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PubMed1998

Cryoablation of localized prostate cancer: neoadjuvant downsizing of prostate cancer with LH-RH analogue depot before cryosurgery.

Radical prostatovesiculectomy, radiation therapy, and complete androgen deprivation are acknowledged therapeutic concepts in the treatment of organ-confined prostate cancer. With cryoablation of the prostate, minimal invasive therapy has become available since 1991. Improvements in cryotechnique and progress in transrectal high-resolution ultrasound permit thermo-induced damage to the whole gland to be curative. Downstaging of prostate cancer by hormone ablative therapy remains a controversial issue at this time, but the use of androgen ablation decreases the size of the prostate gland which facilitates cryosurgery and improves the results. The freezing equipment has a limited capacity, and in certain instances large gland volumes prevent adequate freezing of the prostate. Since percutaneous prostate cryosurgery leaves dead tissue in situ to be resorbed over time, downsizing reduces the amount of necrotic tissue to be resorbed, reducing the potential for complications, particularly abscesses. The use of androgen ablation also increases the deposition of fat in the area of the Denonvillier's fascia, making freezing of the rectum less likely during the procedure. In our study androgen ablative therapy was completed before performing cryosurgery in 26 of 43 patients (58%). The 17 patients not given androgen ablation therapy had gland volumes < 40 ml, tumor volumes < 3 ml, and no evidence of extracapsular tumor. The neoadjuvant therapy consisted of a 3- to 10-month course of leuprolide acetate combined with an antiandrogen.

Androgen Antagonists↗

PubMed1997

Family history of prostate cancer in patients with localized prostate cancer: an independent predictor of treatment outcome.

PURPOSE: To determine if familial prostate cancer patients have a less favorable prognosis than patients with sporadic prostate cancer after treatment for localized disease with either radiotherapy (RT) or radical prostatectomy (RP). PATIENTS AND METHODS: One thousand thirty-eight patients treated with either RT (n = 583) or RP (n = 455) were included in this analysis. These patients were noted as having a positive family history if they confirmed the diagnosis of prostate cancer in a first-degree relative. The outcome of interest was biochemical relapse-free survival (bRFS). We used proportional hazards to analyze the effect of the presence of family history and other potential confounding variables (ie, age, treatment modality, stage, biopsy Gleason sum [GS], and initial prostate-specific antigen [iPSA] levels) on treatment outcome. RESULTS: Eleven percent of all patients had a positive family history. The 5-year bRFS rates for patients with negative and positive family histories were 52% and 29%, respectively (P < .001). The potential confounders with bRFS rates were iPSA levels, biopsy GS, and clinical tumor stage; treatment modality and age did not appear to be associated with outcome. After adjusting for potential confounders, family history of prostate cancer remained strongly associated with biochemical failure. CONCLUSION: This is the first study to demonstrate that the presence of a family history of prostate cancer correlates with treatment outcome in a large unselected series of patients. Our findings suggest that familial prostate cancer may have a more aggressive course than nonfamilial prostate cancer, and that clinical and/or pathologic parameters may not adequately predict this course.

Aged↗

PubMed2002

Benign prostatic hyperplasia, prostate cancer and other prostate diseases diagnosed as a result of screening procedure among 1,004 men in the Lublin district.

Urological problems especially connected with prostate diseases appear in older men: prostatitis, benign prostatic hyperplasia, prostate cancer and others. Prostate cancer is the most common cancer in men and the second leading cause of deaths in male population. Therefore, it seems important to early detect prostate cancer in general practice setting due to screening procedures such as digital rectal exam and prostate-specific-antigen test. The aim of the study was to examine the character of diagnoses of a prostate disease among 1,004 men of the Lublin district who reported to a doctor during screening procedure carried out in urology outpatient clinic at Clinical Hospital in Lublin in the year 2000. After physical examination urologists initially diagnosed a prostate disease and sent men suspected to have a prostate cancer to further investigations. There was studied age and place of living. Benign prostate hyperplasia was the most common diagnosis made in 77.1% of subjects. It occurred most often in men aged 51-70 years. Prostate cancer was suspected in 3.5% of subjects. Frequency of benign prostate hyperplasia and prostate cancer suspicion increased with age. On the basis of studies screening procedures seem beneficial in the early detection of prostate cancer in men over 50.

Adult↗

PubMed1994

Cost analyses of prostate cancer screening: frameworks for discussion. Investigators of the American Cancer Society-National Prostate Cancer Detection Project.

