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PubMed1985

On the effects of oestrogen in the male. Some effects of different oestrogenic substances in rats and men with prostatic carcinoma.

In vitro incubations of human testicular tissue responded to human chorionic gonadotrophin with testosterone release in a dose-dependent manner. The release of testosterone increased with incubation time. The stimulated release of testosterone was inhibited by oestradiol and ethinyl oestradiol in a dose-dependent manner, suggesting that these oestrogens exert direct inhibitory effects on the human Leydig cells. Estramustine phosphate, estromustine, diethylstilboestrol and diethylstilboestrol diphosphate did not inhibit testosterone release. Hypophysectomized rats were treated for 8-9 days with human chorionic gonadotrophin, which maintained testicular blood flow within the physiological range. Some of the animals received additional treatment with oestradiol or estromustine. Oestradiol and estromustine depressed plasma testosterone concentration. In contrast to estromustine, oestradiol inhibited testicular blood flow, as measured by the microsphere technique. Intact rats were castrated, supplemented with testosterone and concomitantly treated with different oestrogenic substances. Testosterone supplementation induced increase of prostatic blood flow, which was inhibited by oestradiol, ethinyl oestradiol or diethylstilboestrol. Estramustine and estromustine had no effect on prostatic blood flow. The growth of a transplantable rat prostatic carcinoma (Dunning R3327H) was studied after castration, testosterone substitution or testosterone substitution in combination with oestradiol treatment. Oestradiol inhibited tumour growth, possibly by direct action. The blood flow in tumours in intact animals decreased with increasing tumour volume. Oestradiol treatment enhanced tumour blood flow. The oestrogenic effects of estramustine phosphate, ethinyl oestradiol/polyoestradiol phosphate or orchiectomy were studied in previously untreated prostatic carcinoma patients by measuring serum levels of liver proteins (pregnancy zone protein and sex hormone binding globulin) and pituitary hormones (luteinizing hormone, follicle stimulating hormone and prolactin) during a 6 month period. Both medical treatments induced marked but quite comparable changes of the proteins. Apart from the increase of follicle stimulating and luteinizing hormones, no changes were observed in these serum proteins after orchiectomy.

Adenocarcinoma↗
PubMed1983

[Studies on hormone-polymer composites in urological field--their application in prostatic cancer therapy].

Our studies on the application of hormone-polymer composites in urological field are discussed in this review. We first studied the modes of in vivo and in vitro release of testosterone from vinyl polymer-testosterone composites prepared by radiation-induced polymerization. It was ascertained by our group that in vivo and in vitro release of testosterone from biodegradable copolypeptide -testosterone composites as well as vinyl polymer composites was well controlled. Using this system, we were successful in preparing a testicular prosthesis, which was made of vinyl polymer-testosterone composites and was ascertained to release testosterone constantly for a long period in the dose range of clinical usage. We also applied this sustained release drug delivery system to the method of administration of an LH x RH agonist, which was one of the best therapeutic drugs for androgen dependent prostatic cancer. Sustained release of the LH x RH agonist in the dose range of clinical usage over a period of several months from copolymer-LH x RH agonist composites was confirmed in both male rats and in prostatic cancer patients. Prostatic cancer cells contain a major secretion protein (alpha-protein or estramustine-binding protein) and estramustine has a high affinity for alpha-protein. Therefore, we examined the effect of an estramustine-microsphere containing anticancer drugs, namely, the missile therapy for prostatic cancer. The missile therapy should open the way to specific and selective chemotherapy for prostatic cancer.

Animals↗
PubMed1983

[Estracyt therapy in advanced prostate cancer: current status and personal results].

In addition to surveying biochemistry, clinical findings and side effects of Estramustin Phosphate therapy, this paper gives an account of our own results with primary and secondary Estramustin Phosphate therapy. A total number of 118 patients have been examined in three different studies since 1970. Apart from conventional clinical control examinations, an additional accurate parameter applied to control therapy response was cytological analysis of therapy induced regression signs in primary tumor. Thus objective therapy response was established for 87% resp. 93% of the patients on primary Estramustin Phosphate therapy, and for 35% resp. 45% of those on secondary therapy. Patients with cytologically poor therapy response 3 months after beginning of therapy entered significantly earlier into clinical progression than patients with favorable therapy response, with clinical progression being additionally and essentially influenced by the pretherapeutical metastatic stage. Gastro-intestinal side-effects were prevalent in 79% of cases on intravenous administration of the drug, while on oral administration they were found to be three times less.

