bluuebunny/crossref_metadata_2025_split huggingface dataset:
Socioeconomic status, urbanization grade, and prostate cancer
Authors: van der Gulden J. W. J. , Kolk J. J. , Verbeek A. L. M. 
Published: February 2007

AbstractIn a population‐based case‐referent study, carried out in The Netherlands, the relationship between socioeconomic status (SES) and urbanization grade on the one hand and prostate cancer incidence on the other has been investigated. Two explanations for a potential association have been taken into account. First, there is a relationship with SES class (or with urbanization grade) in the past, referring to an effect on the induction or promotion of prostate cancer caused by variation in exposure to particular risk factors. Second, there is a relationship with current SES (or urbanization grade), resulted in differences in medical screening. Study data were obtained by means of a validated mailed questionnaire, which has been completed and returned by 345 cases (with histologically confirmed prostate cancer) and 1,346 referents (patients with benign prostate hyperplasia). The response was 79%. No clear relationship was observed with SES, based on the major job held between 1960‐1970 (the period of cancer induction), nor was this the case with SES based on the longest‐held job (as a proxy for current SES). A slight, but statistically non‐significant, trend was found of higher risks in subjects living in rural areas, with an urban/ rural ratio of 0.79. Considering the results of this study and those of previous studies reviewed in this paper, it might be doubted that any relationship is to be found between prostate cancer risk and SES or urbanization grade. © 1994 Wiley‐Liss, Inc.
Growth, morphology, and morphometry of human hypertrophic prostate cells treated with suramin in vitro
Authors: De Angeli Sergio , Fandella Andrea , Conconi Maria Teresa , Anselmo Giuseppe , Parnigotto Pier Paolo 
Published: February 2007

AbstractThis work studies the effects of suramin on the growth and morphology of cell strain U285, obtained from human prostate hypertrophic tissue and cultured in vitro. The FRAME cytotoxicity test was performed to evaluate the inhibition of growth induced by suramin. Cells were exposed to suramin at the time of seeding and 24 hours later; neutral red was added with and without suramin. An optical microscope connected to a computer‐aided system and a scanning electron microscope were used to study morphological changes induced by suramin. Growth inhibition depends on drug concentration and exposure period. Moreover, the effect of suramin on neutral red uptake is reversible. Suramin 1,000 μM causes the cells to become spheroid, and they fail to form a monolayer. Our data indicate that the addition of suramin during the lag phase decreases the rate of cell proliferation. © 1994 Wiley‐Liss, Inc.
Comparative analysis of epidermal growth factor receptor gene expression and protein product in benign, premalignant, and malignant prostate tissue
Authors: Turkeri Levent N. , Sakr Wael A. , Wykes Susan M. , Grignon David J. , Pontes J. Edson , Macoska Jill A. 
Published: February 2007

AbstractIn order to more clearly define the status of epidermal growth factor receptor (EGFR) in prostate cancer, expression of EGFR transcript and protein was analyzed in paired samples of benign and malignant tissues from 30 radical prostatectomy specimens. Prostate tumors and high grade prostatic intraepithelial neoplasias (PINs) expressed significantly less EGFR protein than benign tissues or low grade PINs (P < 0.001). Expression of EGFR mRNA was analyzed in a subset of the same samples, and was higher in more prostate tumors than benign specimens (P < 0.05). However, differences in mean mRNA expression between malignant and benign tissues were not significant. EGFR mRNA was expressed at moderate or low levels in equivalent numbers of PIN lesions. These results suggest that, although EGFR mRNA expression is somewhat elevated in prostate tumors, EGFR protein expression may be down‐regulated in the same malignant tissues. Furthermore, our data demonstrate phenotypic similarity between prostate tumors and high grade PIN at the level of EGFR protein expression. © 1994 Wiley‐Liss, Inc.
Western blot assay for prostate‐specific membrane antigen in serum of prostate cancer patients
Authors: Rochon Yvan P. , Horoszewicz Julius S. , Boynton Alton L. , Holmes Eric H. , Barren Robert J. , Erickson Sheila J. , Kenny Gerald M. , Murphy Gerald P. 
Published: February 2007

