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PubMed1999

Advances in the application of prostate-specific antigen in the detection of early-stage prostate cancer.

Prostate-specific antigen (PSA) has revolutionized the detection of prostate cancer. PSA-based screening has been shown to be effective in detecting prostate cancer at an early, potentially curable stage; however, this tumor marker is limited by appreciable false-positive and false-negative results. This is especially problematic when the PSA level is in the upper limit of normal (2.5 to 4.0 ng/mL) or the intermediately increased range (4.1 to 10.0 ng/mL). Several PSA-related indexes and assays have been proposed in an attempt to improve the power of PSA in the early detection of prostate cancer: PSA density (PSAD), age-referenced PSA, volume-referenced PSA, PSAD of the transition zone (PSA-TZ), ProstAsure Index, (Global Health Net, Savannah, GA) and percent free PSA. These indexes may improve the sensitivity and specificity of PSA-based screening, facilitating the early detection of prostate cancer and reducing the number of unnecessary biopsies.

Age Factors↗

PubMed2006

Id proteins expression in prostate cancer: high-level expression of Id-4 in primary prostate cancer is associated with development of metastases.

A major cause of treatment failure for prostate cancer is the development of androgen-independent metastatic disease. Id protein family, a group of basic helix-loop-helix transcription factors, has been shown to be involved in carcinogenesis and a prognostic marker in several types of human cancers. In this study, we examined the expressions of four Id proteins, Id-1, -2, -3 and -4, in 125 clinical prostate cancer specimens as well as 40 nodular hyperplasia specimens by immunohistochemistry. The expressions of Id proteins were correlated with Gleason grading and metastatic progress of the tumors. We found that Id proteins were dysregulated in prostate cancer. Id-1 and -2 expressions were elevated while Id-3 and -4 expressions were reduced in prostate cancers compared to nodular hyperplasia. Cytoplasmic staining of Id-1 (P=0.013) and nuclear staining of Id-2 (P=0.001) and Id-4 (P<0.001) were positively correlated with Gleason score. The results indicate that these Id proteins may play a positive role in the development of prostate cancer. In contrast, Id-3 might have an inverse relationship with prostate neoplastic transformation (P=0.002) and cancer progression (P=0.022). We found that Id-4 nuclear overexpression in the primary prostate cancers significantly increased the risks to the development of metastasis in the patients (odds ratio=3.215, 95% confidence interval=1.150-8.987, P=0.026). Our results suggest that in prostate cancer patients, differential Id proteins expressions may be a useful marker for poor prognosis, and Id-4 may be a potential prognostic marker for distant metastasis.

Aged↗

PubMed2000

Prostate-specific antigen and androgens in African-American and white normal subjects and prostate cancer patients.

Prostate cancer in African Americans is more aggressive and common than in any other racial group. An endocrine mechanism has been proposed to account for this racial difference. However, androgen levels in African-American elderly normal subjects and prostate cancer patients have been insufficiently studied. Because the Albert Einstein Medical Center (AEMC) has a large African-American population, we could contribute racial data from which observations could be made within this study and in past and future studies. Blood from 38 screened men (mean age 65) with prostate-specific antigen (PSA) less than 4 ng/mL and normal rectal examination seen at the AEMC Cancer Center was studied using standard radioimmunoassays. The blood samples also served as our control. Our experimental group consisted of 51 prostate cancer patients (mean age 71 years), all of whom had nonmetastatic prostate cancer. Subjects were categorized by cancer status, race, and age group. In our screened subjects, PSA, testosterone, and dihydrotestosterone were not higher in African Americans than in whites. Furthermore, our prostate cancer patients demonstrated no significant racial variation for PSA, testosterone, and dihydrotestosterone. Our data also did not indicate any correlation between PSA and androgen levels in our cancer patients. In our population of elderly men, no racial differences in androgen levels were found. Androgen levels did not correlate with PSA levels in prostate cancer patients.

Black or African American↗

PubMed2003

Genome-wide scan for prostate cancer susceptibility genes using families from the University of Michigan prostate cancer genetics project finds evidence for linkage on chromosome 17 near BRCA1.