Aged↗
PubMed2000

Different microtubule network alterations induced by pachymatismin, a new marine glycoprotein, on two prostatic cell lines.

Pachymatismin is a new cytostatic factor extracted from the marine sponge Pachymatisma johnstonii Bowerbank. To investigate the mechanism of action of pachymatismin, we studied its effects on two human prostate cell lines (DU145 and E4) of tumor origin. Immunocytochemistry demonstrated that the drug caused depolymerization of microtubules in DU145 cells, this effect being similar to that of estramustine, known to be a microtubule-depolymerizing agent. E4 cells, described to be resistant to the microtubule-depolymerizing agent estramustine, were also found resistant to pachymatismin. Pachymatismin at the same dose that destroys microtubule organization in DU145 cells is not able to induce microtubule depolymerization in E4 cells. Compared to the estramustine- and pachymatismin-sensitive DU145 cells, E4 cells revealed an increase of betaI+II, betaIII, betaIV isotypes as well as post-translational modifications of tubulin, such as polyglutamylation and acetylation. In addition, the level of tau protein was also enhanced in E4 cells compared to DU145 cells. The effects of pachymatismin were tested in vitro using calf brain microtubules. It was shown that the drug lowers the capacity of microtubules to reassemble in vitro. Interestingly, pachymatismin has been found to inhibit microtubule assembly less efficiently when the ratio of tau to tubulin is increased. Taken together, pachymastismin has been shown to induce in vivo microtubule depolymerization following binding to microtubule proteins. Changes in microtubule components such as tubulin isoforms or tau may be involved in a decrease of sensitivity to pachymatismin.

Animals↗
PubMed2005

Docetaxel in hormone-refractory metastatic prostate cancer.

The taxoid analogue docetaxel is a potent inhibitor of microtubular depolymerisation and, in hormone-refractory metastatic prostate cancer, it also counters the effects of the anti-apoptotic protein Bcl-2. Overall survival was significantly increased in patients with hormone-refractory metastatic prostate cancer receiving intravenous docetaxel every 3 weeks plus oral prednisone or estramustine, compared with patients receiving intravenous mitoxantrone every 3 weeks plus prednisone in two large phase III trials (TAX 327 and SWOG [Southwest Oncology Group] 9916). In the TAX 327 study, patients receiving docetaxel 75 mg/m(2) every 3 weeks plus prednisone had a median overall survival duration of 18.9 months; in the SWOG 9916 study, median overall survival duration was 17.5 months with docetaxel 60 mg/m(2) every 3 weeks plus estramustine 280 mg three times daily on days 1-5. The median overall survival duration for the control arm of mitoxantrone 12 mg/m(2) every 3 weeks plus prednisone was 16-17 months. Compared with mitoxantrone plus prednisone, docetaxel plus prednisone improved prostate specific antigen response rate, pain and health-related quality of life, and docetaxel plus estramustine increased progression-free survival. Adverse events were more common with docetaxel- than mitoxantrone-based treatment regimens, but most events associated with docetaxel were mild-to-moderate in severity.

Antineoplastic Agents, Phytogenic↗
PubMed1981

On the presence of prostatic secretion protein in rat seminal fluid.

The copulating plug collected from the tip of the penis from rats immediately after decapitation contains a protein very similar and probably identical to PSP (prostatic secretion protein); this protein has earlier been purified from rat prostatic cytosol and characterized. The protein present in the copulating plug interacts with [3H]estramustine and binds to the antibody raised against rat PSP. The concentration of the protein in the copulating plug is 400 ng/mg of total protein, when measured using the radioimmunoassay technique developed earlier for measurement of PSP in rat prostate. The [3H]estramustine-protein complex formed in a preparation of the copulating plug has an apparent molecular weight of about 50,000 and a sedimentation coefficient of about 3S when analyzed using sucrose density gradient centrifugation. The complex was retained on Concanavalin-A Sepharose indicating that the protein is a glycoprotein. Binding of the complex was also observed on hydroxylapatite and DEAE-Sephadex columns, from which it was eluted at 0.18 M KCl. Light microscope autoradiograms of rat sperms incubated with 125I-labeled PSP indicated that PSP is bound to all parts of the sperms. A macromolecule interacting with the PSP-antibodies is also present in human seminal fluid but at a concentration considerably lower than in rat seminal fluid. The present study shows that a macromolecule probably identical to prostatic secretion protein is present in the copulating plug from the rat. The biological role of this protein in normal male fertility is discussed.

