androstanolone/testosterone ratio in the receptor-containing peak was high (1.7), whereas in the incubation medium it was very low (0.08). In the peak containing the SBP-like protein, the ratio was 0.74, which may suggest that all or part had been exposed to the predominant androstanolone environment inside the prostatic cell.

Aged↗

Evaluation of serum arginase activity in benign prostatic hypertrophy and prostatic cancer.

Activities of arginase, prostatic acid phosphatase (PAP) and prostate specific antigen (PSA) were determined in sera of healthy male controls, benign prostatic hypertrophy (BPH) and prostatic cancer patients. Serum arginase activity in the cancer group (22.8+/-11.6 U/l) was significantly lower than in both the control (33.64+/-16.19 U/l) and the BPH group (58.8+/-11.6 U/l) (p<0.001, respectively), while the BPH group had significantly higher levels compared to the controls (p<0.05). However, serum arginase levels in all groups had no statistically significant correlation with PAP and PSA. Serum arginase activity correlated inversely with the Gleason grades. These results suggest that serum arginase assay may be used for the pretreatment evaluation of patients with prostatic diseases.

Acid Phosphatase↗

Free to total prostate-specific antigen (PSA) ratio is superior to total-PSA in differentiating benign prostate hypertrophy from prostate cancer.

BACKGROUND: Serum prostate-specific antigen (PSA) exists in different molecular forms, and their respective concentration has been proposed as a useful tool to improve discrimination between benign prostatic hypertrophy (BPH) and prostate cancer (PC). METHODS: The relevance of the free to total PSA ratio was prospectively studied in a selected urology clinic population of 420 patients. Total serum PSA ranged from 2.1 to 30 ng/ml; 154 had PC and 266 had BPH. RESULTS: Receiver operating characteristic (ROC) curves were constructed for the total population (total-PSA range from 2.1 to 30 ng/ml) and for the diagnostic gray zone of 2.1-10 ng/ml. For the two groups, the free to total PSA ratio had a higher specificity than total-PSA for all sensitivity levels. Cut-off values were found to, vary with prostate weight. CONCLUSIONS: Although free to total PSA ratio demonstrated better performances than total-PSA, its use in screening appears problematic, due to the low prevalence of prostate cancer.

Aged↗

Alpha-1 adrenoceptors in human prostate: characterization and alteration in benign prostatic hypertrophy.

Alpha-1 adrenoceptors in hypertrophied prostates of humans were characterized by a binding assay using [3H]prazosin as a radioligand. Specific [3H]prazosin binding in hypertrophied prostates of humans was saturable and of high affinity (Kd = 0.6 nM) with a maximal number of binding sites of 106 fmol/mg of protein, and it showed a pharmacological specificity as well as stereo-selectivity which characterized alpha-1 adrenoceptors. Adrenergic antagonists competed for the binding in order: R-(-)-YM-12617(5-[2-[[2-(o-ethoxyphenoxy)ethyl]amino]propyl]-2- methoxybenzenesulfonamide HCl) greater than (+/-)-YM-12617 = prazosin greater than phentolamine greater than S-(+)-YM-12617 greater than idazoxan. R-(-)- and (+/-)-YM-12617, alpha-1 adrenoceptor antagonists, have been shown to exhibit an extremely high affinity for prostatic [3H]prazosin binding sites (Ki = 0.6 and 1.1 nM, respectively). In addition, R-(-)-YM-12617 was approximately 100 times as potent as the S-(+)-isomer. The affinities of prazosin and YM-12617 compounds for [3H]prazosin binding sites in hypertrophied prostates of humans correlated closely with their pharmacological potencies in prostates reported previously. The blockade of [3H]prazosin binding sites in hypertrophied prostates of humans induced by (+/-)-YM-12617 was easily reversed by washing. There was a significant 35% increase in the maximal number of binding sites for [3H] prazosin binding in hypertrophied prostates from benign prostatic hypertrophy compared to normal tissues, whereas the hypertrophy had little effect on the Kd value.(ABSTRACT TRUNCATED AT 250 WORDS)

Binding, Competitive↗

Prostate specific antigen density: a means of distinguishing benign prostatic hypertrophy and prostate cancer.

