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At least 991 records · Page 55Linked to original sources
PubMed1996

Free and complexed prostate-specific antigen serum ratios to predict probability of primary prostate cancer and benign prostatic hyperplasia.

OBJECTIVES: Ratios of free to total prostate-specific antigen (f/t PSA ratio) improved differentiation of benign prostatic hyperplasia (BPH) from prostate cancer (CaP). Using sera obtained at least 1 month prior to biopsy-confirmed diagnosis and logistic regression adjusted for disease prevalence, probability curves are constructed to predict the presence of CaP. METHODS: The patient population included 122 (44%) BPH sera and 155 (56%) prostate carcinoma sera collected prior to any therapy. The total PSA range = 2.0-20.0 ng/mL; median age = 69 years. External reference standards for both free and total PSA assays were used to standardize the assays and correct the ratio. Probability curves and tables for cancer incidence were formulated for a subset of the total test population (total PSA range = 2.0-10.0 ng/mL; 98 BPH, 118 CaP patients) by using logistic regression and prior cancer prevalence statistics derived from a published patient screening study. RESULTS: Median f/t PSA ratios were 0.18 and 0.12 in the overall sample and 0.19 and 0.12 in the subset for BPH and CaP, respectively (P = 0.0001). The median total PSA concentrations for BPH and CaP were 5.8 and 6.7 ng/mL when total PSA range = 2.0-20.0 ng/mL and were 4.9 and 5.9 ng/mL when total PSA range = 2.0-10.0, respectively. CONCLUSIONS: Cancer probability curves were constructed to help guide decisions concerning biopsy and other aspects of prostate cancer disease management. Further validation of this approach in another series of patients is necessary and is planned.

Adult↗
PubMed1989

Receptors for luteinizing hormone-releasing hormone, somatostatin, prolactin, and epidermal growth factor in rat and human prostate cancers and in benign prostate hyperplasia.

Using sensitive multipoint micromethods, we estimated membrane receptors for [D-Trp6]-luteinizing hormone-releasing hormone ([ D-Trp6]-LH-RH), somatostatin (SS-14), human prolactin (hPRL), and epidermal growth factor (EGF) in experimental Dunning rat prostate cancers and in samples of normal human prostate, benign prostatic hyperplasia (BPH), and human prostate cancer (PC) obtained from biopsy, after prostatectomy, or at autopsy. In the Dunning R-3327 rat prostate adenocarcinoma specimens, the receptors were characterized in untreated animals and following in vivo treatment with microcapsules of the agonist [D-Trp6]-LH-RH and the somatostatin analog RC-160. Two populations of binding sites were found for [D-Trp6]-LH-RH, one with high affinity and low capacity and another with low affinity and high capacity. Treatment with [D-Trp6]-LH-RH and RC-160 alone or with the combination of these analogs increased the binding capacity (Bmax) of the low-affinity binding sites for [D-Trp6]-LH-RH and decreased Bmax for hPRL and EGF. Therapy with [D-Trp6]-LH-RH also reduced Bmax of SS-14 binding and dissociation binding constant of high-affinity binding sites for [D-Trp6]-LH-RH, whereas administration of RC-160 or the combination treatment with both analogs increased Bmax of SS-14 binding. These findings are compatible with the view that analogs of LH-RH and SS-14 might exert some direct inhibitory effects on the Dunning prostate cancer. Among 13 human BPH samples examined, only one had receptors for [D-Trp6]-LH-RH, and seven specimens exhibited binding for prolactin. [D-Trp6]-LH-RH receptors were found in all seven samples of human PC but not in any of the eight specimens of normal human prostate. All samples of normal human prostate, BPH, and human PC exhibited binding sites for EGF but not for SS-14. Our findings on the membrane receptors in the human and rat prostate cancers raise the intriguing possibility that LH-RH, acting as a growth factor, along with EGF and prolactin, might be involved in complex interactions that contribute to the promotion of prostate cancer in man.