AbstractThere is a need for the development of new diagnostic tools for the early detection of prostate cancer. A candidate molecule for a new screening test is a prostate‐specific membrane antigen (PSM) recognized by the monoclonal antibody 7E11.C5. We carried out studies aimed at identifying PSM in the serum of normal and benign prostatic hyperplasia (BPH) donors and patients with adenocarcinoma of the prostate, in order to judge whether the development of a serum assay using this marker was feasible. By Western blotting, we found significant levels of PSM in serum samples from prostatic cancer patients, in the seminal fluid of pooled normal donors, in BPH patients, and in normal male sera. Similar to prostate‐specific antigen (PSA), PSM was present in seminal plasma in higher concentrations than in serum, and PSM levels in prostatic cancer patients were significantly higher than in normal controls. These data suggest that the development of an assay utilizing the PSM and new monoclonal antibodies directed against the antigen, could provide a feasible test for prostatic cancers. © 1994 Wiley‐Liss, Inc.
Accumulation of the p53 protein occurs more frequently in metastatic than in localized prostatic adenocarcinomas
Authors: Myers Russell B. , Oelschlager Denise , Srivastava Sudhir , Grizzle William E. 
Published: February 2007

AbstractMutations of the p53 gene result in increased stability and accumulation of the p53 protein, permitting p53 protein detection by immunohistochemical techniques. We have utilized immunohistochemistry to examine accumulation of the p53 protein at various stages of progression in prostatic adenocarcinomas. p53 protein accumulation was detected using the monoclonal antibody BP53‐12‐1 in 3 of 28 (11%) localized prostatic adenocarcinomas, and in prostatic intraepithelial neoplasia (PIN) in 1 of 16 (6%) specimens. In contrast, p53 protein was detected in 9 of 16 (56%) primary prostatic adenocarcinomas that were metastatic (stage D), and in 10 of 18 (56%) matching metastases to lymph nodes from these same patients. Thus, we observed a higher incidence of p53 protein accumulation in matching primary and metastatic lesions of patients with stage D adenocarcinoma than in localized (nonmetastatic) adenocarcinomas. We also found that an antigen retrieval solution (ARS) aided in the detection of p53 protein accumulation in prostatic adenocarcinomas. The results indicate that accumulation of p53 protein occurs prior to metastasis, and identifies a subclass of prostatic adenocarcinomas that express a high potential for metastasis. © 1994 Wiley‐Liss, Inc.
Proliferation‐dependent vs. independent programmed cell death of prostatic cancer cells involves distinct gene regulation
Authors: Furuya Yuzo , Isaacs John T. 
Published: February 2007

AbstractAndrogen‐independent Dunning R‐3327 AT‐3 rat prostatic cancer cells can be induced to undergo programmed cell death in either a proliferation‐dependent or independent manner depending upon the therapeutic agent used. In the present study, 5‐fluorodeoxyuridine (5‐FrdU) was used to induce proliferation‐dependent death of the AT‐3 cells via its ability to inhibit thymidylate synthetase. Ionomycin and thapsigargin were used to induce proliferation‐independent death of these cells via their ability to sustain an elevation in intracellular free Ca2+. Based upon the temporal sequence of DNA fragmentation, morphologic changes, and loss of cell viability, each of the three test agents, at the doses used, induces the programmed death of AT‐3 cells with essentially identical kinetics. Based upon these similarities, comparisons of the pattern of gene expression during the proliferation‐dependent (i.e., 5‐FrdU‐induced) vs. proliferation‐independent (i.e., ionomycin and thapsigargin‐induced) programmed death of AT‐3 cells allow identification of genes whose enhanced expression is involved in the initiation vs. completion of programmed cell death. Based upon this approach, enhanced H‐ras and TRPM‐2 expression is associated with initiation of proliferation‐dependent programmed death of AT‐3 cells while enhanced c‐myc, calmdulin, and α‐prothymosin expression is associated with initiation of proliferation‐independent programmed death of these cells. In contrast, enhanced expression of glucose‐regulated 78 kilodalton and tissue transglutaminase genes are associated with the completion of programmed cell death, since their expression is enhanced in both proliferation‐dependent and independent programmed cell death of AT‐3 cells. © 1994 Wiley‐Liss, Inc.
Mitotic activity and prognosis in prostatic adenocarcinoma
Authors: Vesalainen S. , Talja M. , Lipponen Pertti , Syrjänen K. 
Published: February 2007