Isolated prostate specific antigen (PSA) determinations in asymptomatic individuals have not demonstrated sufficient sensitivity and specificity to be useful in the routine evaluation of prostate disease. To enhance the accuracy of serum PSA we have used a quotient of serum PSA and prostate volume, which we refer to as prostate specific antigen density (PSAD). Prostate volume in this study was calculated from magnetic resonance imaging determinations of benign prostatic hypertrophy (BPH) or from the dimensions of the surgical specimen of cancer using the formula, length x width x depth x 0.5 = volume. A total of 61 patients with prostatic disease clinically confined to the prostate glands (41 with prostate cancer undergoing radical prostatectomy and 20 with BPH) was evaluated. The mean PSAD for prostate cancer was 0.581 while that for BPH was 0.044 (p less than 0.002). No patient with BPH had a PSAD of greater than 0.117 and only 1 patient had a density of 0.1 or greater. Of 34 patients with a PSAD of 0.1 or greater 33 had prostate cancer. Only 2 of the 41 prostate cancer patients and 14 of the BPH patients had a PSAD of 0.05 or less. There were 11 patients with a PSAD of greater than 0.05 and less than 0.1, including 6 with prostate cancer (1 with P0 disease) and 5 with BPH. Of the 6 prostate cancer patients 5 had a PSA of 4.0 or less and among the 5 patients with BPH 4 had a serum PSA of greater than 4.0 and 1 had a PSA of greater than 10. These results suggest that PSAD may be useful in distinguishing BPH and prostate cancer.

Antigens, Neoplasm↗

[Mass screening of prostate in Shiribeshi area in Hokkaido--incidence and clinical symptoms of benign prostatic hypertrophy and prostatic carcinoma].

A prostate mass screening was performed in 6 towns in Shiribeshi area in Hokkaido Prefecture on 384 males who were over 50 years old. The screening included digital palpation, uroflowmetry, blood sampling for tumor markers, questionnaire for voiding disturbances and transrectal sonography. Prostatic carcinoma was found in 9 (2.3%) of 384 males. An incidence of benign prostatic hypertrophy was 15.6% in 384 males. Atypical hyperplasia was found in 4 among 35 biopsied cases. Incidence of voiding disturbance such as retardation, prolongation and nocturia significantly increased with age as well as prostate size.

Aged↗

Excretion of three major prostatic secretory proteins in the urine of normal men and patients with benign prostatic hypertrophy or prostate cancer.

We have studied the mode of excretion of three prostatic secretory proteins, namely acid phosphatase (PAP), prostate-specific antigen (PSA) and beta-inhibin, in the urine of normal adult men, and we have determined the urinary levels of these proteins in men with benign prostatic hypertrophy (BPH) or adenocarcinoma. The output of the three proteins was highly variable during the day. In order to minimize these variations, 24-hour urine samples were collected thereafter. Our study showed that PAP concentrations in 50% of men with or without symptomatic BPH were similar to those of normal young men. In the remaining 50%, PAP was undetectable. In contrast, average PSA and beta-inhibin concentrations were higher in patients with BPH than in young men (p less than 0.05). The three markers were decreased or nondetectable in about half of the patients with untreated prostatic cancer. This phenomenon was even more pronounced in patients receiving hormonal treatment (castration or diethylstilbestrol). However, some of these patients still excreted normal amounts of PAP, PSA, and beta-inhibin. Urinary and serum PAP levels showed no correlation. These results indicate that urinary prostatic markers provide an easy means to study the behavior of the primary prostatic tumor. This information may be of potential value since it is not obtained with serum markers which originate mostly from metastatic cells.

Acid Phosphatase↗

[The relationship of PSA to age and prostatic volume in patients with benign prostatic hypertrophy].

Prostate specific antigen (PSA) is the most useful market for the diagnosis, staging and monitoring of prostate cancer. However, the effect of benign prostate hyperplasia on PSA levels is less well known. It has been reported that 20-45% of all adult males with BPH have PSA values over the normal range. To study this confounding factor we have analyzed the likely relationships between monoclonal PSA, age and prostate size as determined by ultrasound, in our series of 163 patients with BPH undergoing adenomectomy. Within the studied factors, the most conditioning parameter of PSA variability was prostate size. The correlation coefficient (r) was 0.61, with the determination coefficient (r2) being 0.037 (p < 0.001). Age correlation, although less important (r = 0.31), was statistically significant. Both variables were independent and resulted jointly in a correlation coefficient of 0.64. Also included is the mathematical formula used in our series to correlate PSA with age and prostate volume. Its application could mean an increased specificity of this tumoral marker.

Aged↗

Incidence of surgically treated benign prostatic hypertrophy and of prostate cancer among blacks and whites in a prepaid health care plan.

The incidence of surgically treated benign prostatic hypertrophy and of prostate cancer was examined to December 1987 in 14,897 men (2,175 blacks and 12,722 whites) who received multiphasic health checkups during 1971-1972 while members of the Kaiser Permanente Medical Care Program (San Francisco-Oakland, California). Prostate cancer incidence was higher in blacks than in whites for all age groups (age-adjusted relative risk (RR) = 1.8, 95% confidence interval (CI) 1.4-2.3). The incidence of benign prostatic hypertrophy was somewhat higher in blacks than in whites until age 65 years, after which it was higher in whites. In contrast to the risk of prostate cancer, the age-adjusted risk of benign prostatic hypertrophy was the same for blacks as for whites (RR = 1.0, 95% Cl 0.8-1.2).

Adult↗