Adenocarcinoma↗
PubMed1984

[Tissue plasminogen activator activity in early prostatic cancer and in bone metastases of prostatic cancer].

Most malignant cells exhibit increased plasminogen activator activity which, in turn, leads to the formation of the fibrinolytically active enzyme, plasmin. Since solid tumours in man are surrounded by a fibrin network, the fibrinolytic activity of the tumour may influence tumour growth and metastasis. In the present study plasminogen activator activity, as assessed in purified extracts, was compared in benign hyperplasia of the prostate (group A, n = 6), non-metastasizing+ prostatic carcinoma (group B, n = 26), and in prostatic carcinoma with bone metastasis (group C, n = 10). Plasminogen activator activity was significantly higher in prostatic carcinoma than in hyperplasia, but there was no significant difference in plasminogen activator activity between prostate carcinoma with or without bone metastasis. However, plasminogen activator activity in the bone metastasis cells was significantly higher than in the primary tumour. If a positive correlation between fibrinolytic activity of the tumour and the metastasizing capacity were postulated, particular importance could be attached to bone metastasis in prostatic cancer.

Bone Neoplasms↗
PubMed2005

Molecular and phenotypic heterogeneity of metastatic prostate cancer.

Metastatic prostate cancer remains a prevalent disease in the United States that requires detailed characterization of its pathobiology. In the December 2004 issue of Cancer Research, a comprehensive study by Shah et al. demonstrated that metastatic androgen-independent prostate cancer is a collective group of diseases even within the same patient. Understanding the molecular and phenotypic determinants of this heterogeneity is essential in assessing therapeutic outcomes in the management of prostate cancer progression.

Genetic Heterogeneity↗
PubMed1996

p53 immunoreactivity as prognostic marker for cancer-specific survival in prostate cancer.

OBJECTIVES: The objective of this study was to evaluate the role of p53 immunoreactivity as a prognostic marker in prostate cancer. METHODS: The nuclear accumulation of the aberrant p53 protein was determined by immunohisto-chemistry on surgical specimens and related to stage, grade and cancer-specific survival in 186 prostate cancer patients treated with transurethral resection and subsequent surveillance. RESULTS: There was a significant correlation between p53 staining and grade: 2% of the highly differentiated, 8% of intermediately, and 21% of the poorly differentiated tumors stained. Patients with p53-positive tumors had a significantly shorter survival (52 months) than the p53-negative group (123 months). However, in a Cox multiple regression analysis of p53 status, tumor stage, grade, metastasis and age, p53 lost its significance as an independent predictor. CONCLUSIONS: p53 is a rare and late event in prostate cancer, indicating that other molecular mechanisms may be of greater importance in the development of prostate cancer. The predictive value of p53 apparently depends on its association with high grade and advanced stage, and it is not a useful prognostic marker in prostate cancer. However, p53 status could play a role in the evaluation of patients prior to radiotherapy since p53 inactivation may produce radioresistant tumors.

Adult↗
PubMed2003

Identification of new prostate stem cell antigen-derived peptides immunogenic in HLA-A2(+) patients with hormone-refractory prostate cancer.

PURPOSE: Prostate cancer refractory to hormonal manipulation requires new treatment modalities. In the present study we attempted to identify prostate stem cell antigen (PSCA)-derived peptides immunogenic in HLA-A2+ prostate cancer patients in order to develop peptide-based immunotherapy against hormone-refractory prostate cancer (HRPC). METHODS: Eleven different PSCA-derived peptides, which were prepared based on the HLA-A2 binding motif, were examined to determine whether they would be recognized by cellular and humoral immune responses in 12 HLA-A2+ patients (11 with HRPC and 1 with non-HRPC). RESULTS: Among the PSCA-derived peptides, PSCA 7-15 and PSCA 21-30 peptides effectively induced HLA-A2-restricted peptide-specific and tumor-reactive cytotoxic T lymphocytes (CTLs) from peripheral blood mononuclear cells (PBMCs) of HLA-A2+ patients. The PSCA 21-30 peptide was capable of inducing peptide-specific CTLs in both cancer patients and healthy donors, whereas the PSCA 7-15 peptide was immunogenic in only cancer patients. Immunoglobulin G (IgG) reactive to the PSCA 21-30 peptide was detected in plasma of most patients and healthy donors, whereas IgG reactive to PSCA 7-15 was undetectable in all cases. These results indicate that the former peptide elicits both cellular and humoral immune responses in both patients and healthy donors, whereas the latter elicits only cellular responses in patients. CONCLUSION: These two PSCA peptides should be considered for use in clinical trials of immunotherapy for HLA-A2+ HRPC patients.

