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PubMed2004

G proteins in cancer: the prostate cancer paradigm.

Signal transduction research investigating mechanisms of androgen-independent prostate cancer cell proliferation has historically focused on the role of androgen and peptide growth factor receptors. More recent work has raised the idea that intracellular signaling mechanisms triggered by extracellular hormonal factors acting through heterotrimeric guanine nucleotide-binding protein (G protein)-coupled receptors (GPCRs) can also mediate and sustain this pathologic process. Prostate cancer patients with advanced disease express elevated levels of GPCRs and GPCR ligands, suggesting that the GPCR system is activated in the cancerous gland and may contribute to tumor growth. Importantly, inhibition of G protein signaling attenuates prostate cancer cell growth in animal models. The nature of intracellular signaling pathways mediating mitogenic effects of GPCRs in prostate cancer is poorly defined, although the G protein-dependent activation of the Ras-to-mitogen-activated protein kinase pathway has emerged as a critical regulatory event. Activated GPCRs may also exert their mitogenic effects in the prostate by activating the androgen receptor.

Animals↗

PubMed2000

Prevention of prostate cancer.

Prostate cancer lends itself ideally to chemoprevention due to a number of specific features of the disease. These include a high prevalence, long latency time, hormone dependency, the availability of an ideal marker (prostate serum antigen) and, last but not least, the availability of a defined precursor lesion (prostatic intraepithelial neoplasia) among the pathways leading to clinical disease. The large variability in the incidence of the tumor in different geographical regions suggests the possibility of nutritional influences regarding the stimulation and/or inhibition of clinical cancer, as there is a similar prevalence worldwide of the precursor lesion. A great number of publications have dealt with a number of nutritional factors, including fat, phytoestrogens, vitamins (especially vitamin E) and minerals such as selenium and calcium. These are among the most reported substances with a possible influence on disease development; however, unfortunately there are no conclusive results or study outcomes at present which satisfy accepted standards of evidence. Ongoing studies on nutrition and prostate cancer may bring the required evidence to support what is still only an hypothesis at present.

Adenocarcinoma↗

PubMed2003

Prostatic calculi do not influence the level of serum prostate specific antigen in men without clinically detectable prostate cancer or prostatitis.

PURPOSE: Prostatic calculi are common but little is known of their effect on serum prostate specific antigen (PSA). We investigated whether prostatic calculi might influence serum PSA in men with clinically undetectable prostatic cancer or prostatitis. MATERIALS AND METHODS: Between November 1999 and November 2001, 581 consecutive patients underwent serum PSA determination and digital rectal examination. Of these patients 486 without detectable prostatic cancer, or a history or symptoms of prostatitis and with other specified exclusion criteria were included in the study. The detection and volume measurement of prostatic calculi, and the measurement of prostate volume were performed by transrectal ultrasonography. RESULTS: Prostatic calculi were detected in 198 of the 486 men (40.7%). Mean patient age, prostate volume and serum PSA were not significantly different in men with and without prostatic calculi. Prostate volume was significantly greater in patients with abnormally elevated serum PSA than in those with normal levels. However, no significant difference was found between the percent of men with prostatic calculi or the volumes of prostatic calculi in the 2 groups. Univariate logistic regression analysis indicated that the presence or volume of prostatic calculi was not a risk factor for elevated PSA. Multivariate analysis showed that age and prostate volume were associated with elevated PSA. CONCLUSIONS: The presence or volume of prostatic calculi had no significant effect on serum PSA. Our results suggest that the influence of prostatic calculi is irrelevant in men with elevated PSA.

Calculi↗

PubMed2004

Tartrate-resistant acid phosphatase as a marker of bone metastases in patients with breast cancer and prostate cancer.

Serum activity of tartrate-resistant acid phosphatase 5b (TRAP 5b) in patients with breast cancer and prostate cancer having bone metastases was much higher than in healthy donors and patients without skeletal injuries. TRAP 5b activity in patients with breast cancer and multiple bone metastases surpassed that in patients with single bone metastases. The mean activity of TRAP 5b and range of enzyme activity in women treated with bisphosphonates were significantly lower than in patients not receiving antiresorptive therapy. Diagnostic sensitivity and specificity of TRAP 5b as a marker of skeletal metastases in patients with breast cancer were 82 and 87%, respectively. In patients with prostate cancer these indexes were 71 and 83.4%, respectively. Detection of this marker in tumor patients holds much promise for early diagnostics of bone metastases, estimation of the severity of skeletal metastases, and monitoring of the efficiency of bisphosphonate therapy.

