Disease relevance of Prostate

• ATBF1 mRNA was abundant in normal prostates but more scarce in approximately half of prostate cancers tested [1].
• With the concentration of monoclonal antibody used in this study, epithelial and stromal cells from subjects with normal prostates and from 19 patients with benign prostatic hyperplasia were negative for p21 antigen [2].
• PGHS-2 was not detected in normal prostates, but it was expressed by epithelial tumor cells in 18 (75%) of the 24 adenocarcinomas (P =.01) [3].
• Simultaneous implantation of intact Noble (Nb) rats with testosterone and 17 beta-estradiol (E2)-filled silastic capsules for 16 weeks caused atypical hyperplasia (dysplasia) and striking enlargement exclusively in the dorsolateral prostates (DLPs) of all animals [4].
• In autoimmune prostatitis (EAP) of the day-3 thymectomized (d3tx) mice, male Tregs suppressed EAP 3 times better than Tregs from female mice or male mice without prostates [5].

High impact information on Prostate

• In vivo, androgen ablation increased PEDF in normal rat prostates and in human cancer biopsies [6].
• By inhibiting the activity of arginase and nitric oxide synthase, key enzymes of L-arginine metabolism that are highly expressed in malignant but not in normal prostates, reduced tyrosine nitration and restoration of TIL responsiveness to tumor were achieved [7].
• RESULTS: PGHS-1 immunostaining was localized to stromal fibroblasts and vascular endothelium in normal and cancerous prostates [3].
• At 140 weeks of age, the animals were killed, and the prostates were removed and examined for histopathologic features in addition to being assayed for androgen concentrations [8].
• The dihydrotestosterone content in normal prostates (mean +/- SE, 5.1 +/- 0.4 ng/g tissue) and in benign hyperplastic prostates (5.0 +/- 0.4) was similar [9].

Chemical compound and disease context of Prostate

• Prostatic carcinomas contain less (p less than 0.001) creatine kinase activity (units/g) than do prostates with benign prostatic hyperplasia [10].
• Our results are consistent with the hypothesis that aggressive prostate cancers exhibit decreased expression of E-cadherin and demonstrate the feasibility of long-term prognostic studies of this molecule in the usually multiple prostate cancers found in whole, formalin-fixed, paraffin-embedded resected prostates [11].
• Analyses of steroid hormone receptors were performed using a dextran-coated charcoal technique in cytosolic preparations from 40 cases of benign prostatic hyperplasia (BPH) and 10 normal human prostates [12].
• Melatonin produced no effects in intact animals whereas in rats with either peripheral anosmia or bulbectomy it reduced the weight of body, accessory sexual glands, and prostates [13].
• Induction of atypical hyperplasia, apoptosis, and type II estrogen-binding sites in the ventral prostates of Noble rats treated with testosterone and pharmacologic doses of estradiol-17 beta [14].

Biological context of Prostate

• Effects of androgen and polyamines on the phosphorylation of nucleolar proteins from rat ventral prostates with particular reference to 110-kDa phosphoprotein [15].
• The staining for DNA breaks and the tTG staining also indicate that an increased rate of apoptosis is occurring transiently in these prostates [16].
• Multiple binding sites for estradiol were observed in the cytosol as well as in the nuclear salt extractable and salt-resistant compartments of normal, benign hyperplastic, and cancerous human prostates [17].
• We show that BMP7(lacZ/lacZ) null prostates show a two-fold increase in prostate branching, while recombinant BMP7 inhibits prostate morphogenesis in organ culture in a concentration-dependent manner [18].
• When 2-yr-old dogs with starting prostates already at their maximum normal cellular content are subsequently treated for 4 months with dihydrotestosterone (DHT), such treatment induces an additional 2-fold abnormal proliferative increase in prostatic cell number above that seen in normal glands from untreated dogs of any age [19].