BACKGROUND: Previous linkage studies have suggested prostate cancer susceptibility genes located on chromosomes 1, 20, and X. Several putative prostate cancer candidate genes have also been identified including RNASEL, MSR1, and ELAC2. Presently, these linkage regions and candidate genes appear to explain only a small proportion of hereditary prostate cancer cases suggesting the need for additional whole genome analyses. METHODS: A genome-wide mode-of-inheritance-free linkage scan, using 405 genetic markers, was conducted on 175 pedigrees, the majority containing three or more affected individuals diagnosed with prostate cancer. Stratified linkage analyses were performed based on previously established criteria. RESULTS: Results based on the entire set of 175 pedigrees showed strong suggestive evidence for linkage on chromosome 17q (LOD = 2.36), with strongest evidence coming from the subset of pedigrees with four or more affected individuals (LOD = 3.27). Race specific analyses revealed strong suggestive evidence for linkage in our African-American pedigrees on chromosome 22q (LOD = 2.35). CONCLUSIONS: Genome-wide analysis of a large set of prostate cancer families indicates new areas of the genome that may harbor prostate cancer susceptibility genes. Specifically, our linkage results suggest that there is a prostate cancer susceptibility gene on chromosome 17 that is independent of ELAC2. Further research including combined analyses of independent genome-wide scan data may clarify the most important regions for future investigation.

Age of Onset↗

PubMed2001

Ki-67 index in metastatic prostate cancer.

OBJECTIVE: Prostate cancer in bone is generally thought to progress more rapidly than in its primary site, a supposition that is supported by studies of prostate-specific antigen velocity. However, descriptions of proliferative rates in metastases have relied on inferred data from in vitro studies of cell lines derived from metastases. The aim of this study was to determine directly the proliferative rate within bone metastases arising from prostate cancer. PATIENTS AND METHODS: 10 bone biopsies containing metastatic deposits of untreated prostatic cancer were obtained. These were immunohistochemically stained for the Ki-67 protein with the monoclonal antibody MIB-1, using the streptavidin-biotin complex technique. Benign prostatic tissue was used as the control. Using an image analyser, the Ki-67 index (% of cells staining positively) in each specimen was determined. RESULTS: In the 10 specimens the Ki-67 index ranged from 0.15 to 7.82%. Wide overlap was seen between groups of differing tumour differentiation. CONCLUSION: The proliferative rate as determined by the Ki-67 index in bone metastases of prostate cancer is similar to that reported in primary tumours. There does not appear to be a relationship between tumour grade and proliferative index in these specimens.

Adenocarcinoma↗

PubMed2006

[The search for better markers for prostate cancer than prostate-specific antigen].

Prostate-specific antigen (PSA) is currently the most important biochemical marker for the diagnosis of prostate cancer. Because of the limited specificity of PSA, clinically irrelevant tumours and benign abnormalities are also detected that potentially lead to over-treatment and the accompanying physical and emotional burden for the patient. In addition, PSA is used as an indicator of progression or clinical response after treatment for prostate cancer, but the prognostic value of this marker is limited. Current studies are evaluating a number of alternative markers, such as PSA-related parameters, human kallikrein 2, osteoprotegerin and the gene DD3(PCA3), that may improve the specificity of current PSA-based diagnostics and the prognostic value of PSA.

Antigens, Neoplasm↗

PubMed2004

Has there been a change in practice of screening for prostate cancer with prostate-specific antigen in Ontario?

OBJECTIVE: To determine whether there has been a change in the rate of screening in Ontario in 2002 compared to 1995. METHODS: A questionnaire was mailed to 520 physicians, associated with PSA records selected randomly from the database of a large community laboratory. Physicians were asked to consult their records as to the reasons for PSA testing. RESULTS: There were 285 usable responses from 520 mailings (response rate 55%), mostly (91%) from family or general practice. Reasons for testing, expressed as proportions of responses, were as follows (this study, 1995 study and P value for the differences): screening for prostate cancer (74%, 63%; P = 0.059), diagnosis of urinary symptoms (30%, 40%; P = 0.027), follow-up of a medical procedure or drug therapy (14%, 32%; P = 0.001), confirmation of a previous PSA result (14%, 6%; P = 0.015) and other reasons (7%, 8%; P = 0.73). Of those records with screening as one reason for testing, 80% vs. 66% (P = 0.003) indicated it was the only reason; 86% vs. 73% (P = 0.003) indicated that it was part of a routine examination, and 54% vs. 64% (P = 0.052) indicated that the test was requested by the patient. CONCLUSION: These findings are consistent with increased screening for prostate cancer with PSA.