Animals↗
PubMed1989

Differential reaction of secretory and non-secretory proteins in hormone-treated Dunning tumor.

Tumor cells from of the Dunning R-3327 PAP tumor were grown in vivo in the flank region of male Copenhagen rats for 4 months. Untreated control animals, castrated animals, and untreated or castrated animals supplemented with testosterone and estramustine (alone or in combination) bearing tumors were used for immunocytochemical studies of the tumor cells. Antibodies against the following secretory proteins were applied to paraffin sections of formalin-fixed tissue: anti-SVS II, anti-PBP, anti-transglutaminase, anti-acid phosphatase (isoenzymes, isoelectric points [pI] 5.6, 7.1, 8.0), non-secretory proteins comprised antiglucocorticoid-receptor, and antibodies against extracellular matrix proteins and intermediate filaments. A differential expression of marker proteins subsequent to the various treatments was observed immunohistochemically. Castration induced a loss of secretory activity, an increase in keratin-immunoreactive cells, and regressive activity in the secretory cells. Immunoreactivity of the glucocorticoid receptor in the nuclei of the basal cells was also decreased. Testosterone substitution only partially restored secretory activity of tumor cells in castrated animals. In experiments where estramustine had been administered to normal or castrated animals, metaplastic transformation of the epithelium, focal reduction, or increase of secretory and/or regressive activity and persistence of glucocorticoid receptor-like immunoreactivity was observed. The findings indicate that different hormonal situations provide conditions for the development of rather heterogeneous reaction patterns of different tumor cells, allowing partial regression of individual clones of tumor cells along with stimulation of others.

Adenocarcinoma↗
PubMed1999

Phosphorylation/dephosphorylation of androgen receptor as a determinant of androgen agonistic or antagonistic activity.

Protein phosphorylation/dephosphorylation is an important posttranslational modification that plays a critical role in signal transduction. The androgen receptor (AR) is under such control. We demonstrate that androgen receptor phosphorylation determines whether or not AR ligands perform as agonists or antagonists in LNCaP cells. Androgen receptor ligands (such as dihydrotestosterone and beta-estradiol) stimulate receptor expression and phosphorylation and, as a result, they act as agonists or partial agonists. In contrast, agents such as bicalutamide and estramustine inhibit the receptor phosphorylation and act as antagonists. This model is supported by gene expression and transactivation assays. Significant increases in levels of both mRNA and protein of prostate-specific antigen (PSA), a natural AR target gene, occur following the treatment of LNCaP cells with DHT, beta-estradiol, or hydroxyflutamide. In contrast, exposure of LNCaP cells to bicalutamide or estramustine results in a sharp decrease of PSA expression. Agonistic or antagonistic effect of these compounds on PSA expression parallels the level of phosphorylated, but not dephosphorylated androgen receptors. These agonistic or antagonistic effects are also observed in HeLa cells transfected with wild-type AR expression plasmid (pAR0) and AR-driven luciferase expression plasmid GRE-tk-LUC in the presence of different groups of AR blockers. Our data indicate that the functional status of androgen receptors is strongly correlated with the phosphorylation status of the receptors, and that the phosphorylated androgen receptor is the form of the receptor transcriptionally active in regulation. Thus the androgen receptor phosphorylation/dephosphorylation may serve as a new molecular target for screening androgen antagonists for the treatment of prostate cancer.

Androgen Antagonists↗
PubMed1992

Effect of oral clodronate on bone pain. A controlled study in patients with metastic prostatic cancer.

