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PubMed1994

Prostate specific antigen cannot distinguish stage T1a (A1) prostate cancer from benign prostatic hyperplasia.

To determine if serum prostate specific antigen (PSA) has decreased the prevalence of stages T1a (A1) and T1b (A2) prostate cancer, and to compare the PSA values for patients with stages T1a and T1b prostate cancer and men with symptomatic benign prostatic hyperplasia, 966 patients undergoing transurethral resection of the prostate were evaluated retrospectively. Included in the study population were 499 consecutive patients who underwent transurethral resection of the prostate for obstructive urinary symptoms in 1986 (no PSA group), and 467 consecutive patients who underwent resection in 1989 and 1990 who were evaluated with serum PSA preoperatively (PSA group). The mean age for the no PSA group was 71 years compared to 70 years for the PSA group (p = 0.36). The overall prevalence of stages T1a and T1b prostate cancer in the no PSA group was 8.6% compared to 10.3% in the PSA group (p = 0.37). The prevalence of stages T1a and T1b prostate cancer in the no PSA group was 3.6% and 5.0%, respectively, compared to 7.3% and 3.0%, respectively, for the PSA group (p = 0.01). In the PSA group the median PSA value for patients with stages T1a and T1b prostate cancer was 3.8 ng/ml compared to 3.4 ng/ml for the patients without cancer (p = 0.59). The median PSA level for the stage T1a cancer patients was 2.4 ng/ml, which was not statistically different from that in patients without cancer (p = 0.31), and the median PSA level for the stage T1b cancer patients was 5.9 ng/ml, which was statistically different than that in patients without cancer (p = 0.01). These findings suggest that the routine use of serum PSA does not decrease the prevalence of stage T1a prostate cancer and that PSA may decrease the prevalence of stage T1b tumors but a larger study would be necessary to document this finding.

Adult↗

PubMed2004

NGEP, a gene encoding a membrane protein detected only in prostate cancer and normal prostate.

We identified a gene (NGEP) that is expressed only in prostate cancer and normal prostate. The two NGEP transcripts are 0.9 kb and 3.5 kb in size and are generated by a differential splicing event. The short variant (NGEP-S) is derived from four exons and encodes a 20-kDa intracellular protein. The long form (NGEP-L) is derived from 18 exons and encodes a 95-kDa protein that is predicted to contain seven-membrane-spanning regions. In situ hybridization shows that NGEP mRNA is localized in epithelial cells of normal prostate and prostate cancers. Immunocytochemical analysis of cells transfected with NGEP cDNAs containing a Myc epitope tag at the carboxyl terminus shows that the protein encoded by the short transcript is localized in the cytoplasm, whereas the protein encoded by the long transcript is present on the plasma membrane. Because of its selective expression in prostate cancer and its presence on the cell surface, NGEP-L is a promising target for the antibody-based therapies of prostate cancer.

Animals↗

PubMed2006

Androgen-deprivation therapy as primary treatment for localized prostate cancer: data from Cancer of the Prostate Strategic Urologic Research Endeavor (CaPSURE).