Adult↗

PubMed2004

A phase I trial of DNA vaccination with a plasmid expressing prostate-specific antigen in patients with hormone-refractory prostate cancer.

Prostate-specific antigen (PSA) is a serine protease secreted at low levels by normal luminal epithelial cells of the prostate and in significantly higher levels by prostate cancer cells. Therefore, PSA is a potential target for various immunotherapeutical approaches against prostate cancer. DNA vaccination has been investigated as immunotherapy for infectious diseases in patients and for specific treatment of cancer in certain animal models. In animal studies, we have demonstrated that vaccination with plasmid vector pVAX/PSA results in PSA-specific cellular response and protection against tumour challenge. The purpose of the trial was to evaluate the safety, feasibility and biological efficacy of pVAX/PSA vaccine in the clinic. A phase I trial of pVAX/PSA, together with cytokine granulocyte/macrophage-colony stimulating factor (GM-CSF) (Molgramostim) and IL-2 (Aldesleukin) as vaccine adjuvants, was carried out in patients with hormone-refractory prostate cancer. To evaluate the biologically active dose, the vaccine was administered during five cycles in doses of 100, 300 and 900 microg, with three patients in each cohort. Eight patients were evaluable. A PSA-specific cellular immune response, measured by IFN-gamma production against recombinant PSA protein, and a rise in anti-PSA IgG were detected in two of three patients after vaccination in the highest dose cohort. A decrease in the slope of PSA was observed in the two patients exhibiting IFN-gamma production to PSA. No adverse effects (WHO grade >2) were observed in any dose cohort. We demonstrate that DNA vaccination with a PSA-coding plasmid vector, given with GM-CSF and IL-2 to patients with prostate cancer, is safe and in doses of 900 microg the vaccine can induce cellular and humoral immune responses against PSA protein.

Adenocarcinoma↗

PubMed2026

Lifestyle, anthropometric factors and clinically significant prostate cancer diagnosis in men with suspected prostate cancer.

OBJECTIVE: Lifestyle and anthropometric factors may influence prostate cancer (PCa) risk, yet evidence remains inconclusive. This study reports the associations between lifestyle and anthropometric factors and clinically significant PCa (csPCa; ISUP grade > 1) among men with clinical suspicion of PCa. MATERIALS AND METHODS: In this registered (NCT06116851), single-institution, prospective cohort trial, men referred for PCa diagnostics due to elevated prostate-specific antigen or abnormal digital rectal examination were included. Subjects underwent prostate diagnostics and completed detailed surveys of lifestyle, medical and family history. Physical activity was measured using a triaxial accelerometer. Anthropometric assessments included body mass index, waist circumference and magnetic resonance imaging-based body composition analyses. RESULTS: Among 298 included men, 143 (48%) were diagnosed with csPCa. In multivariate logistic regression, higher physical activity, measured by step count (odds ratio [OR]: 0.91, 95% confidence interval [CI]: 0.82-0.99) and active smoking compared to never-smokers (OR: 0.38, 95% CI: 0.14-0.96) were inversely associated with detection of csPCa. Higher prostate-specific antigen density was associated with increased risk (OR: 1.78, 95% CI: 1.39-2.35). Body composition was not associated with csPCa. Study strengths include comprehensive data collection. Primary limitation is partial reliance on self-reported data. CONCLUSIONS: Higher measured physical activity was inversely associated with detection of csPCa in men with suspicion of PCa. Active smoking also showed an inverse association. Both findings merit further investigation.

