bluuebunny/crossref_metadata_2025_split huggingface dataset:
Looking for human glandular kallikrein‐1 in the prostate
Authors: Paradis Gilles , Tremblay Roland R. , Dubé Jean Y. 
Published: February 2007

AbstractBased on recent studies indicating that human glandular kallikrein‐1 (hGK‐l) mRNA was present in the prostate, we have undertaken to determine whether the prostate contained trypsin‐like proteases with properties compatible with those deduced from hGK‐1 gene nucleotide sequence. The first series of experiments showed that only minimal levels of trypsin‐like enzymatic activity, determined with synthetic substrates, were present in chromatographic fractions of prostatic glycoproteins having a molecular weight in the range expected for hGK‐l, i. e., 25,000‐35,000. Because of this, we used [3H]diisopropylfluorophosphate (DFP) labeling alone or in the presence of various serine‐protease inhibitors to identify trypsin‐like proteases in the prostate. Two‐dimensional gel electrophoresis of prostatic glycoproteins showed the presence of minor spots of 18‐32 kDa. These spots were slightly more acidic than were those of prostate specific antigen (PSA) and were completely inhibited by preincubation with tosyl lysine chloromethyl ketone and p‐nitrophenyl‐p‐guanidobenzoate in contrast to PSA spots that were not affected by these treatments. When a similar procedure was applied to total cytosolic proteins instead of glycoproteins, an additional 30 kDa DFP binding protein was observed. This relatively abundant protein was much more acidic than was PSA and was not inhibited by any of the protease inhibitors tested. In conclusion, this study has permitted us to demonstrate the presence of two sets of proteins that have physicochemical properties compatible with those that can be deduced from the information contained in the hGK‐1 gene.
Effect of the steroidal androgen receptor antagonist win 49,596 on steroid‐induced benign prostatic hyperplasia in the castrate beagle dog
Authors: Juniewicz P. E. , Lemp B. M. , Barbolt T. A. , Labrie T. K. , McCarthy M. , Reel J. R. , Batzold F. H. 
Published: February 2007

AbstractThe effects of the steroidal androgen receptor antagonist Win 49,596 on steroid‐induced prostatic growth, histomorphology, and secretory function were studied in the castrate male beagle dog. At oral doses ranging from 0.625 to 40 mg/kg/day for 12 weeks, Win 49,596 inhibited prostatic growth in terms of both weight and total DNA in a dose‐dependent manner. In addition, both the incidence and severity of diffuse glandular hyperplasia/hypertrophy were dose‐dependently inhibited by Win 49,596, resulting in diffuse glandular atrophy. Prostatic secretory function was also inhibited by Win 49,596 treatment. The effects of Win 49,596 at a dosage of 40 mg/kg/day were similar to that observed for the nonsteroidal androgen receptor antagonist flutamide at 10 mg/kg/day. Oral administration of Win 49,596 to castrate dogs at a dosage of 40 mg/kg/day for 12 weeks failed to produce any evidence of agonist activity. These results demonstrate that Win 49,596 prevented the experimental induction of benign prostatic hyperplasia in dogs and suggest that on further evaluation this compound may be efficacious in the treatment of the numan disease.
Evidence of mucin M1 antigens in seminal plasma and normal cells of human prostatic urethra in relation to embryonic development and tumors
Authors: Daher N. , Gonzales J. , Gautier R. , Bara J. 
Published: February 2007

AbstractBy employing immunoperoxidase methodology, using monoclonal antibodies against the peptide core of gastric mucins (M1 antigens), we demonstrate the presence of M1 mucinproducing cells that are associated with the prostatic urethral epithelium and located mainly in the veru montanum area near the prostatic ductal and utriculus junctions. The significance of these M1 cells is not yet clear. Using an immunoradiometric assay, these M1 mucins were found predominantly in the prostatic fraction obtained from seminal plasma. By chromatography on Sepharose 6B and 2B and cesium chloride gradient centrifugation, we demonstrate that high‐molecular‐weight components (> 107 Da) show a density of 1.45 g/ml, similar to mucins, and are immunochemically related to peptidic gastric M1 mucins. The particular location of these M1 antigens in prostatic adult urethra and their fetal expression in cloacal structures suggest that, in males, the prostatic urethral epithelium includes some remnant cells from the enteric cloaca. Finally, the presence of mucincontaining cells in the prostatic urethra could possibly explain the histogenesis of the rare benign villous tumors and primary mucinous adenocarcinomas arising from the prostatic urethral epithelium.
Radiolocalization of human prostate tumor in a mouse subrenal capsule model by monoclonal antibody turp‐27
Authors: Wright George L. , Wilson Eileen , Klinger Mark , Roland Wendy , Beckett Mary Lou , Daddona Peter E. 
Published: February 2007