BACKGROUND: Prostate cancer is largely an androgen-sensitive disease. Androgen-deprivation therapy (ADT) generally has been used for patients with advanced disease. However, ADT is used increasingly as monotherapy for patients with clinically localized disease. The objective of the current report was to describe the characteristics of patients who underwent ADT for the management of localized disease. METHODS: Cancer of the Prostate Strategic Urologic Endeavor (CaPSURE), which is a national disease registry of men with prostate cancer, was screened to identify patients who received treatment with primary ADT (PADT) between 1989 and 2002 for clinically localized disease (T1-T3,Nx/N0,Mx/M0). Clinical data (including Gleason score, prostate-specific antigen [PSA] level, and T classification) and sociodemographic data (including age, race, education, income, and insurance coverage) were analyzed with chi-square statistical tests. Time to failure data were analyzed using log-rank tests, the Kaplan-Meier method, and Cox proportional hazards regression analyses. RESULTS: Of 7045 men, 993 patients (14.1%) with clinically localized disease received primary ADT. Compared with patients who underwent standard treatment, patients who received PADT had higher risk disease (as defined by PSA level, T classification, and Gleason score) and had more comorbidities. Patients who underwent PADT were older, less educated, had lower income, and were more likely to have Medicare than private insurance. The dominant forms of hormone therapy were luteinizing hormone-releasing hormone (LHRH) monotherapy (48.6%) and combined androgen blockade (LHRH agonist and antiandrogens; 38.8%). At 5 years after the initiation of PADT, 67.3% of patients still were receiving treatment with only androgen deprivation, 103 patients (13.8%) had gone on to receive definitive second treatment (radical prostatectomy, external beam radiotherapy, brachytherapy, or cryotherapy), 27 patients (3.9%) underwent second-line therapy (chemotherapy or alternative hormone-deprivation therapy), 22 patients (4.1%) died of prostate cancer, and 146 patients (19%) died of all causes. CONCLUSIONS: The use of PADT therapy appeared to control disease in the majority of patients who received it, at least for an intermediate period. However, such patients appeared to be unique based on sociodemographic characteristics, comorbidity status, and risk factors compared with patients who received other forms of therapy. The impact of PADT on quality of life needs to be compared with standard therapy, and its long-term durability should be assessed better in patients with prostate cancer.

Adenocarcinoma↗

PubMed2004

Prostate stem cell antigen (PSCA) expression in human prostate cancer tissues and its potential role in prostate carcinogenesis and progression of prostate cancer.

BACKGROUND: Prostate stem cell antigen (PSCA) is a recently defined homologue of the Thy-1/Ly-6 family of glycosylphosphatidylinositol (GPI)-anchored cell surface antigens. The purpose of the present study was to examine the expression status of PSCA protein and mRNA in clinical specimens of human prostate cancer (Pca) and to validate it as a potential molecular target for diagnosis and treatment of Pca. MATERIALS AND METHODS: Immunohistochemical (IHC) and in situ hybridization (ISH) analyses of PSCA expression were simultaneously performed on paraffin-embedded sections from 20 benign prostatic hyperplasia (BPH), 20 prostatic intraepithelial neoplasm (PIN) and 48 prostate cancer (Pca) tissues, including 9 androgen-independent prostate cancers. The level of PSCA expression was semiquantitatively scored by assessing both the percentage and intensity of PSCA-positive staining cells in the specimens. Then compared PSCA expression between BPH, PIN and Pca tissues and analysed the correlations of PSCA expression level with pathological grade, clinical stage and progression to androgen-independence in Pca. RESULTS: In BPH and low grade PIN, PSCA protein and mRNA staining were weak or negative and less intense and uniform than that seen in HGPIN and Pca. There were moderate to strong PSCA protein and mRNA expression in 8 of 11 (72.7%) HGPIN and in 40 of 48 (83.4%) Pca specimens examined by IHC and ISH analyses, with statistical significance compared with BPH (20%) and low grade PIN (22.2%) samples (p < 0.05, respectively). The expression level of PSCA increased with high Gleason grade, advanced stage and progression to androgen-independence (p < 0.05, respectively). In addition, IHC and ISH staining showed a high degree of correlation between PSCA protein and mRNA overexpression. CONCLUSIONS: Our data demonstrate that PSCA as a new cell surface marker is overexpressed by a majority of human Pca. PSCA expression correlates positively with adverse tumor characteristics, such as increasing pathological grade (poor cell differentiation), worsening clinical stage and androgen-independence, and speculatively with prostate carcinogenesis. PSCA protein overexpression results from upregulated transcription of PSCA mRNA. PSCA may have prognostic utility and may be a promising molecular target for diagnosis and treatment of Pca.

Duplicate Publication↗

PubMed1998

Leptin in relation to prostate cancer and benign prostatic hyperplasia.

The aim of our study was to determine whether leptin, a hormone implicated in both energy-balance and reproductive function, is involved in the etiology of prostate cancer or benign prostatic hyperplasia (BPH). We compared the serum leptin levels of 43 cases of incident prostate cancer, 41 patients with BPH, and 48 healthy controls, all recruited in Athens, Greece. Multiple logistic regression modeling was used, with adjustment for age, height, body mass index, education, estradiol, testosterone, dihydrotestosterone, dehydroepiandrosterone sulfate, sex hormone-binding globulin and insulin like growth factor 1. Odds ratios per 4 ng/ml increment of leptin were 0.70 [95% confidence interval (CI) (0.32,1.55)] for prostate cancer and 1.06 [95% CI (0.67,1.67)] for BPH. After adjustment for body mass index, serum leptin levels were not significantly correlated with levels of any of the other hormones under study. Leptin levels are unlikely to affect the risk of either prostate cancer or BPH substantially.

