bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inhibition of prostatic epithelial cell proliferation by a factor secreted specifically by prostatic stromal cells
Authors: Kooistra Anko , J. König Josée , Keizer Diederick M. , Romijn Johan C. , Schröder Fritz H. 
Published: February 2007

AbstractStromal cells from the prostate were recently shown to inhibit clonal growth of the prostatic carcinoma cell lines PC‐3 (hormone‐independent) and LNCaP (hormone‐sensitive) in coculture. Our study revealed that stromal cell‐conditioned medium strongly inhibited proliferation of PC‐3 and LNCaP cells when grown in monolayer culture. Antiproliferative activity was found to be reversible, and was produced specifically by prostatic stromal cells and not by stromal cells derived from skin, foreskin, uterus, kidney, and Wilms' tumor. Inhibition was not species‐specific, since the cell lines AT‐2.1 and MATLyLu, derived from the Dunning rat prostate tumor, were also sensitive. No inhibition, however, occurred on breast and renal carcinoma cell lines, suggesting a prostate‐specific action. The putative inhibiting factor(s) could be concentrated and partially purified by ammonium sulfate precipitation. The possible role in stromal control of epithelial cell proliferation is discussed.
Comparison of prostate specific antigen, prostate specific membrane antigen, and LNCaP‐based enzyme‐linked immunosorbent assays in prostatic cancer patients and patients with benign prostatic enlargement
Authors: Murphy Gerald. P. , Holmes E. H. , Boynton A. L. , Kenny G. M. , Erickson S. J. , Barren R. J. , Ostenson R. C. 
Published: February 2007

AbstractSerum assays for prostate specific antigen (PSA; monoclonal), for prostate specific membrane antigen (PSM; Western blot), and a LNCaP/7E11.C5‐based competitive enzyme‐linked immunosorbent assay (ELISA) were evaluated in a small number of prostate cancer patients with localized or disseminated disease, and judged to be in clinical progression or remission based on National Prostate Cancer Project (NPCP) criteria. PSA values recognized the presence of clinical progression in localized disease (B1‐C) and to a lesser degree disseminated disease (D1‐D2). In contrast, to a limited degree the ELISA test recognized clinical progression mainly in disseminated disease and chiefly in stage D2. PSM values were elevated in both D1 and D2 but not in a linear fashion as observed with PSA. The ELISA and PSM results may be assessing a different clinical response to prostatic cancer than that recognized by PSA. This could reflect a developing clone of resistant prostatic cells as previously postulated. To further pursue this possibility a secondary generation of monoclonal antibodies to PSM is being developed. The ELISA levels for benign prostatic enlargement were not elevated above normal. In contrast both with PSA and PSM the assays reflected levels significantly above the normal range in benign prostatic hypertrophy (BPH).
Immunohistochemical localization of cathepsin B in neoplastic human prostate
Authors: Sinha Akhouri A. , Wilson Michael J. , Reddy Pratap K. , Gleason Donald F. , Sameni Mansoureh , Sloane Bonnie F. 
Published: February 2007

AbstractCathepsin B (CB) has been shown to degrade extracellular matrix (ECM) proteins, and has been reported to be involved in invasion and metastasis of several types of solid organ tumors in human and animals, but CB has not been studied in human prostate cancer (CAP). Our objective was to determine the CB protein immunostaining pattern in CAP and to correlate the immunostaining with the degree of malignancy as reflected in the Gleason grading system. We used two types of CB antibodies (namely, monospecific, polyclonal antibodies to human liver CB prepared in rabbits, and polyclonal antibody produced in sheep) to establish CB localization patterns in neoplastic prostate. Our analysis showed a heterogeneous CB immunostaining pattern in the neoplastic human prostate. CB immunostaining occurred in many, but not all, of the neoplastic columnar/cuboidal cells of acini and isolated cells, i.e., in small ragged glands and clusters (groups) of invasive cells in the prostatic stroma. We have shown that, in general, there was a positive correlation of the intensity of CB immunostaining with the Gleason histologic score (or Gleason grade sum) tumors, i.e., from the lowest scores through score 8, but many of the tumors with scores 9 and 10 showed little CB immunostaining. Our study indicated that the increased CB immunostaining in the Gleason grade sum 5–8 tumors may be associated with increased degradation of ECM, but not in 9 and 10 despite the fact that the latter tumors are more malignant clinically. In well‐differentiated tumors, fewer CB immunostaining cells were present than the moderately‐differentiated tumors. In other words, most of the stromal invasion of the prostatic ECM occurred in tumors of Gleason grade sums 5–8. We suggest that CB immunostaining might be a useful method to assess stromal invasion of prostatic carcinoma, especially in the higher grade tumors.
Growth inhibition of human prostate tumor cells by an agonist of gonadotrophin‐releasing hormone
Authors: Loop Stephen M. , Gorder Christine A. , Lewis Suzanne M. , Saiers Joseph H. , Drivdahl Rolf H. , Ostenson Richard C. 
Published: February 2007