Aged↗

PubMed2006

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

The serine protease Omi/HtrA2 is released from mitochondria into the cytosol after apoptotic stimuli, inducing apoptosis in a caspase-independent manner through its protease activity and in a caspase-dependent manner by neutralizing the inhibition of inhibitor of apoptosis proteins (IAPs) on caspases. Alteration of apoptosis is essential for cancer development, and cancer cell death by radiation and chemotherapy is largely dependent upon apoptosis. Thus, analysis of the expression status of Omi/HtrA2, a regulator of apoptosis, in cancer tissues is needed for an understanding of cancer development. In the current study we analyzed the expression of Omi/HtrA2 in 65 prostate cancer, 40 benign prostatic hyperplasia and 10 normal prostate specimens by immunohistochemistry. Omi/HtrA2 mRNA levels of in vivo prostate cancer and benign prostatic hyperplasia samples were also assayed by semiquantitative reverse transcription-polymerase chain reaction. Immunopositivity (defined as > or =30%) was observed for Omi/HtrA2 in most of the prostate cancers, and the positive rate of Omi/HtrA2 was lower in the well-differentiated group than in the poorly and moderately differentiated groups (p<0.005). By contrast, the cells in the normal prostate and benign prostatic hyperplasia groups showed no or only weak expression of Omi/HtrA2. Meanwhile, the Omi/HtrA2 mRNA level of prostate cancer is much higher than that of benign prostatic hyperplasia (p<0.001). Taken together, these results suggest that prostate cancer cells in vivo may need Omi/HtrA2 expression for apoptosis, and that Omi/HtrA2 expression might be involved in prostate cancer development.

Aged↗

PubMed2000

Meta-analysis for combining relative risks of alcohol consumption and prostate cancer.

BACKGROUND: Prostate cancer has become the most common cancer among men in the United States, but little is known about factors associated with prostate cancer incidence. METHODS: A meta-analysis of studies published prior to July 1998 was conducted to pool relative risk (RR) estimates from the existing literature on the association between prostate cancer and alcohol consumption, in an attempt to determine whether there is an association, and if so, what its magnitude is. RESULTS: The overall pooled RR estimate was 1. 05 for both fixed and random effects models, based on six cohort studies and 27 case-control studies. The RR estimate varied little by study design. Among types of consumption, the highest risk was found for beer (RR = 1.27), but this was based on only eight studies that reported type of alcohol consumed. A linear dose-response was fit to the 15 studies reporting amount of alcohol consumed, finding a RR of 1.05 (95% confidence interval (CI), 0.91-1.20) for each additional drink of alcohol per day or a RR of 1.21 for 4 drinks per day. When the average drinks per day consumed in the 15 studies were used to estimate the overall risk for all 33 studies, a RR of 1.02 was found for each additional drink of alcohol per day. CONCLUSIONS: Overall, no association between prostate cancer and alcohol consumption was seen. While some categories of consumption showed an increased risk, the studies reporting such categories appeared to be biased towards reporting a positive association among the categories.

Alcohol Drinking↗

PubMed2004

Update on screening for prostate cancer with prostate-specific antigen.

Serum prostate-specific antigen (PSA) determination in conjunction with digital rectal examination (DRE) is recommended by the majority of clinical guidelines for early detection(opportunistic screening) of prostate cancer provided the patient is well informed and has a life-expectancy of at least 10 years. The major disadvantage of PSA is its lack of specificity. Various static and dynamic concepts have been developed to improve the diagnostic performance of PSA of which free/total PSA ratio and PSA doubling time seem to be the most promising. Apart from early detection, population screening(mass screening) is a distinct topic. The effect of the latter one with regard to reduction of prostate cancer specific mortality and quality of life issues is not yet clear. Several national and international prospective trials are currently being conducted to answer these important questions but results will only be available in a few years.

Biomarkers, Tumor↗

PubMed1999

Improved discrimination of prostate cancer and benign prostatic hyperplasia by means of the quotient of free and total PSA.