AbstractThe subrenal capsule assay was used to determine if 125I‐labeled anti‐prostate monoclonal antibody TURP‐27 could target human prostate tumor fragments implanted under the renal capsule of normal immunocompetent C57 BL/6 mice. Maximal binding and optimal tumor to non‐tumor tissue ratios occurred within 24–48 hours postadministration of 125I‐TURP‐27. No significant localization was observed in mice bearing TURP‐27 antigen‐negative human colon tumor tissue implants or with an isotype‐matched control monoclonal antibody. These preclinical data suggest that TURP‐27 may have clinical application for imaging metastatic prostate tumors and further application in immunoconjugate and/or radiotherapy of prostate cancer.
Production of epidermal growth factor and transforming growth factor‐α by the androgen‐responsive LNCaP human prostate cancer cell line
Authors: Connolly Jeanne M. , Rose David P. 
Published: February 2007

AbstractEpidermal growth factor (EGF)‐related polypeptides may be involved in the growth of human prostate cancer cells, and in the androgen stimulation of hormone‐responsive prostatic carcinomas. We have shown that androgen‐responsive LNCaP cells, like the autonomous DU 145 human prostate cancer cell line, synthesize and secrete EGF and related polypeptides, including immunoreactive transforming growth factor‐α (TGF‐α). As determined by radioimmunoassay, intracellular EGF levels were approximately 100 times those of TGF‐α, but together these accounted for less than half of the total EGF‐like polypeptides detected in a radioreceptor assay. Although LNCaP cell growth was stimulated by dihydrotestosterone (DHT), there was no evident effect on immunoreactive EGF levels in the medium after correction for cell number. Moreover, metabolic labeling experiments showed no effect of the androgen on EGF synthesis by LNCaP cells. Gel filtration chromatography of conditioned medium showed both high molecular weight species and the mature 6,000 dalton form of immunoreactive EGF. We conclude that although LNCaP prostate cancer cell growth is stimulated by DHT, it is unlikely that this is mediated directly via increased EGF synthesis by the tumor cells.
Effects of epidermal growth factor and androgen influences on accessory sex glands in prepubertal swiss‐webster mice
Authors: Lehman Brenda L. , Smith Roger , Leichty Kerry D. , Kauffman Clint L. , Miller Roman J. 
Published: February 2007

AbstractThe effects of epidermal growth factor (EGF) on androgen stimulation of accessory sex gland growth and biochemistry were determined for prepubertal male Swiss‐Webster mice. For the seminal vesicle and anterior prostate, 5αdihydrotestosterone (5αDHT) treatment significantly increased the quantitative levels of organ wet weight, DNA content, polyamine content, and stereologically determined epithelium and lumen volumes above the control group. EGF treatment alone slightly enhanced the levels of most measured parameters from control values. However, when a combined EGF5αDHT treatment was compared with 5αDHT treatment alone, the 5αDHT treatment effects on epithelial and lumen volumes and polyamine content were antagonized by the action of EGF.
Androgen regulation of polyamine synthesis in seminal vesicle and in different lobes of the rat prostate
Authors: Fjösne Hans E. , Östensen Mari‐Ann , Haarstad Helge , Sunde Arne 
Published: February 2007

AbstractEndogenous levels of the polyamines putrescine, spermidine, and spermine have been examined in the 106 m/s2 supernatant of different lobes of the rat prostate and in the seminal vesicles of castrates, androgen‐stimulated castrates, and intact controls.Content of the polyamines varied between the lobes, with spermidine highest in intact animals. After castration, the content of polyamines fell significantly in all lobes but the coagulating gland (CG). Spermidine levels were highest, except in the lateral prostate (LP) and CG, where the content of putrescine was highest. In castrated animals treated with testosterone propionate for 72 h, the amount of the three polyamines examined increased dramatically in the ventral prostate (VP) and moderately in the CG and seminal vesicle (SV). Concerning individual polyamines, spermidine increased significantly in all lobes, while putrescine increased significantly only in the two saccular parts of rat prostate, i.e., CG and SV. Spermidine content decreased significantly in the DP.Major differences in the content of the three polyamines—putrescine, spermidine, and spermine—in the various tissues studied have been found. Moreover, distinct differences among intact, castrated, and testosterone‐treated castrated animals have been revealed.
Induction of chemical castration in male rats by a new long‐acting LHRH‐antagonist
Authors: Habenicht Ursula‐F. , Schneider Martin R. , Etreby M. Fathy El 
Published: February 2007