AbstractThe effect of [D‐Leu6, des‐Gly‐NH210, Proethylamide9]‐GnRH, leuprolide, was determined for the human primary prostate tumor cell line ALVA‐31 by in vitro mitogenic assays. Prostate tumor cell proliferation was inhibited up to 50% by leuprolide. Inhibition was not observed in parallel cultures treated with other low molecular weight bioactive peptides. The incorporation and metabolic reduction of testosterone was not affected by concentrations of leuprolide that were inhibitory in the mitogenic assay. Specific high‐affinity binding of 125I‐labeled leuprolide was also demonstrated on intact tumor cells with an estimated effective median dose (ED50) of <1 × 10–9M. Inhibition of prostate tumor growth was further demonstrated in Balb/c athymic intact and castrate male mice bearing ALVA‐31 tumor xenografts following chronic administration of leuprolide. These data clearly demonstrate that leuprolide can inhibit the growth of a human prostate carcinoma cell line. Studies conducted in castrate animals further suggest an alternative mechanism of growth inhibition that appears to be independent of the suppression of steroid hormone biosynthesis by LHRH analogues.
Isolation of cDNAs that are differentially expressed between androgen‐dependent and androgen‐independent prostate carcinoma cells using differential display PCR
Authors: Blok Leen J. , Vijay Kumar M. , Tindall Donald J. 
Published: February 2007

AbstractIn the development of prostate cancer there is an important transition from androgen‐dependent growth (which can be treated) to androgen‐independent growth (which is beyond medical control). This transition is probably accompanied by genetic changes, resulting in the activation of oncogenes or the inactivation of tumor suppressor genes. In the present manuscript, the isolation of genes that may be involved in advanced, androgen‐independent prostate cancer growth is described.Using differential display PCR, 13 cDNAs were isolated representing genes that are differentially expressed between the androgen‐dependent prostate carcinoma cell line LNCaP and the androgen‐independent prostate carcinoma cell lines PC‐3 and DU 145. These clones were divided into four groups: androgen‐responsive genes (TL5, TL25, TL32, and TL35); genes with a marked decreased expression in one of the prostate cancer cell lines (TL27); genes with a marked, increased expression in one or more of the prostate cancer cell lines (TL4, TL16, TL21, and TL22); and genes with minor (but repeatable) changes in expression between prostate cancer cell lines (TL7, TL15, TL18, and TL33). The 13 genes were analyzed for their sequence information, tissue specificity, and androgen responsiveness in order to identify genes of interest.In summary, differential display PCR appears to provide an attractive alternative to existing molecular techniques to screen for differentially expressed genes in prostate cancer cells.
Inhibition of tumor angiogenesis and the therapeutic ability of linomide against rat prostatic cancers
Authors: Vukanovic Jasminka , Isaacs John T. , Hartley‐Asp Beryl 
Published: February 2007

AbstractLinomide, a quinoline‐3‐carboxamide, has growth‐inhibitory effects against a series of Dunning R‐3327 rat prostatic cancers in vivo [Ichikawa et al.: Cancer Res 52:3022–3028, 1992]. In addition, we have demonstrated that daily linomide treatment can inhibit angiogenic responses in nontumor‐bearing rats and reduce tumor blood flow in tumor‐bearing rats [Vukanovic et al.: Cancer Res 53:1833, 1993]. In the present study we have demonstrated that the reduced tumor blood flow is due to linomide's ability to inhibit tumor angiogenesis, as documented by decreased number of blood vessels in prostatic carcinomas growing in rats treated daily with linomide. Due to linomide's ability to inhibit tumor angiogenesis, and since tumor angiogenesis is required not only for the growth of the primary cancer but also for its ability to metastasize, the effect of linomide on metastasis was directly tested using a quantitation metastasis assay. These in vivo experiments demonstrated that daily linomide treatment decreased by 3‐fold the extent of dissemination of cancer cells to the lungs.To test if this antimetastatic response is due to direct effects of linomide on the metastatic cells themselves as well as an induced effect upon inhibition of tumor angiogenesis, additional studies were performed. These studies demonstrated that linomide is not converted in vivo to metabolite(s) which are directly cytotoxic or cytostatic to the prostatic cancer cells themselves. These studies also demonstrated that linomide does not decrease the attachment, migration, or invasive abilities of metastatic cancer cells. These results suggest that the major mechanism for the antitumor and antimetastatic effects of linomide is via its inhibition of tumor angiogenesis. Additional studies have demonstrated that in vivo linomide treatment results in the apoptotic death of thymocytes. This cytotoxic effect is not required for linomide's antitumor effect, nor is it due to elevated plasma levels of glucocorticoid.
Effects of age, sex steroids, and family relationships on volumes of prostate zones in men with and without prostate cancer
Authors: Meikle A. W. , McWhorter W. P. , Stephenson R. A. , Middleton R. G. , Skolnick M. H. 
Published: February 2007