Acid Phosphatase↗

PubMed1991

[Intra-arterial infusion chemotherapy for advanced bladder cancer and prostate cancer using reservoir system].

Eight patients with bladder cancer and two patients with prostate cancer were given intra-arterial infusion chemotherapy using the reservoir system. The tip of the catheter was inserted through the femoral artery to the common iliac artery and we compressed both femoral arteries during infusion. Five patients with locally advanced bladder cancer and two patients with prostate cancer were evaluated for the clinical and pathological efficacy of the treatment. Clinically, the efficacy of four of the five patients with bladder cancer was CR or PR and pathologically (according to Shimosato's criteria), the efficacy was two in IVb or III, and three in IIb. Clinically, the efficacy in two patients with prostate cancer was CR or PR, and pathologically the efficacy was IVb or IIb. Three patients had complications of the reservoir system. These results suggest that good therapeutic efficacy and an improved quality of life can be obtained by intra-arterial chemotherapy using the reservoir system.

Aged↗

PubMed2004

Up-regulation of cathepsin X in prostate cancer and prostatic intraepithelial neoplasia.

BACKGROUND: Evidence is accumulating that several proteases are involved in prostate cancer progression. A locus which is often amplified in prostate cancer is the chromosomal region 20q13. Interestingly, one of the genes encoding the cysteine protease cathepsin X maps to this region. The aim of this study was to assess the expression pattern of cathepsin X in malignant and non-malignant prostatic tissue samples. METHODS: Matched malignant and non-malignant tissue specimens were obtained from 56 men after radical prostatectomy. Cathepsin X was quantified at both protein and mRNA levels using several detection methods: Western blotting, immunohistochemistry, quantitative RT-PCR, and in situ hybridization. Furthermore, genomic DNA was analyzed by PCR for possible gene amplification. RESULTS: Immunohistochemical analysis of formalin-fixed, paraffin-embedded sections of radical prostatectomy specimens was performed utilizing a polyclonal antibody against human procathepsin X and revealed staining of acinar basal cells in normal prostate glands. Prostatic intraepithelial neoplasias (PINs) and prostate carcinomas stained highly positive for cathepsin X, showing a significant difference to the staining of normal prostate glands. In contrast, relatively weak and heterogeneous staining was observed for cathepsins F, B, and L. Up-regulation of cathepsin X at the protein level was confirmed by Western blotting. No statistically significant difference was observed at the mRNA level. PCR of genomic DNA revealed that cathepsin X up-regulation most likely occurs in the absence of genomic amplification. CONCLUSIONS: The high expression levels of cathepsin X both in PIN and invasive adenocarcinomas of the prostate suggest that cathepsin X may play a role in the early tumorigenesis of prostate cancer. Further studies are needed to define the utility of this cysteine protease as a diagnostic marker for the early detection of prostate cancer.

Aged↗

PubMed2005

Is screening for prostate cancer with prostate specific antigen an appropriate public health measure?

Screening and treatment for prostate cancer is controversial. In the absence of randomized trials, several prominent medical organizations in the United States and Europe have formulated policies that range from enthusiastic support to significant skepticism concerning the efficacy of screening and subsequent treatment for prostate cancer. Sharp rises in the incidence of prostate cancer have occurred whenever PSA testing has been introduced on a wide scale. Unfortunately, it is unclear whether declines in prostate cancer mortality can be attributed to PSA testing. Other explanations include the early use of anti-androgen therapy or changes in environmental factors such as diet. Repeated testing for serum PSA has produced significant shifts in the types of cases being identified and has raised the possibility of significant over-diagnosis of this disease. The European screening trial and the PLCO trial in the US will hopefully provide some insights into the value of population-based testing.

Europe↗

PubMed1986

[A case of primary malignant neoplasms associated with penile cancer and prostatic cancer].

A case of a 79-year-old man with penile cancer and prostate cancer is reported. The pathological study of surgical specimens disclosed well-differentiated squamous cell carcinoma of the penis and poorly differentiated adenocarcinoma of the prostate. This is a rare case of multiple primary malignant neoplasms associated with penile cancer and prostate cancer.

Adenocarcinoma↗

PubMed1995

Studies of rhodamine-123: effect on rat prostate cancer and human prostate cancer cells in vitro.