Our recent cost analysis of prostate cancer early detection evaluated the economic performance of various prostate specific antigen (PSA) screening approaches, detected marginal cost variations with time and used a benefit-cost calculation as a framework for further discussion. Receiver operator characteristic analysis initially suggested an optimal test performance for PSA of 2 to 3 ng./ml. when used alone and at approximately 3 ng./ml. in combination with digital rectal examination. However, lower PSA decision levels require cost justifications. Marginal cost analysis demonstrated markedly decreased use of digital rectal examination by year 3 due to significantly lower sensitivity for incident cancer. The benefit-cost equation acknowledges that many parameters of cost and probability are not definitive to date yet illustrated major points for discussion. The cost parameters most sensitive to incremental change in decreasing order are the specificity of the screening test, benefits obtained from early therapy and prevalence of the disease. Discussions about improving the likelihood of overall benefit for the United States population should focus on these parameters, as well as social and ethical implications. If we assume minimized future expenditures for terminal cancer care via decreases in therapy choices or coverage, no economic benefit for screening exists. If we also assume that potential costs to society are not roughly approximated by any benefits, we may engender inappropriate attempts at cost reduction by effectively discouraging screening in the highest risk groups. Perhaps the greatest immediate cost control issue is the marked increase in prostate cancer detection in the oldest age groups who have the least likelihood of mortality or morbidity benefits. Current cost savings may be possible with improved public health education about the appropriateness of early detection in the oldest age groups or those with significant preexisting medical conditions.

American Cancer Society↗

PubMed1994

[Epidemiology of prostate cancer and its implications in public health].

Among potentially fatal cancers, prostatic cancer has the peculiarity of a considerable difference between a high prevalence of characteristic histological lesions and a low clinical prevalence (low prevalence of clinical manifestations?). Its second peculiarity is a prevalence that clearly increases with age. These two notions, no doubt partially linked to slow tumour growth, explain the present difficulties in defining a screening or a diagnostic strategy for this type of cancer. Aging of the population, with the "baby boomers" reaching ages that are affected by prostatic cancer, diagnostic methods that despite progress are still imperfect, and a probable real increase in the incidence of cancer underline the need for epidemiologic studies on prostatic cancer and its consequences.

Aged↗

PubMed2006

Health outcomes in older men with localized prostate cancer: results from the Prostate Cancer Outcomes Study.

PURPOSE: We compared health-related quality-of-life (HRQOL) outcomes and survival of men with localized prostate cancer who received aggressive treatment with those receiving conservative management. METHODS: We conducted a population-based cohort study of men aged 75 to 84 years when diagnosed with a clinically localized cancer in 1994 or 1995. We used medical record abstractions and patient surveys to obtain clinical and HRQOL data at diagnosis and 24-month follow-up. We used a propensity score method to adjust for baseline differences between men treated with radical prostatectomy or radiation therapy (n = 175) and men who received hormone therapy or no treatment (n = 290). Propensity scores were used in regression analyses comparing HRQOL outcomes between treatment groups. Overall and disease-specific survivals were estimated with multivariate proportional hazards models. RESULTS: At 24 months following diagnosis, aggressively treated men were more likely to report daily urinary leakage (odds ratio [OR] = 2.9, 95% confidence interval [CI] 1.2-7.0) and to be bothered by urinary problems (OR = 5.1, 95% CI, 1.3-9.1) and sexual problems (OR = 2.8, 95% CI, 1.2-6.3). The adjusted disease-specific mortality hazard ratio was 0.43 (95% CI, 0.15, 1.28), favoring aggressive treatment. However, the absolute 5-year disease-specific survival difference was only 6% (98% vs 92%). Over 80% of all deaths were from other causes. CONCLUSIONS: Aggressive treatment was associated with significant decreases in disease-specific HRQOL. However, men who were aggressively treated for localized cancer had a minimally reduced absolute risk of dying from prostate cancer. Physicians and older patients should consider these outcomes in making decisions about screening and treatment.

Age Factors↗

PubMed2003

Prostate-specific antigen (PSA) protein does not affect growth of prostate cancer cells in vitro or prostate cancer xenografts in vivo.