Aged↗

PubMed1995

Citrate as an in vivo marker to discriminate prostate cancer from benign prostatic hyperplasia and normal prostate peripheral zone: detection via localized proton spectroscopy.

OBJECTIVES: This study was designed to determine whether citrate levels detected by localized 1H spectroscopy could reliably discriminate regions of prostate adenocarcinoma from surrounding regions of normal peripheral zone and benign prostatic hyperplasia (BPH). METHODS: In 28 patients and 5 volunteers stimulated echo proton spectroscopy was used in conjunction with endorectal surface coils to obtain water-suppressed 1H spectra from regions of normal prostate peripheral zone, BPH, and prostate cancer. 1H spectra from prostate cancer patients were correlated with pathologic areas identified on T2-weighted endorectal coil magnetic resonance (MR) images and histologic study of the step-sectioned gland after surgery. RESULTS: The major finding of in vivo studies was consistently lower citrate levels in prostate cancer compared with BPH and normal prostate peripheral zone. This was reflected by significantly (P < 0.05) lower mean citrate/(creatine plus choline) peak area ratio observed for regions of cancer (0.67 +/- 0.17) compared with BPH (1.21 +/- 0.29) and normal peripheral zone (1.46 +/- 0.28). Moreover, there was no overlap of individual cancer and normal peripheral zone citrate ratios and no significant difference between citrate ratios in regions of normal peripheral zone in young volunteers (1.28 +/- 0.14) and age-matched patients (1.46 +/- 0.28). The observed alterations in vivo citrate levels were supported by citrate concentration data obtained from extracts of histologically proven samples of normal, benign, and malignant prostatic tissues removed at surgery. In vitro citrate levels in the normal peripheral zone (30.9 +/- 8.5 mumol/g wet weight) and BPH (46.3 +/- 5.4 mumol/g wet weight) were significantly higher than those for prostate cancer (3.74 +/- 0.54 mumol/g wet weight). CONCLUSIONS: These studies further demonstrate the potential of citrate as an in vivo marker for discriminating prostate cancer from surrounding regions of normal peripheral zone and BPH.

Adenocarcinoma↗

PubMed1997

Vascular endothelial growth factor (VEGF) expression in prostate cancer and benign prostatic hyperplasia.

PURPOSE: Vascular endothelial growth factor (VEGF) is a potent inducer of endothelial cell growth and is expressed at elevated levels in several tumor types. In this study immunohistochemical localization and distribution of isoforms of VEGF were examined in malignant and non-malignant human prostatic tissues. MATERIALS AND METHODS: Immunohistochemical localization of VEGF was performed on thirty well, moderately and poorly differentiated stage D2 prostate cancer specimens and twenty benign prostatic hyperplasia (BPH) specimens. VEGF mRNA was determined by polymerase chain reaction and VEGF protein isoforms were detected by Western blotting of prostate cancer and BPH specimens. RESULTS: Cytoplasmic immunoreactivity for VEGF was detected in tumor cells and peritumoral stromal cells of prostate cancer specimens and in non-malignant glandular epithelial cells and interglandular stromal cells in BPH specimens. Staining was focal with areas of strongly to weakly stained cells adjacent to negatively staining areas. mRNA's for VEGF121, VEGF165 and VEGF189 were present in all benign and malignant prostate specimens. VEGF protein isoforms of molecular sizes corresponding to VEGF165 and VEGF189 were detected in cytosolic extracts of prostate cancers and BPH specimens by Western blotting. In addition, two novel higher molecular weight immunoreactive bands were detected in the prostate specimens. CONCLUSIONS: Widespread distribution of VEGF in prostate cancers and BPH specimens suggest that the VEGF165, VEGF189 isoforms and novel 90 and 110 kD forms detected may contribute to the establishment or progression of these conditions.