AbstractLHRH‐antagonists might represent a useful new type of androgen deprivation to treat prostatic cancer. In this context adult intact male rats were treated subcutaneously with different concentrations of the new LHRH‐antagonist antide either once (1, 3, 6, 10, 15 mg/kg) or on 5 consecutive days (5 × 3 mg/kg). The effect on serum concentration of LH and testosterone and the effect on the weights of testes, prostate, and seminal vesicles was investigated after different periods of time (24 hours, 1,2,3,5, and 8 weeks). Histological evaluation of the testes was also performed. A clear dose‐dependent inhibitory effect on the above‐mentioned parameters was observed. The most effective treatment schedule was the single application of 15 mg/kg resulting in castration‐like inhibition of prostate weights and marked inhibition of spermatogenesis within 2 weeks, which was maintained 8 weeks after the injection.Serum LH and serum testosterone concentrations were below the detection limit of the assay within 2 weeks and showed first signs of recovery after 8 weeks. Histologically, no signs indicative of irreversible effects (testes) were observed. To summarize, the LHRH‐antagonist antide was found to have a profound long‐lasting inhibitory but reversible effect on the reproductive system of adult intact male rats. These data emphasize the suitability of this type of compound for the treatment of prostatic cancer.
Treatment of hormone‐refractory stage D carcinoma of prostate with coumarin (1,2‐benzopyrone) and cimetidine: A pilot study
Authors: Marshall M. Ernest , Butler Karen , Hermansen Dane 
Published: February 2007

AbstractThe combination of coumarin (1,2‐benzopyrone) and cimetidine has been reported to render objective tumor regressions among patients with metastatic renal cell carcinoma and malignant melanoma. Subsequently, a pilot trial was conducted to evaluate this regimen for the treatment of stage D hormone‐refractory carcinoma of the prostate. Patients received coumarin 100 mg orally as a single daily dose for 14 days; on day 15 cimetidine 300 mg four times daily was added, and both drugs were continued until progression of disease. Fourteen patients with advanced prostate cancer were treated. Nine patients had evaluable disease only, whereas five patients had both measurable and evaluable disease. All patients had bone metastases. Although there was no objective evidence of tumor regression, three patients (with evaluable disease only) experienced significant improvement in bone pain with decreased analgesic use that persisted until disease progression at 3, 5.5 +, and 9 months. Although coumarin caused no symptomatic or organ dysfunction toxicity, one elderly patient experienced reversible mental confusion from cimetidine. Coumarin and cimetidine, at the dose and schedule described, are not effective for the treatment of advanced prostate cancer. However, the results of laboratory investigations suggest that further clinical trials of coumarin, at higher doses, may be warranted for the treatment of this disease.
Tissue‐specific decline in cytosolic casein kinase II of the ventral prostate in aging rats
Authors: Goueli Said A. 
Published: February 2007

AbstractAn age‐associated decline in the activity of cytosolic casein kinase II in the rat ventral prostate was observed. The decrease in specific and total activity of casein kinase II of prostatic cytosol obtained from 12‐month old rats compared with that from 3‐month old rats was 50% and 70%, respectively. This decrease was tissue specific since no such alteration in enzymic activity was found in liver, lung, or heart. The decline in activity was not due to an increase in the concentration of a casein kinase inhibitor or to altered androgenic status with aging. Rather, the reduction in the activity of the enzyme was commensurate with the decrease in the total concentration of the enzyme protein as determined by an ELISA using anti‐casein kinase II antibodies. The activity of casein kinase II in the nuclear fraction of the rat prostate was not altered in aging animals. It may be concluded that the cytosolic form of casein kinase II in the prostate of older animals is regulated at the transcriptional level (but not via the androgen‐receptor complex mechanism). An alternative explanation for this observation may relate to altered stability of the enzyme in the prostate of older animals.
Analysis of somatic cell hybrids derived from normal human prostatic epithelial cells fused with HeLa cells
Authors: Peehl Donna M. , Wong Stephen T. , McNeal John E. , Stamey Thomas A. 
Published: February 2007