AbstractMitotic figures were quantitated by two different methods (number of mitotic figures in 10 high power fields, MI; number of mitotic figures/mm2of neoplastic epithelium, M/V) in a series of 303 prostatic adenocarcinomas, and the results were related to clinical and histological features as well as to prognosis. Gleason score and mitotic indices were significantly interrelated. Invasive T3–4 tumors showed higher mitosis counts than did the local ones, and metastasis at the time of diagnosis was related to mitotic indices as well. Progression and progression‐free survival were related significantly to Gleason score and mitoric indices. In univariate survival analysis, T‐category, M‐category, Gleason score, MI, and M/V were significant prognostic factors. In multivariate analysis, independent predictors of survival were M‐category, T‐category, Gleason score, patient age, and the M/V index. If the Gleason score was not included, M/V included all the available prognostic information in T1–2M0 carcinomas. The results show that, in addition to the conventional Gleason grading system, mitotic indices are useful prognostic parameters while evaluating the long‐term prognosis in prostatic adenocarcinoma.
Evaluation of three different AgNOR counting methods in advanced carcinoma of the prostate
Authors: Ahiskah Rengin , Ekicioǧlu Gülsün , Küllü Sevgi , Alican Yusuf , Çevik Ibrahim , Akdaş Atif 
Published: February 2007

AbstractWe applied the silver staining of nucleolar organizer regions (AgNOR) technique to the pretreatment biopsies of 50 cases of advanced prostate cancer. Three different counting methods were utilized in the enumeration of AgNORs. All methods yielded statistically significant differences of mean AgNOR counts of groups defined by high and low WHO, and by Gleason grades. However, there was overlap among groups, and further analysis of counts by grouping of patients according to their stage, response to treatment, and prognosis was not conclusive. Replicate counts were performed in 10 cases. While intraobserver reproducibility was high by all methods, only the second counting method yielded nonsignificant interobserver variability. There was a significant intratumoral heterogeneity of AgNOR scores. Lack of technical standardization, low reproducibility, and lack of correlation with prognosis limit the use of AgNOR counts in advanced carcinoma of the prostate. &1995 Wiley‐Liss, Inc.
Identification of a prostate inhibitory substance in a pollen extract
Authors: Habib Fouad K. , Ross Margaret , Lewenstein Ari , Zhang Xin , Jaton Jean Claude 
Published: February 2007

AbstractRecently, much attention has focused on the treatment of BPH with the pollen extract, Cernilton. The present investigation was designed to identify the active component in this agent which might be responsible for the symptomatic relief of BPH as previously reported [1,2]. Sequential purification of the active component present in the pollen extract was carried out by a combination of dialysis, gel filtration, and reverse phase chromatography. To monitor the biological activity of each of the purified fractions, a biological assay employing the human prostate cancer cell line DU145 was undertaken.While we have identified a number of constituent components in the pollen extract, only one fraction designated V‐7 (FV‐7) maintained a strong inhibitory effect on the growth of DU145 cells. The inhibition was time‐ and dose‐dependent, and the concentrations of FV‐7 required to reduce the cell numbers by 50% (IC50) after 2 days of exposure was 5 μg/ml. FV‐7 was also inhibitory towards the primary culture of prostate stroma and epithelial cells, with the stroma/fibroblast showing greater sensitivity towards the HPLC‐purified component. However, it should be noted that this inhibitory activity measured in the primary culture cells was only achieved at higher concentrations of FV‐7. Preliminary characterization of the active ingredient identified FV‐7 as DIBOA which is a cyclic hydroxamic acid. FV‐7 and DIBOA induce similar inhibitory effects on the growth of DU145 cells.
Genetic instability assessed by sister chromatid exchange analysis in the dunning R‐3327 rat prostatic adenocarcinoma model and its relationship to metastatic potential
Authors: Sharief Yousuf , Mohler James L. 
Published: February 2007