Antibody Formation↗
PubMed2002

A prostate cancer primer.

Prostate cancer is the second most commonly diagnosed malignancy in men and remains the second leading cause of cancer deaths among this population. Early screening and diagnosis, advances in preventive techniques, and existing cutting-edge treatments are part of a multidimensional approach in an ongoing battle to improve the health of millions of men. This primer was designed to familiarize nurses with basic facts about prostate cancer and its management. The epidemiology of prostate cancer and its risk factors, clinical manifestations, screening and early diagnosis, treatment strategies, and implications for urologic nurses are presented.

Humans↗
PubMed2005

Insulin-like growth factor binding protein-6 inhibits prostate cancer cell proliferation: implication for anticancer effect of diethylstilbestrol in hormone refractory prostate cancer.

Diethylstilbestrol (DES) is a synthetic oestrogen, and its anticancer effects are exerted in androgen-dependent prostate cancer. The administration of DES decreases serum testosterone to castration levels. However, in androgen-independent prostate cancer patients, who are already orchiectomised, the administration of DES improves symptoms and decreases prostate-specific antigen (PSA). The mechanisms responsible for these direct inhibitory effects have been explained as biological actions not mediated by oestrogen receptors. We assessed the gene expression profiles of prostate cancer cells treated with DES, and investigated direct inhibitory effects of DES. DES inhibited the proliferation of LNCaP and PC-3 cells. cDNA microarray analysis showed that expression of many genes was downregulated by DES. However, insulin-like growth factor binding protein 6 (IGFBP-6) gene expression levels were upregulated in PC-3 cells. IGFBP-6 gene expression and protein levels significantly increased after DES treatment. Recombinant IGFBP-6 inhibited cell proliferation, and the inhibitory effect of DES was neutralised by anti-IGFBP-6 antibody. From the immunohistochemical analysis of IGFBP-6 using biopsy samples from androgen-independent prostate cancer, we found IGFBP-6 expression in androgen independent prostate cancer, and that DES treatment increased the IGFBP-6 staining intensity of the cancer cells in one sample. These findings suggested that DES induces IGFBP-6, which inhibits cell proliferation in an androgen-independent prostate cancer cell line, PC-3. IGFBP-6 therefore might be involved in the direct effects of DES in androgen-independent prostate cancer.

Antineoplastic Agents, Hormonal↗
PubMed2001

Three-dimensional grayscale ultrasound: evaluation of prostate cancer compared with benign prostatic hyperplasia.

OBJECTIVES: To compare the accuracy of the detection, localization, and staging of prostate cancer using transrectal three-dimensional (3D) grayscale ultrasonography (3D-US) with conventional transrectal two-dimensional grayscale ultrasonography (2D-US). METHODS: Fifty patients with clinical localized prostate cancer scheduled to undergo radical retropubic prostatectomy and 50 patients with clinical benign prostatic hyperplasia underwent transrectal ultrasound investigations (2D and 3D). The prostate images were retrospectively analyzed by two ultrasound experts unaware of the clinical findings. The images of the prostate cancer group were correlated with the whole-mount histologic specimens of the prostate. RESULTS: All percentages are given for experts 1 and 2. The sensitivity, specificity, and accuracy for the detection of prostate cancer without considering the definitive localization of the tumor for 2D-US was 72% and 76%, 50% and 54%, and 63% and 64%, respectively; for 3D-US, the rates were 82% and 88%, 40% and 42%, and 61% and 65%. The sensitivity, specificity, and accuracy of the combination of 2D-US with 3D-US was 88% and 90%, 36% and 38%, and 62% and 64%, respectively. The sensitivity, specificity, and accuracy for the exact localization of the prostate tumor for 2D-US was 44% and 46%, 50% and 54%, and 47% and 50%, respectively; for 3D-US, they were 52% and 62%, 40% and 42%, and 46% and 52%. The staging of prostate cancer using 3D-US was correct in 49% (expert 1) and in 57% (expert 2) of patients. No difference was observed between 2D-US and 3D-US for accurate staging. Both experts judged the interpretation of 3D-US images as superior to that of 2D-US images. CONCLUSIONS: Although 3D-US had statistically significant increased sensitivity in the detection of lesions and decreased specificity compared with 2D-US, 3D-US did not result in significant clinical improvement in the detection and staging of prostate cancer.