BACKGROUND: Prostate-specific antigen (PSA) is produced in high amounts by normal and malignant prostate cancer cells. PSA is a serine protease with substrates that include semenogelin I and II, insulin-like growth factor binding protein 3, fibronectin, and laminin. PSA, via its enzymatic activity, may play a role in growth, invasion, and metastasis of prostate cancer cells. Recent data also suggest that the PSA protein itself, independent of enzymatic activity, may also function as an endothelial cell-specific inhibitor of angiogenesis. METHODS: Human (PC3, DU145) and rat (AT2, AT6) prostate cancer cell lines were transfected with the full PSA gene encoding preproPSA protein. PSA-producing clones of each cell line were selected and the amount of enzymatically active PSA produced by each cell line determined using a PSA-specific fluorescent peptide substrate. In vitro and in vivo growth characteristics of PSA-producing transfectants were compared to neomycin controls and wild type cells. RESULTS: All selected clones produced and secreted PSA (5-120 ng/ml/10(5) cells). None of the PSA-transfected cell lines produced detectable amounts of enzymatically active PSA. Production of enzymatically inactive PSA by prostate cancer cell lines did not alter growth kinetics in vitro. PSA-producing xenograft doubling times in vivo were similar to neomycin controls and wild type. CONCLUSION: Although recent reports suggest the PSA protein itself may be antiangiogenic, our results demonstrate that production of PSA protein by prostate cancer cells does not significantly alter growth in vitro or in vivo.

Animals↗

PubMed1996

Prospective evaluation plan for randomised trials of prostate cancer screening. The International Prostate Cancer Screening Trial Evaluation Group.

To enable pooled analyses of continuing and planned randomised trials of prostate cancer screening, guidelines for minimal data required for such analyses were developed in the recent meeting of the International Prostate Screening Trial Evaluation Group (IPSTEG). The aim of the pooled analysis with data on individual level will be: (a) Estimation of the effect of screening on prostate cancer mortality with greater precision than individual studies (b) Assessment of optimal screening procedures and interval (c) Identification of subgroups within the populations that might receive most benefit from screening (d) Evaluation of the quality of life effects and cost effectiveness of screening. All studies included in the combined analysis share a common core protocol with minimum data requirements. The protocol allows, however, adaptation of the procedures to local circumstances within defined options. It should be noted that the process is continuing and the protocol is subject to evaluation and revision in the meetings of the IPSTEG on a regular basis.

Aged↗

PubMed2005

Silencing of polo-like kinase (Plk) 1 via siRNA causes induction of apoptosis and impairment of mitosis machinery in human prostate cancer cells: implications for the treatment of prostate cancer.

Prostate cancer (PCa) is one of the most common cancers in men. Each year approximately 543,000 new cases are reported worldwide, and the disease kills 200,000 (mostly older men) in developed countries. The existing treatment approaches and surgical intervention have not been able to effectively manage this dreaded cancer and, therefore, continuing efforts are ongoing to explore novel targets and strategies for the management of PCa. The activity of polo-like kinase 1 (Plk1) is elevated in tissues and cells with a high mitotic index, including cancer cells. An increasing body of evidence suggests that the level of Plk1 expression has prognostic value for predicting outcomes in patients with some cancers. A close correlation between Plk1 expression and carcinogenesis has been documented. However, the role of Plk1 in PCa is not known. We propagated a hypothesis that Plk1 inhibition will result in elimination of human PCa cells via a mitotic arrest followed by apoptosis (1). To define the role of Plk1 in PCa, we used the technique of RNA silencing via small interfering RNA (siRNA). First, using a series of human prostate carcinoma cells and normal human prostate epithelial (PrEC) cells, we assessed Plk1 levels in PCa. Immunoblot analyses clearly showed a significant expression of Plk1 in LNCaP, DU145, and PC3 human PCa cells. Interestingly, Plk1 was not detectable in normal PrEC cells. Next, we transfected the PCa cells with Plk 1 siRNA, which resulted in a significant inhibition in Plk1 protein in all PCa cells. Plk1 depletion resulted in a decrease in cell viability and induction of apoptosis in PCa cells but had no appreciable effect in normal PrEC cells. Our data also demonstrated that Plk1 siRNA transfection of PCa cells resulted in 1) a mitotic cell cycle arrest, 2) failure of cytokinesis, and 3) defects in centrosome integrity and maturation. Thus, our study suggested that 1) Plk1 plays a critical role in the process of PCa development and 2) gene therapeutic approaches aimed at Plk1 or the pharmacological inhibitors of Plk1 may be developed for the management of PCa.

Apoptosis↗

PubMed2006

Bicalutamide (Casodex) 150 mg plus standard care in early non-metastatic prostate cancer: results from Early Prostate Cancer Trial 24 at a median 7 years' follow-up.

Trial 24, one of three ongoing trials in the Early Prostate Cancer programme, is evaluating the efficacy and tolerability of bicalutamide (Casodex) 150 mg following standard care (radiotherapy, radical prostatectomy or watchful waiting) in patients with early, non-metastatic prostate cancer. At 7 years' median follow-up, addition of bicalutamide significantly improved objective progression-free survival (PFS) for patients with locally advanced disease, reducing the risk of progression by 34% versus standard care alone (hazard ratio 0.66; 95% confidence interval 0.55, 0.79; P<0.001). In localized disease, a significant difference in objective PFS was not found. There was no significant difference in overall survival.