AbstractBenign prostatic hyperplasia (BPH) and prostate cancer commonly occur together. This suggests that common familial, hormonal, and environmental factors contribute to their development. In men at risk for the development of prostate cancer (at 40 men in 19 families) and aged‐matched unrelated controls (n = 46), we have determined whether familial factors, age, and blood hormone concentrations are related to the transition zone (TZ), peripheral zone (PZ), or total volume of the prostate measured by transrectal ultrasound (TRUS). We determined that the influences of age, prostate cancer (n = 15), and familial status did not significantly affect the relationships reported. Therefore, data from all groups were combined for this study. TZ correlated positively with age (P = 0.003) after controlling for family status, but total prostate volume correlated insignificantly with age (P = 0.08). In addition, the ratio of TZ to PZ volumes also correlated significantly with age in the control group (r = 0.27, P = 0.014). Both TZ and PZ volumes correlated highly (r = 0.91, P < 0.0001, n = 86) with total volume. In addition, total volume correlated significantly (r = 0.71, P < 0.001) with the ratio of the TZ/PZ volumes, which also correlated significantly with each other (r = 0.61, P < 0.0001, n = 86). In contrast to the increase of TZ volume related to total prostate volume, PZ volume declined compared with total volume. Prostate volumes up to 50 ml are predominated by the PZ and above 50 ml by the TZ, which may compress and shrink the PZ. Both TZ and total prostate volume correlated positively with serum estrone concentrations (P = 0.04 and P = 0.003, respectively). These results suggest that the risk of prostate cancer does not contribute to generalized overgrowth of the prostate, including the TZ. However, estrogens and age strongly influence TZ but not PZ volume. Both PZ and TZ volumes rise together until the prostate exceeds 50 ml, when the growth of the TZ appears to exceed the PZ and then to compress it.
Mediation of glucocorticoid receptor function by transforming growth factor beta I expression in human PC‐3 prostate cancer cells
Authors: Reyes‐Moreno Carlos , Frenette Gilles , Boulanger Jocelyn , Lavergne Eliane , Govindan Manjapra V. , Koutsilieris Michael 
Published: February 2007

AbstractWe investigated the role of glucocorticoids in controlling the proliferation of androgen‐independent PC‐3 human prostate cancer cells via the action of transforming growth factor beta 1 (TGF β1). The presence of glucocorticoid receptor (GR) in PC‐3 cells was detected by immunoblotting analysis using a rabbit anti‐GR polyclonal antibody against the synthetic human GR peptide (hGR383–393). In PC‐3 cells, GR bound radiolabeled dexamethasone with an affinity similar to wild‐type GR. In addition, GR‐ligand complex bound radiolabeled DNA as detected by DNA band‐shift analysis on gel electrophoresis and trans‐activated the mouse mammary tumor virus‐thymidine kinase‐chloramphenicol acetyltransferase chimeric gene in transiently transfected PC‐3 cells. Dexamethasone (0.1 up to 100 nM) and TGF β1 (0.5 up to 50 ng/ml) inhibited PC‐3 cell proliferation. TGF β1 and dexamethasone both increased the distribution of PC‐3 cells into the G1/G0 phase of the cell cycle. Platelet‐derived growth factor (PDGF) stimulated the proliferation of PC‐3 cells and overcame dexamethasone's inhibition of PC‐3 cell growth. Dexamethasone's inhibition (10–7M) of PC‐3 cell growth was completely neutralized by RU 486 (10–6M) and partly neutralized by anti‐TGF β1 polyclonal antibody. Furthermore, dexamethasone up modulated the expression of TGF β1 mRNA in PC‐3 cells. Because dexamethasone's inhibition was neutralized at least in part by an anti‐TGF β1 polyclonal antibody and dexamethasone up modulated the expression of TGF β1 mRNA in PC‐3 cells, we conclude that GR function in human PC‐3 prostate cancer cells is mediated at least in part by TGF β1 expression.
In vitro proton magnetic resonance spectroscopy of four human prostate cancer cell lines
Authors: Cornel E. B. , Smits G. A. H. J. , De Ruijter J. E. , Oosterhof G. O. N. , Debruyne F. M. J. , Schalken J. A. , Heerschap A. 
Published: February 2007