The effect of the lipophilic, cationic dye, Rhodamine-123 (Rh-123), on prostate cancer in rats, and on three tumor cell lines in vitro is reported here. The general toxicity of Rh-123 in mice has been found to be minimal. Lobund-Wistar (L-W) rats with the autochthonous prostate cancer of Pollard were treated for six doses with Rh-123 at a dose of 15 mg/kg subcutaneously every other day. Microscopic examination of the tumors revealed cellular and acinar destruction. The effectiveness of Rh-123 as a cytotoxic agent was tested by clonogenic and viability assays in vitro with three human prostate cancer cell lines. Severe (60-95%) growth inhibition was observed following Rh-123 exposure for 2-5 days at doses as low as 1.6 micrograms/ml in all three prostate cancer cell lines.

Adenocarcinoma↗

PubMedDate not supplied

Costs and benefits of prostate cancer screening. Investigators of the American Cancer Society--National Prostate Cancer Detection Project.

Optimal combinations of digital rectal examination (DRE), transrectal ultrasound (TRUS) and prostate specific antigen (PSA) may better detect patients at high risks, as well as those in whom continued screening may not be cost effective. Our recent cost analysis of prostate cancer early detection used current data from three consecutive years of the American Cancer Society's National Prostate Cancer Detection Project. Marginal cost analysis showed marked increased costs for the DRE by year three due to significantly reduced sensitivity for incident cancers. The benefit-cost equation acknowledges that many parameters of both cost and probability are not definitive at this time, 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 > prevalence of the disease. Benefit-cost calculations demonstrated that DRE, when performed by highly skilled examiners, had the lowest cost. However, DRE became one of the most costly detection scenarios when a minor decrease in DRE performance was assumed for more general examiners. If slightly more specific PSA usage (or assay) is developed, the higher prevalence of clinically detectable prostate cancer could make screening less costly than breast cancer screening. If we assume minimized future expenditures for terminal cancer care via reductions 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.(ABSTRACT TRUNCATED AT 250 WORDS)

Cost-Benefit Analysis↗

PubMed2006

Long-term prognostic significance of primary Gleason pattern in patients with Gleason score 7 prostate cancer: impact on prostate cancer specific survival.

PURPOSE: We determined the long-term clinical significance of primary Gleason pattern in patients with Gleason score 7 prostate cancer. MATERIALS AND METHODS: We reviewed the records of all patients who underwent bilateral pelvic lymph node dissection and radical retropubic prostatectomy for Gleason score 7 prostate cancer at our institution. All patients who underwent adjuvant hormonal or radiation therapy were excluded from analysis. Patients were monitored for biochemical failure, that is PSA progression, systemic recurrence and cancer specific survival. RESULTS: We identified 1,688 patients who met admission criteria, of whom 1,256 (74.4%) had primary Gleason pattern 3 and 432 (25.6%) had primary Gleason pattern 4. Median followup was 6.9 years. At 10 years primary Gleason pattern 3 was associated with increased biochemical recurrence-free survival (48% vs 38%, p <0.001), lower systemic recurrence (8% vs 15%, p <0.001) and higher cancer specific survival (97% vs 93%, p = 0.013) for Gleason primary grades 3 and 4, respectively. All of these end points remained significant on multivariate analysis when controlling for preoperative PSA, seminal vesicle involvement, margin status, DNA ploidy and TNM staging. PSA doubling time was shorter in patients with primary Gleason pattern 4 (1.64 vs 1.01 years). Systemic recurrence and cancer specific survival were associated with a PSA doubling time of less than 1 year. CONCLUSIONS: Gleason score 7 prostate cancer is a heterogeneous entity. We should continue to stratify patients according to primary Gleason pattern. Patients with Gleason score 4 + 3 prostate cancer have more aggressive disease and experience higher rates of biochemical failure, systemic recurrence and cancer specific death.

Adult↗

PubMed2005

Longitudinal PSA changes in men with and without prostate cancer: assessment of prostate cancer risk.

BACKGROUND: To determine longitudinal PSA changes over a period of 10 years in patients with and without prostate cancer. METHODS: Serial PSA measurements performed over 10 years were evaluated in 353 men who eventually developed prostate cancer and in 2.462 participants of a screening program without prostatic malignancy. RESULTS: In men with cancer, mean tPSA increased from 2.28 ng/ml at 10 years before diagnosis to 6.37 ng/ml at the time of postive biopsy (PSA velocity: 0.409 ng/ml/year). PSA velocity was significantly associated with Gleason scores and pathologic stage. In the benign group (n=2.462), mean tPSA increased from 1.18 to 1.49 ng/ml over a period of 10 years (PSA velocity of 0.03 ng/ml/year). Of the subjects with tPSA levels of 2 ng/ml or less, 2 years prior to cancer diagnosis, 11.4% had tPSA values of more than 4 ng/ml at the time of biopsy. Of the 972 men with tPSA below 1 ng/ml 2 years before the most recent measurement was obtained, 966 (99.4%) had no evidence of prostate cancer 2 years later, while six were found to have malignancies (0.6%). CONCLUSIONS: Longitudinal PSA changes in men with and without prostate cancer are significantly different. Annual testing may not be required in men with baseline tPSA levels of 1 ng/ml or below, whereas in patients with levels higher than 1 ng/ml, it seems to be indicated because of the significant percentage of men presenting with tPSA levels of more than 4 ng/ml two years later.