The value of t-PSA (total prostate specific antigen) and of the quotient of free and t-PSA (% f-PSA) for the discrimination of BPH (benign prostatic hyperplasia) and PC (prostate cancer) as well as possible influencing factors were subject to examination under study conditions. The sera of 210 patients (131 BPH, 79 PC patients) were examined by means of the Immulite test; thereof 76 male patients (47 BPH, 29 PC patients) were found to have a t-PSA-value between 4 and 10 ng/ml (grey area). Apart from the age and the findings of rectal digital examination, we recorded the prostate volume, indications of non-specific increases in PSA and for PC patients also the TNM-G stage. For patients with prostate cancer the quotient of f- and t-PSA was significantly lower (median: 0.08) than compared to patients with BPH (median: 0.22) (p<0.001). Also in the grey area the quotient was significantly lower in patients with malignant diagnosis (median: 0.12) than for patients with a non-malignant diagnosis (median: 0.21) (p<0.001). ROC curves were prepared in order to compare the capability of discrimination of the two parameters. At this point, the better discrimination potential of the quotient in the grey area became evident. Due to the fact that priority was given to the detection of carcinoma, the threshold value was defined at a level at which high sensitivity (90%) is existent in combination with an acceptable specificity (approx. 50%). The resultant values are for the total PSA area 0.21, for the grey area 0.19 as a cut-off. Neither the age, nor the prostate volume, nor urinary tract infections had any influence upon the quotient. There was also no correlation between the stage or the grading of the tumour and the percentage of the f-PSA. The quotient alleviates the discrimination between BPH and PC, in particular in the diagnostically problematic grey area. Thus, it can serve as an aid for the decision "biopsy or re-biopsy". As there is currently no standardized method for the application of % f-PSA, there is a requirement for further examination under homogeneous criteria.

Adult↗

PubMed1999

Current and projected annual direct costs of screening asymptomatic men for prostate cancer using prostate-specific antigen.

BACKGROUND: Concern over the cost of screening for asymptomatic prostate cancer by means of prostate-specific antigen (PSA) testing has played an important role in PSA screening policy. However, little is known about the true costs of current PSA screening in Canada and how costs may change in the future. METHODS: The authors performed a cost identification study from the perspective of provincial ministries of health. They used data from published reports, hospital discharge data, claims data from several provinces, a laboratory survey, a national survey of knowledge, attitudes and beliefs about screening, a provincial cancer registry and expert opinion to estimate current first-year screening costs. Using demographic data from Statistics Canada and various scenarios regarding changes in screening patterns, the authors derived estimates of the future costs of PSA screening. RESULTS: In 1995 PSA screening cost an estimated $45 million (range $40 million to $84 million). Treatment accounted for over 61% of total costs, whereas screening, diagnosis and staging accounted for 35%. Screening all eligible men in Canada in 1995 would have cost $317 million (range $356 million to $691 million), more than the costs of all prostate cancer care in that year. Annual recurrent screening for all eligible men in 2005 would cost $219 million (range $208 million to $412 million). Projections from existing trends suggest that annual costs of PSA screening in 2000 are likely to increase from the estimated $45 million to approximately $66 million (range $59 million to $126 million). INTERPRETATION: PSA screening is costly, but even universal screening would consume a smaller share of national health expenditures than previous studies have suggested. Costs attributable to PSA screening may increase in the future owing to changes in utilization patterns and demographic shifts.

Aged↗

PubMed2006

Prostate cancer screening in high-risk men: African American Hereditary Prostate Cancer Study Network.

BACKGROUND: There are scant data available on prostate cancer screening among high-risk African American men with positive family histories. It is important to determine whether or not their screening rates differ from those in the general population. METHODS: This study computed rates of previous digital rectal examination (DRE) and prostate-specific antigen (PSA) screening for prostate cancer in cancer-free (unaffected) relatives age 40-69 years from African American families that had four or more men with prostate cancer. The rates for these 134 high-risk African American men from the African American Hereditary Prostate Cancer Study (AAHPC) were compared with nationwide estimates obtained from participants in the 1998 and 2000 National Health Interview Survey (NHIS), for which the numbers of demographically comparable subjects were 5583 (4900 Caucasians, plus 683 African Americans) and 3359 (2948 Caucasians, 411 African Americans), respectively. RESULTS: Men in the AAHPC cohort (with a strong positive family history) had significantly less screening than both African Americans and Caucasians in the NHIS cohorts. Only about one-third (35%) of the men in the AAHPC unaffected cohort had ever had a DRE, and only about 45% of them had ever received a PSA test. These rates were much lower than those obtained for African American men in the NHIS: 45% for DRE and 65% for PSA. These discrepancies increased with age. CONCLUSIONS: Older African American men with positive family histories report surprisingly low rates of DRE and PSA screening compared with their counterparts in the NHIS surveys. At-risk men need to be informed of the benefits and limitations of prostate cancer screening and actively involved in decision-making for or against prostate cancer screening.