AbstractThere is accumulating evidence that some biochemical pathways observable by magnetic resonance spectroscopy, e.g., citrate acid and phospholipid metabolism, are altered in human prostate cancer. Four well‐established human prostate cancer cell lines were therefore studied with magnetic resonance spectroscopy to compare differences in metabolic content with tumor biological behavior. Herein we demonstrate that, although each cell line has its own metabolic profile, relative creatine and citrate levels can be used to discriminate the androgen‐dependent LNCaP cell line from the androgen‐independent DU‐145, TSU, and PC‐3 cell lines.
Cost‐effectiveness analysis in early detection of prostate cancer: An evaluation of six screening strategies in a randomly selected population of 2,400 men
Authors: Gustafsson Ove , Norming Ulf , Nyman Claes R. , Carlsson Per , Svensson Helene 
Published: February 2007

AbstractBased on the findings in an early detection study for prostate cancer [Gustafsson et al.: J Urol 148:1827–1831, 1992] using digital rectal examination (DRE), transrectal ultrasound (TRUS), and prostate‐specific antigen (PSA), a cost‐effectiveness analysis was performed based on 6 screening strategies, namely: 1) DRE of all individuals; 2) TRUS of all individuals; 3) DRE, TRUS, and PSA analysis followed by reexamination of individuals with PSAs ≥7 ng/ml; 4) DRE of individuals with PSAs of ≥4 ng/ml; 5) TRUS of individuals with PSAs of ≥4 ng/ml; 6) DRE and PSA analysis followed by TRUS on individuals with PSAs ≥4 ng/ml.The detection rates of prostate cancer using these 6 strategies were 2.4%, 3.3%, 3.6%, 2.0%, 2.6%, and 3.2%, respectively. Except for costs per detected cancer, costs were also calculated per detected small cancer (≤1.5 cm) and per detected cancer treated for cure. The cost calculations were based on total costs, i.e., direct plus indirect costs.When the 6 strategies were compared, taking into account the detection rate of cancers treated for cure and cost‐effectiveness with respect to cancers treated for cure, strategies 1), 2), 3), and 4) were ruled out as less favorable than the remaining 2 strategies.TRUS of individuals with PSAs ≥4 ng/ml (strategy 5) was the most cost‐effective strategy and detected 80% of the cancers actually treated for cure. Screening with DRE and PSA analysis followed by TRUS of individuals with PSAs ≥4 ng/ml (strategy 6) had a somewhat lower cost‐effectiveness, but detected 90% of the cancers treated for cure.
Survival of patients with localized prostate cancer treated with percutaneous transperineal placement of radioactive gold seeds: Stages A2, B, and C
Authors: Hochstetler Jerald A. , Kreder Karl J. , Loening Stefan A. , Brown C. Kice 
Published: February 2007

AbstractBetween 1984 and 1991, a total of 177 patients with adenocarcinoma of the prostate were treated with transcutaneous, transperineal radioactive gold seeds. Of these 177 patients, 20 were determined to have pelvic lymph node involvement and were excluded from this review. The remaining 157 patients received a median radioactivity dose of 164 mCi with a median follow‐up of 48 months. Cancer‐specific survival at 5 years was 100% for stage A2 and B1, 90% for stage B2, and 76% for stage C cancer. Covariates of grade, total radioactivity administered, age of the patient, and number of seeds implanted did not influence disease‐free survival in a statistically significant manner. Significant complications were observed in two patients.The survival rates of patients treated with 198Au seed implanation for localized cancer are equivalent or better when compared to historical data of patients treated with 125I implantation, external beam radiotherapy, combination radioactive gold seed implantation and external irradiation, and radical prostatectomy. In addition, these comparable survival rates using intersitial 198Au seeds may be achieved with less morbidity.
Prognostic significance of capsular invasion and capsular penetration in patients with clinically localized prostate cancer undergoing radical prostatectomy
Authors: Theiss Matthias , Wirth Manfred P. , Manseck Andreas , Frohmüller Hubert G. W. 
Published: February 2007