Although osteosclerotic metastases are characteristic of prostatic carcinoma, bone resorption is also accelerated. Since clodronate inhibits bone resorption and relieves bone pain, we have given it to patients with painful bone disease from prostatic cancer after failure of hormonal therapy. All patients received estramustine phosphate orally. Simultaneously they were randomly allocated to clodronate (36) and placebo (39) groups. Clodronate was given by mouth. The dose was 3.2 g for the first month, thereafter 1.6 g. Pain relief was more distinct in the clodronate group where one third of patients were totally free of bone pain. The use of analgesics stopped in 38% of patients on clodronate and in 18% on placebo which effect probably belongs to estramustine phosphate. Serum calcium concentration decreased more markedly in the clodronate group. Clodronate dose of 3.2 g seemed to be more potent than that of 1.6 g. Side effects were uncommon and occurred equally in both groups. No significant differences were seen in median survival or survival rates between the groups.

Administration, Oral↗
PubMed1982

The synthesis of 3H labelled steroid-nitrogen mustard derivatives and studies on their action in rat and human prostate.

Tissue receptor proteins are thought to be a key factor in selective retention and nuclear translocation of steroid hormones in their target tissues. Steroid-cytotoxic derivatives with high affinity for these receptor proteins may, therefore, be useful as site directed agents in the treatment of hormone dependent cancers. The prostatic retention and subcellular localisation of estramustine and a 17 beta nitrogen mustard derivative of 5 alpha-dihydrotestosterone have been compared since the latter compound has higher androgen receptor binding affinity than the former. The 5 alpha-dihydrotestosterone derivative was not retained more avidly than estramustine by either human or rat ventral prostatic tissue. Nuclear localisation could not be detected with either compound. The cytotoxic action of these compounds requires the liberation of the nitrogen mustard moiety. The cleavage rate of both compounds was low but similar in both benign and malignant prostatic tissues. We conclude that steroids are unlikely to be suitable agents for directing cytotoxic compounds to prostatic tissue particularly if the steroid-cytotoxic derivative requires metabolism for the expression of the cytotoxic activity.

Animals↗
PubMed1982

Fractionation of the rat ventral prostate with respect to isolation and exocytosis of the prostatic secretion protein.

The ventral prostate was fractionated into one mitochondrial and three microsomal fractions. The different fractions were characterized morphologically and chemically. An interesting finding was that upon homogenization the endoplasmic reticulum membranes often turned 'inside-out' giving rise to microsomes with ribosomes attached to the inside of the vesicles. The secretion of the prostatic secretion protein was studied by means of isotopic pulse labeling using radioactive leucine. Peak radioactivity in the microsomal fraction was obtained at 2 h after injection with a relatively rapid fall. The radioactivity in the secretory fluid displayed a continuous increase up to 8 h followed by a plateau. When prostatic secretion protein was purified from secretory fluid and microsomes using a Con A-Sepharose column it showed a typical precursor-product relationship with an early peak at 60 min in microsomal prostatic secretion protein followed by a peak in secretory fluid at 4 h. Vinblastine blocked the release of labeled secretion protein into the secretory fluid, a phenomenon characteristic for secretory proteins which are exocytosed by means of fusion between secretory granules and the plasma membrane. Following intravenous injection of [3H]estramustine, accumulation was seen in the secretory fluid. Some estramustine probably binds to newly synthesized prostatic secretion protein and follows the same route of intracellular transport and extracellular discharge as does prostatic secretion protein.

Animals↗
PubMed2004

Identification of a novel first exon of the human ABCA2 transporter gene encoding a unique N-terminus.

The human ABCA2 transporter is a member of a large family of ATP-binding proteins that transport a variety of molecules across biological membranes. Using RNA ligation-mediated PCR (RLM-PCR), we have identified a novel first exon, which we designate 1B that is located 699 bp upstream of the previously characterized first exon, which we designate 1A. These first exons are alternatively spliced to the second exon of the ABCA2 transcript resulting in a protein that has a unique amino terminus. For exon 1B, the new amino terminus encoded by the first exon is 52 amino acids and for exon 1A, 22 amino acids. We observed that among adult tissues examined, the highest expression of the 1B isoform was in peripheral blood leukocytes (PBL). Laser scanning confocal microscopy revealed that the 1A isoform and the 1B isoform co-localize with lysosome-associated membrane proteins-1 and -2 (LAMP-1 and -2). Cytotoxicity assays suggested a role for ABCA2 in estramustine and estradiol resistance, and overexpression of ABCA2 is seen in an estramustine-resistant prostate carcinoma line. Since both isoforms of the ABCA2 transporter have identical subcellular localization and both are overexpressed in a resistant cell line, we propose that they are also functionally redundant. It is likely that expression of ABCA2 by two independent promoters constitutes locus of regulation controlling expression of the protein to meet requirements in different tissues.