Adult↗

PubMed1997

Detection of circulating tumor cells in patients with prostate cancer using prostate specific membrane-derived primers in the polymerase chain reaction.

BACKGROUND: Prostate specific membrane antigen (PSM) is a transmembrane glycoprotein that has been described as human prostate specific. It is possible that PSM could be used as a biomarker for staging prostate cancer. METHODS: Peripheral blood mononuclear cells from 2 groups of patients with prostate cancer were used for the detection of PSM messenger ribonucleic acid (mRNA) using the reverse transcriptase-polymerase chain reaction (RT PCR) method. Group 1 consisted of 29 untreated patients (13 stage B cancer, 5 stage C, and 11 stage D cancers). Group 2 consisted of 40 treated patients (23 responded well and 17 had recurrence after treatment). In addition, blood specimens from 30 patients with benign prostatic hyperplasia, 5 women, and 5 men undergoing cystoprostatectomy for invasive bladder cancer were used as controls. We then correlated patient and disease characteristics with PCR assay results. RESULTS: Samples of all 40 controls were negative for PSM-mRNA. Thirteen of 29 patients of group 1 (45%) were positive for PSM-mRNA. The PCR positive rate did not correlate with clinical stage, pathologic stage, tumor grade, or serum PSA levels. Nine of 40 patients (22%) in group 2 were positive for PSM-mRNA, and the majority (8 of 9) were derived from the group of patients with recurrent disease. CONCLUSIONS: A nested RT PCR assay for PSM mRNA can detect circulating tumor cells in the peripheral blood of patients with prostatic cancer. These results suggest that the detection of circulating tumor cells could be useful for monitoring disease progression of prostatic cancer.

Adenocarcinoma↗

PubMed2006

Correlation between serum prostate-specific antigen and alpha-1-antitrypsin in men without and with prostate cancer.

Prostate specific antigen (PSA) is frequently used for prostate cancer (PCa) screening, but serum levels are also increased by prostate inflammation. Elevations in serum levels of alpha1-antitrypsin (ATT), a marker of inflammation, in cancer patients are well documented. However, an association between PSA and ATT has never been investigated. The authors, therefore, measured serum acute phase proteins (APPs) ATT, alpha1-acid glycoprotein, C-reactive protein, and alpha1-antichymotrypsin in 174 men without and 34 with newly diagnosed untreated PCa (38-80 years old). As expected, men with PCa had higher mean PSA levels than those without PCa (P < 0.00001). Men with PCa and those without PCa but with PSA >2 ng/mL (n = 68) had significantly higher ATT concentrations than those without these conditions (n = 106) (mean +/- SEM g/L): 1.94+/-0.083, 1.92+/-0.066, 1.25+/-0.043, respectively; p <0.005). Interestingly, African-American men without PCa (n=111) had higher ATT levels than Caucasian men (n=63) (1.565+/-0.045 g/l versus 1.395+/-0.056 g/l; p <0.005); and differences persisted in men with PSA >2 ng/ml (2.094+/-0.07 g/l versus 1.593 for all0.095 g/l; p<0.0002). There were no differences among groups in the levels of other APP. ATT showed the strongest correlation with PSA (r = 0.346 to 0.395; p <0.001) than any other APP (r < or =0.245). Our data suggest that men with PCa have higher ATT levels than those without PCa; and African-American men without PCa have higher ATT levels than Caucasian men. The possible implications of elevated ATT levels in African-American men on the risk of PCa are discussed.

Acute-Phase Proteins↗

PubMed2002

Transition to androgen-independence in prostate cancer.