AbstractOne hundred thirty patients with an observed follow‐up of more than 10 years after radical prostatectomy were restaged with regard to local extent of the tumor in relation to the prostate capsule. Of 112 patients with surgically staged negative pelvic lymph nodes, 62 had a tumor‐free prostate capsule, 24 had capsular invasion without penetration, and 26 had tumors extending through the capsule of the prostate.Observed overall and disease‐free 10‐year‐survival rates were 79% and 69.4%, respectively, in patients with absence of capsular involvement and 70.8% and 66.7%, respectively, in patients with capsular invasion alone. In patients with capsular penetration, however, the survival rates significantly decreased to 57.7% (P= 0.018) and to 38.5 (P= 0.017), respectively.The overall progression rate was found to be significantly higher in patients with tumors extending through the prostatic capsule (46.2%), as compared to those with absence of capsular involvement (21%;P= 0.014) as well as to those with capsular invasion alone without penetration (25%;P= 0.034).Thus, in contrast to capsular invasion alone, capsular penetration means a poor prognostic indicator, which accounts for a reduced survival expectancy and a higher progression rate following radical prostatectomy. Therefore, tumors with capsular invasion and those with capsular penetration should not be grouped together in the same tumor stage as done in the 1987 edition of the TNM tumor clasification system. © 1995 Wiley‐Liss, Inc.
Tumor suppressor gene P53 mutations in human prostate cancer
Authors: Kubota Yoshinobu , Shuin Taro , Uemura Hiroji , Fujinami Kiyoshi , Miyamoto Hiroshi , Torigoe Soichiro , Dobashi Yasushi , Kitamura Hitoshi , Iwasaki Yoshiko , Danenberg Kathleen , Danenberg Peter V. 
Published: February 2007

AbstractThe genetic background underlying the growth and development of human prostatic cancer is not yet clear. Here we searched for possible mutations in the entire coding region of tumor suppressor gene p53 in primary human prostatic carcinomas, using polymerase chain reaction and single‐strand conformational polymorphism analysis of RNA.We found p53 gene mutations in 4 of 21 cases (19%). DNA sequencing of the polymerase chain reaction products revealed missense point mutations that resulted in amino acid changes in exon 5 or 3 in three cases and single base deletions in exon 7 in two cases. One case contained both a missense point mutation and a single base deletion. Three of these four cases were pathologically diagnosed as poorly differentiated adenocarcinomas, and three of the four cases were clinically localized to stage C or D. None of seven noncancerous prostate tissues nor three well‐differentiated adenocarcinoma tissues showed any mutations.The present results suggest that p53 gene mutation is involved in the late progression steps of human prostate carcinogenesis. © 1995 Wiley‐Liss, Inc.
In vivo and in vitro complex formation of prostate specific antigen with αi‐anti‐chymotrypsin
Authors: Huber Peter R. , Mattarelli Gianfranco , Strittmatter Bernadette , van Steenbrugge Gert Jan , Schmid Hans‐Peter , Maurer Andreas 
Published: February 2007

AbstractComplex formation of prostate specific antigen (PSA) with its inhibitor α1‐anti‐chymotrypsin (ACT) in vivo and in vitro was studied. Patients with benign prostatic hyperplasia (BPH) were treated with the computer assisted device “Prostatron ®.” This instrument acts by means of thermal destruction of prostatic tissue. The effect of the treatment was followed by measurement of serum PSA concentrations using commercially available immunoassays from Roche (Cobas® Core), Wallac (Delfia®) and Abbot (IMx®) and Hybritech Tandem®. Serum samples were further analyzed by molecular sieving on S.300 (Pharmacia) and analyzed for PSA by immuno assay. The complex formation of PSA with ACT in serum was studied, demonstrating this process to be influenced by external stimulus. Patient sera revealing initially normal PSA levels (3 to 5 ng/ml) were stimulated to very high levels of PSA (≥ 140 ng/ml) by Prostatron® treatment. The absolute PSA level depends on the assay system and not only on the staging of the prostate tumor. In addition, complex formation was studied in athymic nude mice and in vitro revealing the possible pathways of PSA release. PSA from LNCAP cells kept in vitro show predominantly uncomplexed (free) PSA, whereas PSA from LNCAP cells injected into nude mice appears in the serum of the animals in complexed form. This demonstrates how in the immunization process free and complexed PSA serve as antigens in the standard procedure for the production of antisera for PSA. This model system also can be used for studies of the release mechanism of PSA into blood circulation. © 1995 Wiley‐Liss, Inc.