Anatomical context of Prostate

• To investigate the mechanism of this synergism, cytosol androgen binding was measured by a density gradient technique in prostates of control and 17 beta-estradiol-treated castrate dogs [20].
• Murine 8-lipoxygenase (8-LOX), homologue of the 15-LOX-2 enzyme that is expressed in benign human prostatic epithelium and reduced in Pca, was not detected in wild-type or LPB-Tag prostates as determined by enzyme assay, reverse transcription-PCR, and immunohistochemistry [21].
• Using the substrate poly[Glu80Na,Tyr20] [poly(GT)] and the autoradiographic detection of alkali-resistant phosphoproteins after sodium dodecyl sulfate-polyacrylamide gel electrophoresis, tyrosine protein kinase (TPK) has been evidenced in human hyperplastic prostates (BPH) and the prostatic carcinoma cell lines PC3 and DU145 [22].
• In contrast, pp125FAK and paxillin were up-regulated by androgen deprivation (castration) and further increased by estrogen treatment, which yielded metaplastic prostates mostly composed of proliferating basal epithelial cells [23].
• Three weeks after transplantation, the animals were sacrificed by decapitation and a significant increase in plasma prolactin was observed, which was accompanied by a highly significant increase in the weights of seminal vesicles, ventral and dorsal prostates, and adrenals [24].

Associations of Prostate with chemical compounds

• These findings fail to confirm the widespread belief that dihydrotestosterone content is elevated in benign hyperplastic prostates [9].
• The compounds also reduced the concentration of testosterone in rat prostates by 35-75% [25].
• The BB form of creatine kinase accounts for 98% of the activity in prostatic carcinoma and in prostates without cancer [10].
• The photoaffinity labeling of the regulatory subunits of adenosine cyclic 3':5'-monophosphate-dependent soluble protein kinases with an adenosine cyclic 3':5' monophosphate analogue, 8-azidoadenosine cyclic 3':5'-monophosphate (8-N3-cAMP) was compared in normal prostates and prostatic (Dunning) tumors [26].
• There was a gradual decrease in the vitamin A content of the prostates of the 4-HPR-treated group as compared with the control, such that by the end of the study period, the CON+4HPR group averaged 0.166 +/- 0.0827 (mean +/- SD) REs, whereas the CON group was 0.732 +/- 0.190 REs [27].

Gene context of Prostate

• In prostates from mice in which the ERbeta gene has been inactivated (BERKO), androgen receptor (AR) levels are elevated, and the tissue contains multiple hyperplastic foci [28].
• Abnormalities in Pten mutant skin consisted of mild epidermal hyperplasia, whereas prostates from these mice exhibited high-grade prostatic intraepithelial neoplasia (HGPIN) that frequently progressed to focally invasive cancer [29].
• Treatment of developing prostates with SFRP1 in culture led to increased organ growth [30].
• Conversely, GRP receptors were identified in only a few hyperplastic prostates and were localized in very low density in glandular tissue and, focally, in some stromal tissue [31].
• The present study shows that the ERbeta gene is expressed together with ERalpha in normal prostates and NPECs, whereas it is barely detectable in prostate cancer and CPECS: Moreover, in some CPECs, the ERalpha gene may be transcribed in a changed protein, resulting from the expression of a deletion variant [32].

Analytical, diagnostic and therapeutic context of Prostate

• DNA microarray studies revealed 122 mRNAs that were increased >/=2-fold in duplicate assays of 16-week-old CR2-TAg versus normal prostates [33].
• While the pattern of expression of alpha-tubulin indicated some minor fluctuations, with the highest level occurring 7 days after castration, the prostates of the cortisol-treated group had essentially the same concentration of this mRNA as the noncastrates [34].
• Organ culture studies with lateral prostates confirmed that estradiol suppressed Shh-ptc-gli expression directly at the prostatic level [35].
• The concentration of dihydrotestosterone was measured by radioimmunoassay in nuclear and cytoplasmic extracts from rat ventral prostates [36].
• TRH and a TRH precursor peptide, TRH-Gly (pGlu-His-Pro-Gly), were measured in ventral prostates from 2-, 5-, and 18-month-old Fisher 344 male rats using a combination of HPLC and specific RIAs for TRH and TRH-Gly [37].

References