Adenocarcinoma↗
PubMed2004

Bicalutamide 150 mg in addition to standard care in patients with localized or locally advanced prostate cancer: results from the second analysis of the early prostate cancer program at median followup of 5.4 years.

PURPOSE: We evaluated the efficacy and tolerability of 150 mg bicalutamide daily given in addition to standard care, in patients with localized or locally advanced prostate cancer. MATERIALS AND METHODS: The bicalutamide Early Prostate Cancer program consists of 3 randomized, double blind, placebo controlled trials prospectively designed for combined analysis. A total of 8,113 men with T1b-T4, M0, any N (N0 in 1 trial) prostate cancer were randomized to bicalutamide 150 mg/day (4,052) or placebo (4,061) in addition to standard care (radical prostatectomy, radiotherapy or watchful waiting). Primary end points were objective progression-free survival (PFS) and overall survival. RESULTS: At median 5.4 years of followup (21.6% progression events) bicalutamide significantly improved PFS in the overall population. This result was driven by positive results in trials 24 and 25, with the North American trial (trial 23) showing no difference. Patients with locally advanced disease gained most benefit from bicalutamide in terms of PFS, irrespective of underlying therapy. Overall survival was similar in the bicalutamide and placebo groups, across the program and in each trial. Among watchful waiting patients survival appeared to be improved with bicalutamide in those with locally advanced disease, whereas survival appeared to be reduced with bicalutamide in those with localized disease. The most common adverse events with bicalutamide were gynecomastia and breast pain. Other adverse events occurred with a similarly low incidence in the 2 treatment groups. CONCLUSIONS: This analysis confirms that bicalutamide provides benefit in patients with locally advanced disease. The current data suggest that early or adjuvant hormonal therapy for patients at low risk of disease progression, such as those with localized disease, is not appropriate.

Adult↗
PubMed2000

Hormonal sensitivity following endocrine withdrawal in hormone-refractory prostate cancer.

BACKGROUND: Prostate cancer is proposed to be classified according to hormonal sensitivity. The purpose of this study is to examine hormonal sensitivity of the patient with refractory prostate cancer subsequent to primary hormonal therapy. METHODS: Sixteen patients with refractory prostate cancer subsequent to primary combination hormonal therapy were enrolled in this study. All 16 patients with progressive disease after elimination of oral hormonal agents or after response following hormonal withdrawal received dexamethasone (DXM) (initially 1.5 or 1.0 mg, then tapered to 0.5 mg) orally not only for the purpose of second-line hormonal therapy but also as an indicator of hormonal sensitivity. RESULTS: Overall, 4 patients showed a prostate-specific antigen (PSA) decrease of >50% from baseline on discontinuation of hormonal agents, while another 7 patients showed a PSA decrease of <50%. Five patients showed PSA level was progressed after the withdrawal. In all patients with PSA values that decline not only >50% but also <50% following oral endocrine withdrawal, the fall in PSA values had been >50% following DXM administration. However, the PSA value in the patients with PSA progression following the oral endocrine withdrawal kept rising after DXM administration. CONCLUSIONS: The findings in this study would just suggest a possible relationship between DXM sensitivity and the response to endocrine withdrawal. The patients whose PSA values decline following oral endocrine withdrawal may maintain hormonal sensitivity.