AbstractSomatic cell hybrids have been instrumental in the recognition of specific chromosomes containing genes capable of suppressing the malignant phenotype. As a first step towards the identification of possible suppressor genes in prostate cells, we created hybrids by fusing normal prostate cells with malignant HeLa cells. Similar to hybrids made with other combinations of normal and malignant cells, the normal phenotype was dominant and the malignant phenotype was suppressed. The phenotype of the nontumorigenic hybrids after injection into nude mice resembled that of normal keratinocyte X HeLa hybrids, and tiny, nonprogressive keratinized nodules were produced. One hybrid clone was tumorigenic, possibly due to the loss of a normal suppressor gene, and displayed glandular as well as squamous elements. Further characterization of these hybrids should permit isolation of specific suppressor genes, as well as promote recognition of elements that regulate the glandular phenotype.
Primary yolk sac (endodermal sinus) tumor of the prostate: Case report and review of the literature
Authors: Schriber Jeff , Flax Stanley , Trudeau Maureen , Cook Gerald T. , Weizel Harold , Katz Alan , Keating Armand 
Published: February 2007

AbstractA primary yolk sac (endodermal sinus) tumor of the prostate is described in a 40‐year‐old male. This is the second documented case of a yolk sac tumor occurring in the prostate gland. Treatment included surgical removal and subsequent combination chemotherapy. Four months following diagnosis, the patient died of complications. At autopsy, no residual tumor was detected. The role of combination chemotherapy as potentially curative therapy in the treatment of extragonadal yolk sac tumors is discussed.
Role of calcium in the programmed death of rat prostatic glandular cells
Authors: Martikainen Paula , Isaacs John 
Published: February 2007

AbstractBy using a newly developed and validated rat ventral prostatic organ culture system in which prostatic glandular cells can be induced to undergo programmed cell death, the role of an elevation in the intracellular free Ca2+ concentration in this death process was studied. By using this organ culture system, ventral prostatic glandular epithelial cells can be maintained in culture for a period of more than 14 days with a low daily rate of cell death (i.e., ± 5% die per day) if androgen is included in the media. In contrast, if androgen is not included in the media, the daily rate of prostatic glandular cell death increases approximately 3‐fold (i.e., ± 15% die per day). With this organ culture system it has been demonstrated that the daily rate of programmed death of the glandular epithelial cells can be shifted from 5% to 15% of the cells dying per day when testosterone and 10 μM of the Ca2+ ionophore A23187 are both present in the media. Thus, when the intracellular free Ca2+ is elevated within prostatic cells by means of ionophore treatment, the daily rate of glandular cell death in the presence of testosterone is identical to that induced when testosterone is not present in the media. If the organ cultures are maintained in media lacking testosterone but containing 10 μM of the Ca+2 channel blocker nifedipine to inhibit elevations in the intracellular free Ca2+ derived from the extracellular pools, the rise in the daily rate of cell death from 5 to 15% of the cells dying per day induced by androgen ablation can be inhibited by ± 70%. These results suggest that an increase within prostatic glandular cells in their intracellular free Ca+2 derived from extracellular Ca2+ pools is a critical early event involved in triggering the subsequent process of programmed cell death (i.e., specifically DNA fragmentation) in these cells following androgen ablation.
Flutamide has no effect on adrenal androgen response to acute ACTH stimulation in patients with prostatic cancer
Authors: Carlström Kjell , Pousette Åke , Stege Reinhard 
Published: February 2007

AbstractBasal levels and adrenocorticotropic hormone (ACTH)‐induced increments (Δ‐values) of serum cortisol, dehydroepiandrosterone (DHA), dehydroepiandrosterone sulfate (DHAS), 4‐androstene‐3,17‐dione (A4), and 17‐hydroxyprogesterone (170HP); basal testosterone (T), luteinizing hormone (LH), serum ASAT, gamma‐GT, and albumin were measured in prostatic cancer patients before and after 6 months of treatment with LH‐RH‐agonist, with flutamide, and with LH‐RH‐agonist + flutamide, respectively.Basal DHA and DHAS were decreased during flutamide and LH‐RH‐agonist + flutamide treatment and basal A4 during treatment with LH‐RH‐agonist and with LH‐RH‐agonist + flutamide. Basal 170HP, T, and LH decreased during LH‐RH‐agonist and LH‐RH‐agonist + flutamide treatment and increased during single drug flutamide treatment.Slightly decreased Δ cortisol values were observed during LH‐RH‐agonist and during flutamide treatment and slightly increased Δ 170HP values during LH‐RH‐agonist and LH‐RH‐agonist + flutamide treatment. Values for Δ DHA and Δ A4 were completely unaffected by any of the treatment regimens. Elevated ASAT values were observed during treatment with flutamide and with LH‐RH‐agonist + flutamide.It is concluded that flutamide has no effect on the adrenal androgen response to acute ACTH stimulation.
Characterization of muscarinic cholinergic receptors in membrane preparations from rat prostatic adenocarcinoma
Authors: Batra Satish , Christensson Per‐Inge , Hartley‐Asp Beryl 
Published: February 2007