Blotting, Western↗

PubMed2003

Racial differences in initial treatment for clinically localized prostate cancer. Results from the prostate cancer outcomes study.

OBJECTIVE: We examined whether there were racial differences in initial treatment for clinically localized prostate cancer and investigated whether demographic, socioeconomic, clinical, or tumor characteristics could explain any racial differences. DESIGN: Prospective cohort study. SETTING: Population-based tumor registries in Connecticut, Los Angeles, and Atlanta. PARTICIPANTS: We evaluated 1144 African-American and non-Hispanic white men, aged 50 to 74 years, with clinically localized cancer diagnosed between October 1994 and October 1995. MEASUREMENTS AND MAIN RESULTS: We obtained demographic, socioeconomic, and clinical data from patient surveys and medical record abstractions. We reported adjusted percentages for receiving treatment derived from multinomial logistic regression. We found an interaction between race and tumor aggressiveness. Among men with more aggressive cancers (PSA > or = 20 ng/mL or Gleason score > or = 8), African Americans were less likely to undergo radical prostatectomy than non-Hispanic whites (35.2% vs 52.0%), but more likely to receive conservative management (38.9% vs 16.3%, P=.003). Among the 71% of subjects with less aggressive cancers, African Americans and non-Hispanic whites were equally likely to receive either radical prostatectomy or radiation therapy (80.0% vs 84.5%, P=.2). CONCLUSIONS: African Americans with more aggressive cancers were less likely to undergo radical prostatectomy and more likely to be treated conservatively. These treatment differences may reflect African Americans' greater likelihood for presenting with pathologically advanced cancer for which surgery has limited effectiveness. Among men with less aggressive cancers-the majority of cases-there were no racial differences in undergoing radical prostatectomy or radiation therapy.

Aged↗

PubMed1997

Prognostic factors in patients with metastatic (stage D2) prostate cancer: experience from the Scandinavian Prostatic Cancer Group Study-2.

PURPOSE: Nuclear texture reflects the overall structures of the chromatin organization. We recently reported the principles and prognostic importance of image analysis of nuclei from metastatic prostate cancer. Immunohistochemical up regulation of the adhesion molecule sialyl Lewis(x) is also reported to be a prognostic parameter. Presently we analyzed statistically the prognostic impact of these 2 new parameters compared to well-known clinical parameters in metastatic prostate cancer. MATERIALS AND METHODS: Prognostic factors, such as sedimentation rate, alkaline and acid phosphatases, hemoglobin, testosterone, performance status, pain due to metastasis, T category, histological grade and patient age, were included in a multivariate Cox proportional hazards regression analysis based on 262 patients from the Scandinavian Prostatic Cancer Group Study-2. Extent of bone lesions, deoxyribonucleic acid ploidy, texture analysis and sialyl Lewis(x) molecules based on subsets of these 262 patients were also analyzed in the same multivariate model. RESULTS: This test identified chromatin texture as the most important factor (p < 0.001), followed by reaction of the oligosaccharide sialyl Lewis(x) (p < 0.01). Among the routine clinical and laboratory data, sedimentation rate, alkaline phosphatase and hemoglobin (p < 0.05) showed prognostic importance. Performance status, pain due to metastasis and extent of bone lesions showed prognostic value in the univariate analysis (p < 0.05). CONCLUSIONS: These data indicate that computerized nuclear texture analysis as well as up regulation of sialyl Lewis(x) molecules may be new important prognostic factors in metastatic prostate cancer. Furthermore the prognostic importance of sedimentation rate, alkaline phosphatase and hemoglobin was confirmed.

Aged↗

PubMed2004

Prostate cancer and the met hepatocyte growth factor receptor.

The hepatocyte growth factor/scatter factor (HGF/SF) and its receptor, the Met protein tyrosine kinase, form a classic ligand-receptor system for epithelial-mesenchymal communications in the normal and cancerous prostate. This review illustrates the expression and activities of HGF/SF and Met during prostate development, homeostasis, and carcinogenesis. The participation of HGF/SF in the morphogenetic program of rodent prostate development, the role of Met in normal human prostate epithelium, and underlying mechanisms of deregulated Met expression in localized and metastatic prostate cancer are discussed. On the basis of the commonly observed overexpression of Met in metastatic prostate cancer, HGF/SF-Met-targeted imaging and therapeutic agents can now be applied toward diagnosis and treatment.