ATP-Binding Cassette Transporters↗
PubMedDate not supplied

Influence of p53 and bcl-2 on chemosensitivity in benign and malignant prostatic cell lines.

The administration of cancer chemotherapeutic agents results in an increase in the apoptotic cells in the tumor: therefore, it has been assumed that anticancer drugs exhibit their cytotoxic effects via apoptotic signaling pathways. Characteristics that confer sensitivity to drug-induced apoptosis are, a functional p53 protein and expression of the apoptosis-promoting protein, bax. The role of p53 and bax/bcl-2 in drug-induced apoptosis was assessed in six prostate cell lines, 1532T, 1535T, 1542T, 1542N, BPH-1 and LNCaP using TD(50) concentrations of etoposide, vinblastine and estramustine. Cell death was monitored morphologically by fluorescent microscopy, and by flow cytometry (Annexin-V assay). Apoptotic morphology was rather low and ranged from 0.1% to 12.1%, 3.0% to 6.0% and 0.1% to 8.5% for etoposide, estramustine and vinblastine, respectively. Annexin-V binding and flow cytometry indicated apoptotic propensities of 0% to 4%, 0% to 3% and 0% to 5%, respectively. The percentage of cells responding to drug-induced apoptosis was, on average, higher in the tumor cell lines than in the normal cell lines, but showed no correlation with p53 status. The percentage of cells showing necrosis, assessed by Annexin binding and Propidium Iodide permeability in aqueous medium, tended to be much higher, and was found to be at the level of 5% to 30%. Immunoblotting demonstrated that bax and bcl-2 proteins were expressed at a basal level in all cell lines, but did not increase after exposure to TD(50) doses of the three drugs. The ratio of bax and bcl-2, measured by laser scanning densitometry, was not altered by the drug-induced DNA damage. The results suggest that apoptosis is not a major mechanism of drug-induced cell death in prostate cell lines and appears to be independent of p53 status and bax/bcl-2 expression.

Antineoplastic Agents, Hormonal↗
PubMed2003

Enzyme-mediated precipitation of parent drugs from their phosphate prodrugs.

Many oral phosphate prodrugs have failed to improve the rate or extent of absorption compared to their insoluble parent drugs. Rapid parent drug generation via intestinal alkaline phosphatase can result in supersaturated solutions, leading to parent drug precipitation. The purpose was to (1) investigate whether parent drugs can precipitate from prodrug solutions in presence of alkaline phosphatase; (2) determine whether induction times are influenced by (a) dephosphorylation rate, (b) parent drug supersaturation level, and (c) parent drug solubility. Induction times were determined from increases in optical densities after enzyme addition to prodrug solutions of TAT-59, fosphenytoin and estramustine phosphate. Apparent supersaturation ratios (sigma) were calculated from parent drug solubility at intestinal pH. Precipitation could be generated for all three prodrugs. Induction times decreased with increased enzyme activity and supersaturation level and were within gastrointestinal residence times for TAT-59 concentration>/=21microM (sigma>/=210). Induction times for fosphenytoin were less than the GI residence time (199min) for concentrations of approximately 352 microM (sigma=4.0). At approximately 475 microM (sigma=5.3) the induction times were less than 90min. For estramustine-phosphate, no precipitation was observed within GI residence times. Enzyme-mediated precipitation will depend on apparent supersaturation ratios, parent drug dose, solubility and solubilization by the prodrug.

Alkaline Phosphatase↗
PubMed2001

Modulation of endogenous beta-tubulin isotype expression as a result of human beta(III)cDNA transfection into prostate carcinoma cells.