Adenocarcinoma↗
PubMed2004

Conjugated linoleic acid inhibits proliferation and modulates protein kinase C isoforms in human prostate cancer cells.

Prostate cancer is the second most common cancer in men. The disease etiology is poorly understood, but diet and lifestyle are contributory factors. Conjugated linoleic acids (CLAs), naturally occurring fatty acids in ruminant food products, have antitumor properties in animal models of cancer and antiproliferative effects on cancer cells in vitro. The cellular mechanisms by which CLAs elicit these effects are unclear, particularly for prostate cancer cells. We have previously identified protein kinase C (PKC) isoforms, alpha, delta, iota, mu, and zeta in LNCaP prostate cancer cells. The objective of this study was to determine the effects of CLAs (individual cis-9, trans-11 and trans-10, cis-12 isoforms and a 50:50 mixture) on PKC isoform abundance in LNCaP cells. Confluent cells were treated with 6, 25, and 50 microM CLA for 0.5, 6, and 24 h. Cytosol and membrane protein fractions were assayed for PKC isoforms (mainly alpha and delta but also iota, mu, and zeta) by Western blot analysis using specific antibodies. CLAs clearly modulated the abundance of these PKC isoforms, both positively and negatively, depending on the isoform, concentration of CLAs, and period of treatment. Increased PKC-delta and decreased PKC-iota membrane abundance was consistent with CLAs eliciting increased apoptosis and, in part, with their antitumor effects.

Cell Division↗
PubMed2000

Prostate cancer screening.

Prostate cancer is an important and growing public health problem. PSA testing is able to lead to the identification of large numbers of cases of prostate cancer while still asymptomatic. This provides the potential for important reductions in prostate cancer mortality through the introduction of screening programs. The most reliable evidence that this potential can be realised can only come from randomised controlled trials (RCTs). Alternative sources of evidence are compared with that from RCTs; the costs of a wrong decision would be high and it is argued that the case for RCTs is clear.

Case-Control Studies↗
PubMed2005

4-year prostate specific antigen progression and diagnosis of prostate cancer in the European Randomized Study of Screening for Prostate Cancer, section Rotterdam.

PURPOSE: The European Randomized Study of Screening for Prostate Cancer investigates the impact of screening on prostate cancer mortality and contributes to a better understanding of available screening tests. The present study evaluates the predictive value of a prostate specific antigen (PSA) increase to PSA 3.0 ng/ml or greater in a 4-year period in men who present with low PSA values (less than 3.0 ng/ml) at first screen. MATERIALS AND METHODS: A total of 42,376 men were randomized to screening vs control in Rotterdam. Of 6,467 men 5,771 had PSA values of less than 3.0 ng/ml, did not undergo biopsy at baseline and were rescreened after 4 years with PSA 3.0 ng/ml or greater as biopsy indication. PSA progression in a 4-year interscreening interval is evaluated by determining the positive predictive values, detection rates and parameters of aggressiveness of round 2 cancers. RESULTS: PSA progression to more than 3.0 ng/ml occurred in 0.9%, 9.3% and 48.6% of men who presented with PSA values less than 1.0, 1 to 1.9 and 2 to 2.9 ng/ml, respectively, in round 1. Their respective positive predictive values amounted to 19.0%, 23.8% and 27.9%. Cancer detection rates increased with increasing PSA values in round 1. The distribution of low, moderate and high risk cancers depends on round 2 but not on round 1 PSA ranges. CONCLUSIONS: PSA progression to the (arbitrary) cutoff value of 3.0 ng/ml and the diagnosis of prostate cancer in round 2 screening with a 4-year interval depends strongly on PSA values at the time of the 1st screen. These observations will be helpful to design future screening procedures. With levels less than 2.0 ng/ml PSA progression to levels of 3.0 ng/ml or greater is rare as it was seen only in 4.8% of all men.