Anilides↗

PubMed2000

Combined analysis of hereditary prostate cancer linkage to 1q24-25: results from 772 hereditary prostate cancer families from the International Consortium for Prostate Cancer Genetics.

A previous linkage study provided evidence for a prostate cancer-susceptibility locus at 1q24-25. Subsequent reports in additional collections of families have yielded conflicting results. In addition, evidence for locus heterogeneity has been provided by the identification of other putative hereditary prostate cancer loci on Xq27-28, 1q42-43, and 1p36. The present study describes a combined analysis for six markers in the 1q24-25 region in 772 families affected by hereditary prostate cancer and ascertained by the members of the International Consortium for Prostate Cancer Genetics (ICPCG) from North America, Australia, Finland, Norway, Sweden, and the United Kingdom. Overall, there was some evidence for linkage, with a peak parametric multipoint LOD score assuming heterogeneity (HLOD) of 1.40 (P=.01) at D1S212. The estimated proportion of families (alpha) linked to the locus was.06 (1-LOD support interval.01-.12). This evidence was not observed by a nonparametric approach, presumably because of the extensive heterogeneity. Further parametric analysis revealed a significant effect of the presence of male-to-male disease transmission within the families. In the subset of 491 such families, the peak HLOD was 2.56 (P=.0006) and alpha =.11 (1-LOD support interval.04-.19), compared with HLODs of 0 in the remaining 281 families. Within the families with male-to-male disease transmission, alpha increased with the early mean age at diagnosis (<65 years, alpha =.19, with 1-LOD support interval.06-.34) and the number of affected family members (five or more family members, alpha =.15, with 1-LOD support interval.04-.28). The highest value of alpha was observed for the 48 families that met all three criteria (peak HLOD = 2.25, P=.001, alpha=.29, with 1-LOD support interval.08-.53). These results support the finding of a prostate cancer-susceptibility gene linked to 1q24-25, albeit in a defined subset of prostate cancer families. Although HPC1 accounts for only a small proportion of all families affected by hereditary prostate cancer, it appears to play a more prominent role in the subset of families with several members affected at an early age and with male-to-male disease transmission.

Age of Onset↗

PubMedDate not supplied

Microarray analysis of differential gene expression in androgen independent prostate cancer using a metastatic human prostate cancer cell line model.

Progression to androgen independence (AI) leading to uncontrolled cell growth is the main cause of death in prostate cancer. While almost all patients with metastatic prostate cancer will initially respond to anti-androgen treatments, the majority will fail hormonal treatments in less than 2 yrs. Both genetic and epigenetic alterations in gene expression contribute significantly to the development of AI. To investigate this we have used an in vitro cell line model of AI prostate cancer from which we have identified a number of differentially expressed genes associated with progression to AI in prostate cancer. We used an in vitro cell line model of AI prostate cancer, to study differential gene expression using cDNA microarray analysis and corroborated the microarray results with Ribonuclease Protection Assay (RPA). Approximately 4480 out of 7075 (63.3%) cDNA cloned genes were differentially expressed, of which, 6 genes were differentially expressed by at least fivefold. RPA was used to corroborate the microarray results for the five most highly differentially expressed genes. Using an in vitro cell line model and microarray analysis we have identified a number of candidate genes for further investigation in AI prostate cancer.

Androgen Antagonists↗

PubMed2005

Molecular markers of prostate cancer outcome.

Molecular markers have the potential to serve not only as prognostic factors but may be targets for new therapeutic strategies and predictors of response in a range of cancers. Prostate cancer development and progression is predicated on a series of genetic and epigenetic events within the prostate cell and its milieu. Within this review, we identify candidate molecules involved in diverse processes such as cell proliferation, death and apoptosis, signal transduction, androgen receptor (AR) signalling, cellular adhesion and angiogenesis that are linked to outcome in prostate cancer. Current markers with potential prognostic value include p53, Bcl-2, p16INK4A, p27Kip1, c-Myc, AR, E-cadherin and vascular endothelial growth factor. Evolving technology permits the identification of an increasing number of molecular markers with prognosis and predictive potential. We also review the use of gene microarray analysis in gene discovery as a means of identifying and cosegregating novel markers of prostate cancer outcome. By integrating selected markers into prospective clinical trials, there is potential for us to provide specific targeted therapy tailored for an increasing number of patients.