Increases of individual beta tubulin isotypes in antimicrotubule drug resistant cell lines have been reported by several laboratories. We have previously described elevations in beta(III)and beta(IVa)isotypes in estramustine and paclitaxel resistant human prostate carcinoma cells. To investigate further the function of beta tubulin isotypes in antimicrotubule drug response, human prostate carcinoma cells that normally have very low to undetectable levels of beta(III)were stably transfected with beta(III)cDNA in pZeoSV system. An 18 bp haemagglutinin (HA) epitope tag was added at the 3' end prior to cloning into the vector. Cells were transfected with pZeoSV or pZeoSV-beta(III)plasmids and selected in the presence of Zeocin. Immunofluorescent staining of the transfectant cells have shown significant expression and incorporation of HA-tagged beta(III)tubulin into cellular microtubules. Quantitation of Western blots revealed the HA-tagged beta(III)levels to be approximately 7-fold higher than the vector control cells. RT-PCR analysis confirmed the increase at the transcript level and also revealed a collateral increase of beta(II)and beta(IVb)transcripts. Cell viability assays indicated that sensitivity of beta(III)transfected cells to various antimicrotubule agents was similar to vector transfected cells: IC50 values for estramustine, paclitaxel, colchicine and vinblastine were 4 microM, 4 nM, 22 nM and 2 nM, respectively for both cell lines. Thus, overexpression of beta(III)isotype in human prostate carcinoma cells by stable transfection failed to confer antimicrotubule drug resistance to these cells. Counterregulatory increases of endogenous beta(II)and beta(IVb)tubulin isotypes in these beta(III)transfected cells may be a compensatory mechanism used by the cells to overcome the effects of elevated beta(III)levels on the cellular microtubules. These results highlight the difficulty in isolating the contribution of single tubulin isotypes in drug response studies.

Antineoplastic Agents↗
PubMed1990

Systemic management of prostate cancer.

The objective of this review is to explore different therapeutic options for metastatic adenocarcinoma of the prostate. Orchiectomy, estrogen therapy, synthetic LHRH analogs and possibly antiandrogens are equally effective frontline treatment modalities. Ketoconazole is indicated in emergency situations, but chronic use is prevented by serious idiosyncratic toxicity and by long term complications. Combined androgen blockade (CAB), with leuprolide (or tryptorelin) and flutamide is more effective than single modality treatment in patients capable of strict treatment compliance. Estramustine phosphate may be as effective as CAB and may be the frontline treatment of choice in sexually active patients. Institution of single modality treatment may be delayed until cancer becomes symptomatic. Controversy lingers over whether the institution of CAB at an earlier time may improve progression free survival (PFS) and survival. Research projects of immediate clinical relevance include: comparison of CAB and estramustine; determination of the optimal time for CAB; study of other forms of CAB; and phase II trials of new cytotoxic agents.

Androgen Antagonists↗
PubMed2002

Pattern of somatic androgen receptor gene mutations in patients with hormone-refractory prostate cancer.

Progression to hormone-refractory growth of prostate cancer has been suggested to be mediated by androgen receptor (AR) gene alterations. We analyzed AR for mutations and amplifications in 21 locally recurrent prostate carcinomas treated with orchiectomy, estrogens, or a combination of orchiectomy and estramustine phosphate using fluorescence in situ hybridization, single-strand conformation polymorphism, and DNA sequence analyses. Amplification was observed in 4 of 16 (25%) and amino acid changing mutations was observed in 7 of 21 (33%) of the tumors, respectively. Two (50%) tumors with AR amplification also had missense mutation of the gene. Four of five (80%) cancers that were treated with a combination of orchiectomy and estramustine phosphate had a mutation clustered at codons 514 to 533 in the N-terminal domain of AR. In functional studies, these mutations did not render AR more sensitive to testosterone, dihydrotestosterone, androstenedione, or beta-estradiol. Tumors treated by orchiectomy had mutations predominantly in the ligand-binding domain. In summary, we found molecular alterations of AR in more than half of the prostate carcinomas that recurred locally. Some tumors developed both aberrations, possibly enhancing the cancer cell to respond efficiently to low levels of androgens. Furthermore, localization of point mutations in AR seems to be influenced by the type of treatment.

Estramustine↗
PubMed2003

[Significance of docetaxel in the chemotherapy of hormone-refractory prostate cancer].

Docetaxel (Taxotere) is a taxoid derived from the European yew tree, taxus baccata. In 4 phase-II studies docetaxel has important single agent activity with an overall prostate-specific antigen response rate of 42% in hormone refractory prostate cancer. Other phase-II studies suggest that the addition of estramustine to docetaxel results in a higher response rate but also in an increased toxicity. At present Docetaxel with and without estramustine is being evaluated in phase-III studies that will provide definitive information about its role in hormone refractory prostate cancer.

Antineoplastic Agents, Phytogenic↗