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PubMed1996

Screening and early detection of prostate cancer will decrease morbidity and mortality from prostate cancer: the argument for.

Since prostate cancer represents the most common male malignancy and the second most frequent cause of cancer-related mortality, there is a significant need for methods to either reduce the incidence, improve therapy, or provide early detection. Of these, only the latter appears to be currently at hand. Many investigators have demonstrated that early detection programmes, incorporating a carefully performed digital rectal examination and prostate-specific antigen level testing, have resulted in a significant detection rate of clinically relevant malignancy at a time when it is curable. Although problems such as overdetection, lead- and length-time bias, and significant financial burden are associated with prostate cancer screening, if we are to significantly impact the mortality from this disease, such approaches are probably warranted.

Aged↗

PubMedDate not supplied

Public awareness of prostate cancer and the prostate-specific antigen test.

Prostate cancer and prostate-specific antigen (PSA) testing have been the focus of significant media attention. This study examines the public's knowledge of prostate cancer, knowledge of the PSA test, and among men, the use of the test. The data are from the 1993 Kentucky Health Survey, an annual probability-based statewide telephone survey of adult (18 years of age and older) Kentucky residents (n = 661). Although 92% of the sample reported hearing of prostate cancer, the respondents were basically uninformed about the outcomes of prostate cancer. Men 50 years of age and older were no more informed than was the rest of the sample about prostate cancer or PSA testing. However, 94% of the men who had the test recommended by their physician had undergone the test. These findings indicate that adults remain poorly informed about prostate cancer and possible case-finding strategies. If the American Cancer Society's (ACS) early detection recommendations are to succeed, attention should focus on improving the public's awareness of currently available methods for early detection of prostate cancer.

Health Knowledge, Attitudes, Practice↗

PubMed2002

Reduced plasma levels of coagulation factors in relation to prostate cancer.

BACKGROUND: Prostate cancer has historically been associated with coagulation abnormalities. This study was undertaken to investigate the prevalence of abnormalities of coagulation factors in patients with prostate cancer before and after radical prostatectomy (RP). Because coagulation factors have been shown to be involved in tumor angiogenesis, the vascular density of the prostate tumors was assessed. METHODS: Plasma of 40 consecutive patients with histologically proven prostate cancer was investigated pre-RP and post-RP. The antigen level for antithrombin, plasminogen activator inhibitor-1, and heparin cofactor-II, and the plasma activity of antithrombin and plasminogen were determined by using immunologic and chromogenic assays. The values of these assays were compared with a group of 28 male, age-matched patients without any evidence of cancer and 18 patients with orthopedic interventions preoperatively and postoperatively. The vascular density of the prostate tumors was assessed by staining paraffin sections with an antibody to CD34. RESULTS: The median plasma antigen levels and/or activities of the investigated factors were below normal in the prostate cancer patients before RP. Furthermore, coagulation factors were significantly lower than in the age-matched control group and patients before and after orthopedic surgery. In prostate cancer patients, the median values of all investigated factors went up to normal levels within 2 weeks after RP, whereas postsurgical levels in orthopedic patients remained stable. No correlations to tumor parameters have been observed. CONCLUSION: We assume that the reduction of these coagulation factors is a principle concept in prostate cancer that needs further investigation.

Adult↗

PubMed2003

Annexin II expression is reduced or lost in prostate cancer cells and its re-expression inhibits prostate cancer cell migration.

While studying Bim, a BH3-only proapoptotic protein, we identified an approximately 36 kDa protein, which was abundantly expressed in all five strains of primary normal human prostate (NHP) epithelial cells but significantly reduced or lost in seven prostate cancer cell lines. The approximately 36 kDa protein was subsequently identified as annexin II by proteomic approach and confirmed by Western blotting using an annexin II-specific antibody. Conventional and 2D SDS-PAGE, together with Western blotting, also revealed reduced or lost expression of annexin I in prostate cancer cells. Subcellular localization studies revealed that in NHP cells, annexin II was distributed both in the cytosol and underneath the plasma membrane, but not on the cell surface. Prostate cancer cells showed reduced levels as well as altered expression patterns of annexin II. Since annexins play important roles in maintaining Ca(2+) homeostasis and regulating the cytoskeleton and cell motility, we hypothesized that the reduced or lost expression of annexin I/II might promote certain aggressive phenotypes of prostate cancer cells. In subsequent experiments, we indeed observed that restoration of annexin II expression inhibited the migration of the transfected prostate cancer cells without affecting cell proliferation or apoptosis. Hence, our results suggest that annexin II, and, likely, annexin I, may be endogenous suppressors of prostate cancer cell migration and their reduced or lost expression may contribute to prostate cancer development and progression.

Amino Acid Sequence↗

PubMed2005

A germline DNA polymorphism enhances alternative splicing of the KLF6 tumor suppressor gene and is associated with increased prostate cancer risk.