Adenocarcinoma↗

PubMed2005

Detection of prostate cancer with a blood-based assay for early prostate cancer antigen.

Prostate-specific antigen lacks specificity for prostate cancer, so the identification and characterization of a unique blood-based marker for the disease would provide for a more accurate diagnosis, reducing both unnecessary biopsies and patient uncertainty. We previously identified a novel biomarker for prostate cancer, early prostate cancer antigen (EPCA). EPCA antibodies positively stained the negative biopsies of men who, as much as 5 years later, were diagnosed with prostate cancer. The goal of this study was to determine whether EPCA antibodies could be used in a clinically applicable plasma-based immunoassay to specifically detect prostate cancer. Using an EPCA-based ELISA, the protein was measured in the plasma of 46 individuals, including prostate cancer patients, healthy individuals, other cancer patients, spinal cord injury victims, and patients with prostatitis. With a predetermined cutoff value of 1.7 absorbance at 450 nm, only the prostate cancer population, as a whole, expressed plasma-EPCA levels above the cutoff. Statistical analysis showed a significant difference in EPCA levels between the prostate cancer population and each of the other groups, specifically the healthy donors (P < 0.0001), bladder cancer patients (P = 0.03), and spinal cord injury patients (P = 0.001). Sensitivity of the EPCA assay for prostate cancer patients was 92% whereas the overall specificity was 94%. Specificity for the healthy donors was 100%. Although larger trials are required, this initial study shows the potential of EPCA to serve as a highly specific blood-based marker for prostate cancer. EPCA, when coupled with prostate-specific antigen, may help reduce the number of both unnecessary biopsies and undetected prostate tumors.

Adult↗

PubMed2000

Computed tomography/magnetic resonance based volume changes of the primary tumour in patients with prostate cancer with or without androgen deprivation.

BACKGROUND AND PURPOSE: To evaluate changes of the volume of the cancerous prostatic gland during androgen deprivation (AD) started immediately after diagnosis (IAD). Hypothetically, these data would assist the radiotherapist to determine the appropriate duration of pre-radiotherapy downsizing neoadjuvant luteinizing hormone releasing hormone (LHRH) treatment. A second aim was to assess any increase of the prostatic volume during the 1st year of diagnosis in patients who were allocated to a deferred treatment policy (DAD). METHODS AND MATERIALS Thirteen patients in the IAD cohort and 13 patients in the DAD group, all with T1-3pN1-2M0 prostate cancer, had regular computed tomography/magnetic resonance (CT/MR) examinations during the 1st year after randomization within the EORTC-GU trial 30846. Pre-treatment prostate specific antigen (PSA) values were available in only 12 patients. RESULTS: In the IAD group the prostate gland decreased with significant difference as compared with the DAD patients (P=0.033). As compared with the pre-treatment situation the prostate gland in the IAD group was reduced in size by 18, 35, and 46% at 1, 6, and 12 months, respectively. In four of six evaluable IAD patients the prostatic volume continued to shrink after achievement of the nadir PSA level (at 3 months). In three of the 13 DAD patients the prostate volume increased by >25% during the 1st 3 months after randomization. CONCLUSION: If neoadjuvant androgen deprivation is applied before local treatment to downsize the volume of the cancerous prostate gland, our limited data suggest that such treatment should last at least 6 months in order to achieve a maximal effect in the majority of patients. In about 1/4 of untreated patients an increase in the prostate volume by >25% may occur within 3 months of diagnosis. If no AD is given, radiotherapy should start within this period.

Adult↗

PubMed2000

Optimal predictors of prostate cancer on repeat prostate biopsy: a prospective study of 1,051 men.