Adult↗

PubMedDate not supplied

Is vitamin D deficiency a risk factor for prostate cancer? (Hypothesis).

Prostate cancer is a major cause of cancer death among males, yet little is known about its etiology. We hypothesize that Vitamin (Hormone) D deficiency may underlie the major risks for prostate cancer, including age, Black race, and northern latitudes. These factors all are associated with decreased synthesis of Vitamin D. Mortality rates from prostate cancer in the U.S. are inversely correlated with ultraviolet radiation, the principal source of Vitamin D. This hypothesis is consistent with known antitumor properties of Vitamin D, and may suggest new avenues for research in prostate cancer.

Humans↗

PubMed1995

Effects of age, sex steroids, and family relationships on volumes of prostate zones in men with and without prostate cancer.

Benign prostatic hyperplasia (BPH) and prostate cancer commonly occur together. This suggests that common familial, hormonal, and environmental factors contribute to their development. In men at risk for the development of prostate cancer (at 40 men in 19 families) and aged-matched unrelated controls (n = 46), we have determined whether familial factors, age, and blood hormone concentrations are related to the transition zone (TZ), peripheral zone (PZ), or total volume of the prostate measured by transrectal ultrasound (TRUS). We determined that the influences of age, prostate cancer (n = 15), and familial status did not significantly affect the relationships reported. Therefore, data from all groups were combined for this study. TZ correlated positively with age (P = 0.003) after controlling for family status, but total prostate volume correlated insignificantly with age (P = 0.08). In addition, the ratio of TZ to PZ volumes also correlated significantly with age in the control group (r = 0.27, P = 0.014). Both TZ and PZ volumes correlated highly (r = 0.91, P < 0.0001, n = 86) with total volume. In addition, total volume correlated significantly (r = 0.71, P < 0.001) with the ratio of the TZ/PZ volumes, which also correlated significantly with each other (r = 0.61, P < 0.0001, n = 86). In contrast to the increase of TZ volume related to total prostate volume, PZ volume declined compared with total volume. Prostate volumes up to 50 ml are predominated by the PZ and above 50 ml by the TZ, which may compress and shrink the PZ. Both TZ and total prostate volume correlated positively with serum estrone concentrations (P = 0.04 and P = 0.003, respectively). These results suggest that the risk of prostate cancer does not contribute to generalized overgrowth of the prostate, including the TZ. However, estrogens and age strongly influence TZ but not PZ volume. Both PZ and TZ volumes rise together until the prostate exceeds 50 ml, when the growth of the TZ appears to exceed the PZ and then to compress it.

Aged↗

PubMed2000

Analysis of HPC1, HPCX, and PCaP in Icelandic hereditary prostate cancer.

Putative prostate cancer susceptibility loci have recently been identified by genetic linkage analysis on chromosomes 1q24-25 (HPC1). 1q44.243 (PCaP), and Xq27-28 (HPCX). In order to estimate the genetic linkage in Icelandic prostate cancer families, we genotyped 241 samples from 87 families with eleven markers in the HPC1 region, six markers at PCaP, and eight at HPCX. Concurrently, we assessed allelic imbalance at the HPC1 and PCaP loci in selected tumors from the patients. For each of the candidate regions, the combined parametric and non-parametric LOD scores were strongly negative. Evidence for linkage allowing for genetic heterogeneity was also insignificant for all the regions. The results were negative irrespective of whether calculations were performed for the whole material or for a selected set of early age at onset families. The prevalence of allelic imbalance was relatively low in both the HPC1 (0%-9%) and PCaP (5%-20%) regions and was not elevated in tumors from positively linked families. Our studies indicate that the putative cancer susceptibility genes at chromosomes 1q24-25, 1q44.2-43, and Xq27-28 are unlikely to contribute significantly to hereditary prostate cancer in Iceland and that selective loss of the HPC1 and PCaP loci is a relatively rare somatic event in prostate cancers.

Alleles↗