Apoptosis↗

PubMed2006

Oxidative stress and antioxidant status in non-metastatic prostate cancer and benign prostatic hyperplasia.

OBJECTIVES: We undertook the present study to investigate the possible alteration of oxidant/antioxidant status in the circulation of patients with prostate cancer and benign prostatic hyperplasia. DESIGN AND METHODS: Thiobarbituric acid reactive substances (TBARS), the enzyme activities of superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase (CAT) and copper (Cu) and zinc (Zn) levels were estimated in the erythrocytes of 25 non-metastatic prostate cancer patients, 36 benign prostatic hyperplasia (BPH) patients and 24 age- and sex-matched healthy subjects (controls). RESULTS: TBARS concentrations were significantly increased, while erythrocyte GPX and SOD activities were significantly decreased in the prostate cancer group versus controls (P < 0.001) and BPH group (P < 0.05). Zn levels were lowered in prostate cancer patients versus controls (P < 0.01) with no significant changes between BPH and cancer groups. Similarly, lipid peroxidation was increased (P < 0.05) with decreased SOD activity and Zn level (P < 0.05) in BPH versus controls. CONCLUSION: These results reveal an alteration in the lipid peroxidation index, with concomitant changes in the antioxidant defense system in prostate cancer patients compared to BPH patients. We hypothesize that an altered prooxidant-antioxidant balance may lead to an increase in oxidative damage and consequently may play an important role in prostate carcinogenesis.

Aged↗

PubMed2005

Immunohistochemical analysis of Omi/HtrA2 expression in prostate cancer and benign prostatic hyperplasia.

To study the expression and significance of the serine protease Omi/HtrA2 in prostate cancer and benign prostatic hyperplasia. The expression of Omi/HtrA2 was assayed by means of immunohistochemical technique in 41 prostate cancer (Cap), 20 benign prostatic hyperplasia (BPH) and 10 normal prostate (NP) specimens. Omi/HtrA2 expression was positive in 30 (73.17%) prostate cancer specimens, and the positive rate of Omi/HtrA2 was lower in well differentiated than in poorly and moderately differentiated groups (P < 0.05). By contrast, the cells in normal prostate and benign prostatic hyperplasia groups showed no or weak expression of Omi/HtrA2. Prostate cancer cells in vivo may need Omi/HtrA2 expression for apoptosis, and that Omi/HtrA2 expression might be involved in prostate cancer development.

Adult↗

PubMed1994

[Radical treatment of localized prostatic cancer?].

Prostatic carcinoma, if detected early, may be cured by radical surgery or radiotherapy. In Norway, only a minority of patients (about 5%) received this treatment in 1988. However, diagnosis of possibly localised cancer was made in 31% of patients, most of whom were probably only observed and not treated unless progression occurred. This conservative attitude is representative of European practice but conflicts with the current approach in the United States. In view of the possible complications of such treatment there is no material to prove that radical treatment would benefit the populations as a whole. Nor has this been disproved. Such treatment should only be considered on the basis of strict criteria and for strongly motivated patients, who should be fully informed of the possibilities of complications and of being cured, and also about alternative treatment, including watchful waiting.

Europe↗

PubMed2004

[Clinics in prostate cancer].

The prostate gland is characterized by the age-dependent development of abnormal proliferative disease, i.e., benign prostate hyperplasia and prostate cancer. Prostate cancer is the most important disease in our country among the elderly population. The diagnosis and treatment of prostate cancer have been dramatically improved due to the development of PSA screening, transrectal ultrasonography and new anti-androgen drugs, such as LH-RH analog, with fewer side effects. In this article, the pathogenesis, diagnosis and treatment of prostate cancer are summarized.

Androgen Antagonists↗

PubMed1996

[High-grade intraepithelial prostatic neoplasms: diagnosis and association with prostate cancer].

Prostatic intraepithelial neoplasia (PIN) fulfils the majority of requirements for a premalignant change in the human prostate. Forty-eight patients were diagnosed to have high grade PIN on prostatic needle biopsy. During a follow-up period, 23 (47.9%) were found to have adenocarcinoma on subsequent biopsies. We compared the patients age, the digital examination, the transrectal ultrasound appearance (TRUS) and the serum PSA level between those in whom cancer was detected subsequently and those with PIN alone. There was a statistically significant difference in the transrectal ultrasound appearance (TRUS) and the serum PSA level between the two groups (p < 0.001, p < 0.016 respectively). In conclusion, patients with high grade PIN, elevated serum PSA with hypoechoic zone on TRUS should be rebiopsied 3 months after the initial diagnosis. If the results are negative, close follow-up is mandatory.

Adenocarcinoma↗