PURPOSE: We compare the ability of total prostate specific antigen (PSA), percent free PSA, PSA density and transition zone PSA density to predict the outcome of repeat prostatic biopsy in men with serum total PSA 4 to 10 ng./ml. who were diagnosed with benign prostatic hyperplasia after initial biopsy. MATERIALS AND METHODS: In this prospective study 1,051 men with total PSA 4 to 10 ng./ml. underwent transrectal ultrasound guided sextant biopsy with 2 additional transition zone biopsies. In 254 subjects biopsy specimens were also obtained from suspicious areas identified during transrectal ultrasound and digital rectal examination. All subjects with biopsy specimens negative for prostate cancer underwent repeat biopsy 6 weeks after initial biopsy. The ability of total PSA, percent free PSA, PSA density and transition zone PSA density to improve the diagnostic power of PSA testing was assessed with univariate and multivariate analyses as well as receiver operating characteristics (ROC) curves. RESULTS: Initial biopsy was positive (prostate cancer) in 231 and negative (benign prostatic hyperplasia) in 820 of the 1,051 subjects. Prostate cancer was detected on repeat biopsy in 10% of subjects (83 of 820) with negative initial biopsy. Percent free PSA and transition zone PSA density were the most accurate predictors of prostate cancer in these subjects. At a cutoff of 30% percent free PSA would have detected 90% of cancers (sensitivity) and eliminated 50% of unnecessary repeat biopsies (specificity). Sensitivity and specificity of transition zone PSA density at a cutoff of 0.26 ng./ml./cc was 78% and 52%, respectively. ROC curve analysis also showed that percent free PSA was a significantly better predictor of repeat biopsy results than total PSA, PSA density and transition zone PSA density. The area under the ROC curve was 74.5% for percent free PSA, 69.1% for transition zone PSA density, 61.8% for PSA density and 60.3% for total PSA. CONCLUSIONS: At least 10% of patients with negative initial prostatic biopsy results will be diagnosed with prostate cancer on repeat biopsy. Percent free PSA and transition zone PSA density enhance the specificity of PSA testing compared to total PSA or PSA density when determining which patients should undergo repeat biopsy. Repeat biopsy should be performed in patients with percent free PSA less than 30% or transition zone PSA density 0.26 ng./ml./cc or greater. In our study percent free PSA was the most accurate predictor of prostate cancer in repeat biopsy specimens.

Aged↗

PubMed1996

Soluble CD44 molecules in serum of patients with prostate cancer and benign prostatic hyperplasia.

Recent studies suggest that expression of CD44 splice variants are of prognostic significance for a variety of neoplasias. It was the aim of this study to investigate whether any correlation exists between the concentration of soluble CD44 molecules in serum (CD44 standard form and CD44 splice variants v5 and v6) and the prostate cancer stage. Serum levels of these soluble CD44 isoforms were measured by ELISA tests specific for these proteins in controls (n = 30), patients with benign prostatic hyperplasia (BPH; n = 30), with prostate cancer without metastasis (T1,2,3pN0M0; n = 30) and with locally advanced prostate cancer and/or metastatic disease (T3,4pN1,2M1; n = 19). sCD44std and sCD44v6 concentrations were not significantly different among the four groups studied, with few patients' levels outside the central 95% reference intervals. The mean sCD44v5 concentrations of both prostate cancer and BPH patients were significantly lower than those of the controls. There was no significant difference between the soluble CD44 concentrations of the two groups of prostate cancer patients studied. In contrast to results observed in other carcinomas, the determination of soluble CD44 proteins in serum is not suitable for providing additional prognostic information on patients with prostate cancer.

Adult↗

PubMed1996

Accumulation of p53 and expression of CD44 in human prostatic cancer and benign prostatic hyperplasia: an immunohistochemical study.

OBJECTIVE: To investigate the expression of mutant p53 and wild-type CD44 in human benign and neoplastic prostate. PATIENTS AND METHODS: The accumulation of p53 and the expression of CD44 were investigated immunohistochemically in formalin-fixed and paraffin-embedded tissue specimens (obtained by transurethral resection and open prostatectomy) from 16 patients with primary prostatic cancer (median age 65 years, range 54-75) and six patients with benign prostatic hyperplasia (BPH) (median age 67 years, range 58-75). RESULTS: Positive immunoreactivity for p53 and CD44 was detected in six and eight samples of prostatic cancer tissue, respectively. Additionally, all six prostatic cancer samples showing positive immunoreactivity for p53 were also positive for CD44. There were more samples expressing p53 and CD44 in prostatic cancer with a high Gleason grade score than in samples from cancer with a lower score. In samples from six patients with BPH, positive immunoreactivity for p53 and CD44 was observed in one and two, respectively; stained cells were restricted to the secretory cell layer of the gland. CONCLUSIONS: There was an association between prostatic tumour grade and the increasing expression of p53 and CD44, although there were too few samples for statistical significance. The staining pattern of cells expressing p53 and CD44 may be different between prostatic cancer and BPH tissues.