AbstractThe original Dunning R‐3327 tumor, described in 1961, has given rise to distinct sublines of different metastatic potentials. The different phenotypes cannot be explained by differences in chromosomal number, DNA content, or nuclear pleomorphism. Sister chromatid exchange is an interchange between two strands of DNA indicative of DNA damage. The frequency of sister chromatid exchanges is a well‐accepted measure of genetic instability. To determine whether an assay of genetic instability could distinguish sublines capable of generating cells of the metastatic phenotype, cells from three sublines of low (<10%) metastatic potential and three sublines of high (>90%) metastatic potential were cultured in 10 μM 5‐bromodeoxyuridine to label DNA. Chromosome preparations were made and sister chromatids were differentiated with Hoechst 33258 dye and Giemsa stain. Sixty metaphase spreads from each subline were scored for SCE and chromosome number. The low metastatic sublines G, AT‐1, and AT‐2 had 0.32 ± standard deviation 0.10, 0.38 ± 0.12, and 0.14 ± 0.05 sister chromatid exchanges per chromosome, respectively. The high metastatic sublines AT‐3, MAT‐Lu, and MAT‐LyLu had 0.55 ± 0.17, 0.32 ± 0.1, and 0.33 ± 0.2 sister chromatid exchanges per chromosome, respectively. Subline differences in metastatic potentials cannot be explained by incidences of sister chromatid exchanges.
Inhibition of prostate cancer growth by vinblastine and tamoxifen
Authors: Pienta Kenneth J. , Replogle Tracy , Lehr Jeff E. 
Published: February 2007

AbstractHormone refractory prostate cancer continues to be an aggressive and fatal disease. Agents which inhibit microtubule function have been found to be cytotoxic to prostate cancer cells in preclinical and clinical settings. It was the aim of this study to assess the activity of tamoxifen and vinblastine, two microtubule inhibitors, in hormone refractory prostate cancer. In clinically achievable concentrations, the combination of tamoxifen and vinblastine was cytotoxic to both Dunning rat prostate adenocarcinoma cell line MAT‐LyLu (MLL) and human prostate cancer cells (PC‐3). In cell cycle analysis assays, tamoxifen and vinblastine inhibited cell cycle transit. In vivo, these two agents inhibited the growth of implanted MLL cells. It appears that tamoxifen and vinblastine may be effective agents for the treatment of patients with hormone refractory prostate cancer.
Androgenic and antiandrogenic control on epidermal growth factor, epidermal growth factor receptor, and androgen receptor expression in human prostate cancer cell line LNCaP
Authors: Ravenna L. , Gulino A. , Lubrano C. , Sciarra F. , Di Silverio F. , D'Eramo G. , Vacca A. , Felli M. P. , Maroder M. , Frati L. , Petrangeli E. 
Published: February 2007

AbstractBoth androgen and antiandrogen treatments enhance the proliferation rate of the hormone‐dependent prostate cancer cell line LNCaP, expressing a mutated androgen receptor (AR). We studied the modification of the expression of epidermal growth factor (EGF), of its receptor (EGF‐R), and of androgen receptor (AR) in the LNCaP cell line, under basal conditions and during androgen (R1881) and antiandrogen hydroxy‐flutamide (OH‐FLU) treatment. After prolonged R1881 administration, a marked increase of EGF release was observed, completely blocked by the addition of OH‐FLU. The Scatchard plot analysis of EGF‐R binding revealed two classes of binding sites with high and low affinity. The administration of OH‐FLU alone or combined with R1881 did not modify the affinity constants, while the low‐affinity component disappeared after androgen administration. Both androgen and antiandrogen administration led to a significant increase of the EGF‐R high‐affinity component. AR mRNA and protein levels were downregulated by R1881 treatment. Following OH‐FLU administration, AR mRNA was slightly downregulated, and there was not a strict parallelism between AR mRNA levels and AR binding capacity. When combined with R1881, OH‐FLU partially counteracted the androgen‐induced AR downregulation. Our data show that EGF‐R binding capacity is the only parameter constantly raised in cell proliferation with respect to quiescent cells, and highlights the nonunivocal action of OH‐FLU on androgen‐induced effects.
Clearance of serum PSA after open surgery for benign prostatic hypertrophy, radical cystectomy, and radical prostatectomy
Authors: Haab François , Delmas Vincent , Boccon‐Gibod Laurent , Meulemans Alain , Boccon‐Gibod Liliane , Dauge Marie Christine 
Published: February 2007