AbstractThe binding characteristics of 3H‐quinuclidinyl benzilate (QNB) to muscarinic sites in isolated plasma membrane fractions from R‐3327 Dunning tumors (H and AT‐1 sublines); ventral, dorsolateral prostate; and urinary bladder of the rat were studied. QNB binding to all preparations, except from AT‐1 tumors, was specific, saturable, and of high affinity. The AT‐1 tumors completely lacked specific QNB binding. The muscarinic receptor density in H tumors was twofold and twentyfold higher than that in the ventral prostate and dorsolateral prostate respectively. The receptor density in the urinary bladder was approximately twofold higher than that in H tumors. The Kd values in H tumors and ventral prostate were very similar and significantly higher than that in dorsolateral prostate or the urinary bladder. QNB binding in H tumors was strongly inhibited by classical muscarinic receptor antagonists atropine and scopolamine, but poorly by the agonists carbacholine and pilocarpine. In contrast to scopolamine or atropine, inhibition by pirenzepine and AF‐DX116 was relatively low. These data indicate that the muscarinic receptor in Dunning H tumors is of M3 type.
Immunohistochemical study of androgen receptor in benign hyperplastic and cancerous human prostates
Authors: Masai Motoyuki , Sumiya Hidenori , Akimoto Susumu , Yatani Ryuichi , Chang Chawnshang , Liao Shutsung , Shimazaki Jun 
Published: February 2007

AbstractAndrogen receptor was detected immunohistochemically in benign as well as malignant prostatic tissues by using a monoclonal rat anti‐human androgen receptor antibody (AN 1–15). In both benign and malignant cells, the androgen receptor was exclusively localized in nuclei. In hyperplastic prostate, the androgen receptor was stained in the glandular and the stromal cells. In the gland, cells facing the lumen were stained more intensively than those adjacent to the basal membrane. In cancer tissue, receptor‐positive and ‐negative cancer cells were intermingled. The percent of strongly positive cancer cells was correlated inversely with grade. Relapsed cells showed a low population of strongly positive cells irrespective of grade.
Effect of dimethylsulfoxide on the proliferation and glycosaminoglycan synthesis of rat prostate adenocarcinoma cells (PAIII) in vitro: Isolation and characterization of DMSO‐resistant cells
Authors: Kaneski Christine R. , Constantopoulos George , Brady Roscoe O. 
Published: February 2007

AbstractDimethylsulfoxide (DMSO) modulates the tumorigenicity and other characteristics of some malignant cell lines in vitro. We have investigated DMSO effects on cell proliferation and glycosaminoglycan (GAG) synthesis in rat prostate adenocarcinoma (PAIII) cells in culture. DMSO inhibited cell proliferation and GAG synthesis and shedding. Cells that survived the initial exposure to 2.5% DMSO could be propagated in this concentration of the agent and were designated PAIII‐DMSO resistant (PAIII‐DMSOr). PAIII‐DMSOr cells showed reversible indications of increased differentiation such as decreased growth rate and saturation density. Although the PAIII‐DMSOr cells were grown in 2.5% DMSO, they had normal or elevated GAG content. The major GAG of both PAIII and PAIII‐DMSOr cells was undersulfated heparan sulfate. Verapamil, a calcium channel blocker that reverses drug resistance in tumor cells, stimulated the growth of PAIII‐DMSOr cells in the presence of 2.5% DMSO, but was inhibitory in the absence of DMSO. Growth of PAIII cells was inhibited by the differentiating agents sodium butyrate and retinoic acid and by the ionophore monensin. Interestingly, growth of PAIII‐DMSOr cells in the presence of 2.5% DMSO was largely unaffected by sodium butyrate or retinoic acid. The results suggest that (1) PAIII‐DMSOr cells arise from the induction of a compensation mechanism to DMSO effects in a preexisting population of cells; (2) there is a correlation between GAG synthesis and cell proliferation; and (3) further study of the verapamil effect may help elucidate the mechanism of the DMSO‐induced differentiation of cancer cells.