Prostate carcinoma is the most frequently diagnosed malignancy and the second leading cause of death as a result of cancer in men in the western countries. Withdrawal of androgens or the peripheral blockage of androgen action remain the critical therapeutic options for the treatment of advanced prostate cancer. However, after initial regression, most of the prostate cancers become androgen-independent and progress further, with eventual fatal outcome. Understanding the mechanisms of transition to androgen independence and tumor progression in prostate cancer is critical to finding new ways to treat aged patients that are ineligible for conventional chemotherapy. A large number of different molecular mechanisms might be responsible for the transition to androgen-independence. Many of these involve the androgen receptor (AR) and its signalling pathways, but they might also include genetic changes that affect several genes, which results in the activation of oncogenes or the inactivation of tumor suppressor genes. Here, we discuss the most recent and relevant findings on androgen resistance in prostate cancer in order provide a comprehensive interpretation of the clinical behaviour of tumors at molecular levels.

Androgens↗

PubMed1993

Early detection of prostate cancer following repeated examinations by multiple modalities: results of the American Cancer Society National Prostate Cancer Detection Project.

The American Cancer Society National Prostate Cancer Detection Project (ACS-NPCDP) is a multicenter, interdisciplinary demonstration project to assess the impact on early detection of transrectal ultrasound (TRUS), prostate-specific antigen (PSA), and digital rectal examination (DRE). Preliminary data are available from the first 3-5 y of planned observation. The results show declining rates of detection for each succeeding examination. Cancer detection rates are highly dependent on age. The positive predictive value of a solitary examination is low regardless of modality, but any combination of positive results has a much better predictive value. The cancers detected were predominantly clinically localized tumors, and detection of advanced stage cancer was uncommon after the initial examination. Radical prostatectomy was the most common form of treatment. These findings have implications for prostate cancer early detection guidelines and practice.

Aged↗

PubMed2005

[MRI for troubleshooting detection of prostate cancer].

Prostate cancer is the most common malignancy in males. Men aged 50 and older are recommended to undergo an annual digital rectal examination (DRE) and determination of prostate-specific antigen (PSA) in serum for early detection. However, prostate biopsies guided by transrectal ultrasound (TRUS) come up negative for cancer in many patients despite having PSA levels above 4 ng/ml. T2-weighted Magnetic Resonance Imaging (MRI) is able to represent the prostate including the surrounding anatomy and depict suspicious areas of low intensity within a high-intensity peripheral zone. MRI has a higher sensitivity for detecting prostate carcinomas than DRE and TRUS in patients having an elevated PSA value and a negative core biopsy. However, its specificity is poor since other abnormalities such as prostatic intraepithelial neoplasia (PIN), prostatitis, scars, or haemorrhage have a similar MRI appearance. The use of additional techniques such as MR spectroscopy and contrast-enhanced dynamic MRI improves sensitivity, but in particular it improves the specificity of tumor detection. Newly developed biopsy devices enable the performance of targeted biopsies in areas that appear suspicious in the MRI.

Biopsy↗

PubMed2004

Targeting FSH in androgen-independent prostate cancer: abarelix for prostate cancer progressing after orchiectomy.

OBJECTIVES: To determine the efficacy of the gonadotropin-releasing hormone antagonist abarelix in patients with androgen-independent prostate cancer progressing after orchiectomy and to measure its effect on serum follicle-stimulating hormone (FSH). METHODS: Sixteen patients with prostate cancer progressing after orchiectomy received abarelix-depot 100 mg by intramuscular injection on days 1, 15, and 29 and then every 28 days for up to 24 weeks (52 weeks in patients who met the criteria for a prostate-specific antigen [PSA] response after 24 weeks). PSA response was the primary endpoint and was defined as a 50% reduction confirmed 4 weeks later. The time to progression and effect of therapy on serum FSH were secondary endpoints. RESULTS: No patient met the criteria for a PSA response. Five patients (31%, 95% confidence interval 11% to 58%) experienced confirmed reductions in the PSA level ranging from 9.3% to 31.8%. At the end of the six cycles of therapy, 6 patients remained stable without PSA progression or other signs of disease progression. The median time to progression was 12 weeks (95% confidence interval 6 to 18). The mean serum FSH concentration declined after 4 weeks of study treatment by nearly 90% from a baseline of 45.1 IU/L (95% confidence interval 34.0 to 56.2) and remained suppressed throughout the observation period. Treatment was well tolerated, with one grade 3 allergic reaction. CONCLUSIONS: Treatment with abarelix in patients with androgen-independent prostate cancer after orchiectomy results in marked reduction in circulating FSH. None of the patients met the PSA response criteria; nonetheless, minor reductions in serum PSA were observed in 5 of 16 patients.

Adenocarcinoma↗