AbstractObjective: To study the clearance of serum prostate‐specific antigen (PSA) after several types of prostatic tissue ablation.Methods: Serum PSA levels were measured (YANG Proscheck ultrasensitive assay) just before surgery, immediately after specimen removal, then twice weekly for 5 weeks or until it was undetectable (<0.05 ng/ml) in patients undergoing radical cystoprostatectomy for bladder cancer (n = 10), or radical prostatectomy for T1 T2 prostate cancer (n = 18) and daily for 6 days after open surgery for benign prostatic hypertrophy (BPH) (n = 10).Results: Open enucleation for BPH: the immediately postoperative PSA level was 6 times its preoperative value. It decreased following a monoexponential curve with a very short half‐life of 0.55 ± 0.39 days, range (0.14–1.3), reaching a value lower than the preoperative level in all cases, except one by day 3. After radical cystoprostatectomy: the decrease of serum PSA is monoexponential with a half life of 1.92 ± 1.2 days (0.57–4.24) reaching undetectable level (<0.05 ng/ml) in all patients by day 21. After radical prostatectomy: 11/18 patients (61%) showed a one‐component exponential decrease in PSA with a half‐life of 2.5 ± 1.33 days (range 0.97–4.6 days), and 7/18 showed a two‐component exponential decrease with a first half‐life of 0.94 ± 0.8 days and a second of 7.62 ± 6.35 days); 100% of the patients reached undetectable serum PSA by day 28 in the first group compared to 14.2% of the patients with a two component exponential decrease (P < 0.01). There was no difference between these groups as far as preoperative PSA levels and specimen pathology were concerned.Conclusion: Serum clearance of PSA after extirpative prostatic surgery is closely related to the type and indication of procedure used. Radical cystoprostatectomy is probably the best model in which to study the pharmacokinetics of PSA.
Longitudinal evaluation of serum androgen levels in men with and without prostate cancer
Authors: Carter H. Ballentine , Pearson Jay D. , Metter E. Jeffrey , Chan Daniel W. , Andres Reubin , Fozard James L. , Rosner William , Walsh Patrick C. 
Published: February 2007

AbstractAndrogens are thought to play a role in the pathogenesis of prostate cancer. We evaluated androgen levels in 3 age‐matched groups of men who were part of the Baltimore Longitudinal Study of Aging: 1) 16 men with no prostatic disease by urologic history and exam (control group); 2) 20 men with a histologic diagnosis of benign prostatic hyperplasia (BPH) who had undergone simple prostatectomy; and 3) 20 men with a histologic diagnosis of prostate cancer (16 with local/regional cancer, and 4 with metastatic cancer). Luteinizing hormone (LH), total testosterone (T), and free T were measured on stored AM sera by radioimmunoassay (RIA). Free T was also calculated from the measured concentrations of total T and sex hormone binding globulin (SHBG). The median number of repeated sex steroid measurements ranged from 6–9 over a period from 7–25 years prior to the diagnosis of prostate disease. There were no significant differences in age‐adjusted LH, total T, SHBG, or calculated free T levels among the groups at 0–5, 5–10, and 10–15 years before diagnosis. These data suggest that there are no measurable differences in serum testosterone levels among men who are destined to develop prostate cancer and those without the disease. © 1995 Wiley‐Liss, Inc.
In vitro propagated dendritic cells from prostate cancer patients as a component of prostate cancer immunotherapy
Authors: Tjoa Benjamin , Erickson Sheila , Barren Robert , Ragde Haakon , Kenny Gerald , Boynton Alton , Murphy Gerald 
Published: February 2007

AbstractT cell‐mediated cancer immunotherapy requires efficient antigen‐presenting cells. Dendritic cells (DCs) are arguably the most efficient antigen‐presenting cells studied to date. Individuals with prostate cancer often undergo various therapies which may compromise their immune system, including the state of their DC precursors. We report the in vitro propagation of DCs from peripheral blood of patients with prostate cancer, most of whom are in clinical stages D1 or D2 and have undergone radiation therapy. After 7 days in culture, the number of DCs recovered were 20‐50‐fold higher than those isolated directly from peripheral blood. This number is comparable to findings of previous studies with healthy individuals. Cultured patients' DCs were capable of presenting tetanus toxoid to autologous T cells in vitro. Furthermore, T cells from 2 of 4 patients proliferated when cultured with their DCs and the lysate of a human prostate cancer cell line (LNCaP), demonstrating the potential role of autologous DCs in prostate cancer immunotherapy studies. © 1995 Wiley‐Liss, Inc.