Humans↗
PubMed2005

Description of the International Consortium For Prostate Cancer Genetics, and failure to replicate linkage of hereditary prostate cancer to 20q13.

The International Consortium for Prostate Cancer Genetics (ICPCG) is an international collaborative effort to pool pedigrees with hereditary prostate cancer (PC) in order to replicate linkage findings for PC. A strength of the ICPCG is the large number of well-characterized pedigrees, allowing linkage analyses within large subsets. Given the heterogeneity and complexity of PC, the historical difficulties of synthesizing different studies reporting positive and negative linkage replication, and the use of different statistical analysis methods and different stratification criteria, the ICPCG provides a valuable resource to evaluate linkage for hereditary PC. To date, linkage of chromosome 20 (HPC20) to hereditary PC has been one of the strongest linkage signals, yet the efforts to replicate this linkage have been limited. This paper reports a linkage analysis of chromosome 20 markers for 1,234 pedigrees with multiple cases of PC ascertained through the ICPCG, and represents the most thorough attempt to confirm or refute linkage to chromosome 20. From the original 158 Mayo pedigrees in which linkage was detected, the maximum heterogeneity LOD (HLOD) score, under a recessive model, was 2.78. In contrast, for the 1,076 pedigrees not included in the original study, the maximum HLOD score (recessive model) was 0.06. Although, a few small linkage signals for chromosome 20 were found in various strata of this pooled analysis, this large study failed to replicate linkage to HPC20. This study illustrates the value of the ICPCG family collection to evaluate reported linkage signals and suggests that the HPC20 region does not make a major contribution to PC susceptibility.

Aged↗
PubMed1984

Age, environmental factors and prostatic cancer.

Although prostatic cancer is evident late in life, pathological evidence suggests this disease is initiated earlier in life. As prostatic cancer is an endocrine associated disease and as adult hormone profiles are established during puberty, it was of interest whether difference in pubertal hormone levels occurred in populations at low or high risk for prostatic cancer. Accordingly we have investigated the hormone profiles in rural Black South African and urban white boys during puberty. It has been suggested that the timing of puberty is modified by environmental factors and that there is a concomitant control of gonadotrophin release and food intake by CNS-peptide hormones. It is therefore postulated that dietary factors during puberty modify the gut-CNS peptide hormones which in turn control the hypothalamic-pituitary-testicular axis. Distinct difference in plasma androgen and gonadotrophins between the two races are in part concordant with a modification of CNS-peptide hormones by environmental factors during puberty.

Adolescent↗
PubMed1999

Osteopontin expression in prostate cancer and benign prostatic hyperplasia.

OBJECTIVES: Osteopontin (OPN), a secreted adhesive glycoprotein, has been shown to be produced in excessive amounts in a variety of experimental models of malignancy. Increased levels of OPN exist in blood from the lungs, breasts, and gastrointestinal tracts of cancer patients with metastases. However, there have been no reports on the expression of OPN in human urological malignancies. The present study investigates the presence of OPN in adenocarcinoma of the human prostate and in benign prostatic hyperplasia (BPH). PATIENTS AND METHODS: Using prostate tissue from 34 patients with primary prostate cancer, 13 patients with prostate cancer after having undergone hormonal therapy, and 12 patients with BPH, formalin-fixed paraffin sections were prepared. Specimens were obtained by needle biopsy or radical prostatectomy. Immunohistochemical staining (ABC method) was then performed. Staining was divided into either negative or positive categories. RESULTS: Positive staining of OPN was observed on cancer cells and macrophages in 52.9% of the primary prostate cancers and 14.5% of the prostate cancers after hormonal therapy. In BPH specimens, 66.7% of the cases displayed positive staining of OPN. The staining level of OPN showed no correlation with serum prostate-specific antigen, but did correlate with stage, differentiation, and Gleason's score. CONCLUSIONS: The result postulates that the expression of OPN is an indicator of cell differentiation; however, it cannot be used as a marker of malignancy in prostate cancer.

Adenocarcinoma↗