Aged↗

PubMed2000

The economic burden of prostate cancer in Canada: forecasts from the Montreal Prostate Cancer Model.

BACKGROUND: We developed an economic model of prostate cancer management from diagnosis until death. We have used the Montreal Prostate Cancer Model to estimate the total economic burden of the disease in a cohort of Canadian men. METHODS: Using this Markov state-transition simulation model, we estimated the probability of prostate cancer, annual prostate cancer progression rates and associated direct medical costs according to patient age, tumour stage and grade, and treatment modalities in a 1997 cohort of Canadian men. The estimated lifetime costs of prostate cancer included the costs of clinical staging, initial treatments and complications, follow-up cancer therapies, routine outpatient care, and palliative care following metastatic disease. RESULTS: The clinical burden of prostate cancer forecasted using the model was similar to the projections of the National Cancer Institute. In the 1997 cohort of 5.8 million Canadian men between 40 and 80 years old, prostate cancer would be diagnosed in an estimated 701,491 men (12.1%) over their lifetime. Direct medical costs would total $9.76 billion, or $3.89 billion when discounted 5% annually. INTERPRETATION: The Montreal Prostate Cancer Model indicates that the economic burden of prostate cancer to Canada's health care system will be substantial. Further analyses are needed to identify the most efficient means of treating this disease.

Adult↗

PubMed2003

[Prostate cancer screening].

Prostate cancer has become the most frequent cancer and the second cause of cancer mortality in men. This public health problem is becoming increasingly important due to the increasing life expectancy. At the present time, prostate cancer will be discovered in one in every eight men during their lifetime. Prostate cancer represents 25% of all new cases of male cancers. Prostate cancer screening is designed to detect early stage, asymptomatic prostate cancer, as the patient's chances of cure are higher when the cancer is diagnosed at an early stage. The conclusions of the ANAES evaluation in 1998 did not recommend mass screening for prostate cancer. Several international prospective randomized studies based on serum PSA assay, sometimes associated with digital rectal examination, are currently underway. France is participating in the European ERSPC study (European Randomized Study of Screening for Cancer Prostate) and is organizing a national study on high-risk populations. While waiting for the final results of these studies, a recommendation needs to be proposed to inform general practitioners and specialists about optimal use of the currently available tests. Based on the conclusions of its oncology committee (composed of urologists, medical oncologists, radiotherapists, pathologists and radiologists), the Association Française d'Urologie proposes a recommendation concerning prostate cancer screening and defines its modalities, especially concerning the target population, screening tests and the information given to men before screening. The Association Française d'Urologie recommends prostate cancer screening by PSA assay (prostate specific antigen) and digital rectal examination annually between the ages of 50 and 75 years, and from the age of 45 years in men with a family or ethnic risk. If total PSA is above the normal value of the test or if digital rectal examination is abnormal, referral to a urologist is recommended. Information concerning the limits, benefits and risks of screening and the available treatment options must be given before performing these examinations.

Humans↗

PubMed2001

[Expression of COX-2 in prostatic cancer and benign prostatic hyperplasia].

OBJECTIVE: To investigate the expression of COX-2 in and benign prostatic hyperplasia and prostate cancer and its clinical implications. METHODS: Forty-two patients with and benign prostatic hyperplasia and 16 with prostate cancer were studied by immunohischemistry and western blot. RESULTS: Immunohischemiscal study showed positive results in 15 of the 16 patients and 11 of the 42 patients. Western blot showed that the expression of COX-2 was higher in prostate cancer than in and benign prostatic hyperplasia tissues(P < 0.01). CONCLUSION: Overexpression of COX-2 in prostate cancer may be related to the staging of prostate cancer.

Blotting, Western↗