Prostate cancer is a leading and increasingly prevalent cause of cancer death in men. Whereas family history of disease is one of the strongest prostate cancer risk factors and suggests a hereditary component, the predisposing genetic factors remain unknown. We first showed that KLF6 is a tumor suppressor somatically inactivated in prostate cancer and since then, its functional loss has been further established in prostate cancer cell lines and other human cancers. Wild-type KLF6, but not patient-derived mutants, suppresses cell growth through p53-independent transactivation of p21. Here we show that a germline KLF6 single nucleotide polymorphism, confirmed in a tri-institutional study of 3,411 men, is significantly associated with an increased relative risk of prostate cancer in men, regardless of family history of disease. This prostate cancer-associated allele generates a novel functional SRp40 DNA binding site and increases transcription of three alternatively spliced KLF6 isoforms. The KLF6 variant proteins KLF6-SV1 and KLF6-SV2 are mislocalized to the cytoplasm, antagonize wtKLF6 function, leading to decreased p21 expression and increased cell growth, and are up-regulated in tumor versus normal prostatic tissue. Thus, these results are the first to identify a novel mechanism of self-encoded tumor suppressor gene inactivation and link a relatively common single nucleotide polymorphism to both regulation of alternative splicing and an increased risk in a major human cancer.

Alleles↗

PubMed2001

Ca(2+)-sensing receptor expression and PTHrP secretion in PC-3 human prostate cancer cells.

Prostate cancer metastasizes frequently to bone. Elevated extracellular calcium concentrations ([Ca(2+)](o)) stimulate parathyroid hormone-related protein (PTHrP) secretion from normal and malignant cells, potentially acting via the [Ca(2+)](o)-sensing receptor (CaR). Because prostate cancers produce PTHrP, if high [Ca(2+)](o) stimulates PTHrP secretion via the CaR, this could initiate a mechanism whereby osteolysis caused by bony metastases of prostate cancer promotes further bone resorption. We investigated whether the prostate cancer cell lines LnCaP and PC-3 express the CaR and whether polycationic CaR agonists stimulate PTHrP release. Both PC-3 and LnCaP prostate cancer cell lines expressed bona fide CaR transcripts by Northern analysis and RT-PCR and CaR protein by immunocytochemistry and Western analysis. The polycationic CaR agonists [Ca(2+)](o), neomycin, and spermine each concentration dependently stimulated PTHrP secretion from PC-3 cells, as measured by immunoradiometric assay, with maximal, 3.2-, 3.6-, and 4.2-fold increases, respectively. In addition, adenovirus-mediated infection of PC-3 cells with a dominant negative CaR construct attenuated high [Ca(2+)](o)-evoked PTHrP secretion, further supporting the CaR's mediatory role in this process. Finally, pretreating PC-3 cells with transforming growth factor (TGF)-beta(1) augmented both basal and high [Ca(2+)](o)-stimulated PTHrP secretion. Thus, in PTHrP-secreting prostate cancers metastatic to bone, the CaR could initiate a vicious cycle, whereby PTHrP-induced bone resorption releases [Ca(2+)](o) and TGF-beta stored within bone, further increasing PTHrP release and osteolysis.

Adenoviridae Infections↗

PubMed2003

Men with colorectal cancer are predisposed to prostate cancer.

BACKGROUND: The objective of the present study was to investigate the relationship between colorectal and prostate cancer. METHODS: All Victorian men who developed metachronous colorectal and prostate cancer with the first primary diagnosed between 1982 and 1993 were identified retrospectively from the Victorian Cancer Registry and were followed up to the end of 1995. Analyses were stratified by age group and years of follow up. The cause of death in those men who had prostate cancer following colorectal cancer was determined. The stage of colorectal cancer was compared between men with and without second primary prostate cancer and the grade of prostate cancer was compared with men who did not have a prior colorectal cancer. RESULTS: Men who develop colorectal cancer are at increased risk of prostate cancer, with the greatest risk in men under the age of 65 (Relative risk approximately 2). Men with first primary colorectal cancer are more likely to develop prostate cancer than colorectal second primaries, and men who develop second primary prostate cancer are more likely to die of prostate cancer than colorectal cancer. CONCLUSIONS: Younger men diagnosed with colorectal cancer are at increased risk of prostate cancer. However, there is no direct evidence that screening for prostate cancer leads to a reduction in mortality. This should be considered when discussing long-term follow up.

Age Factors↗

PubMed2005

Androgen deprivation therapy for prostate cancer.

CONTEXT: Prostate cancer is the most common nonskin cancer and second most common cause of cancer mortality in US men. Androgen deprivation therapy (ADT), specifically surgical or medical castration, is the first line of treatment against advanced prostate cancer and is also used as an adjuvant to local treatment of high-risk disease. OBJECTIVE: To review systematically the evidence on the risks and benefits of ADT for prostate cancer as well as clinical management of its adverse effects. EVIDENCE ACQUISITION: We performed MEDLINE searches of English-language literature (1966 to March 2005) using the terms androgen deprivation therapy, hormone treatment, and prostate cancer. We reviewed bibliographies of literature to extract other relevant articles. Studies were selected based on clinical pertinence, with an emphasis on controlled study design. EVIDENCE SYNTHESIS: Androgen deprivation therapy is effective for palliation in many patients with advanced prostate cancer and improves outcomes for high-risk patients treated with radiation therapy for localized disease. Although patients with increasing prostate-specific antigen levels after local treatment without metastatic disease frequently undergo ADT, the benefits of this strategy are not clear. Adverse effects of ADT include decreased libido, impotence, hot flashes, osteopenia with increased fracture risk, metabolic alterations, and changes in cognition and mood. CONCLUSIONS: Androgen deprivation therapy has clear roles in the management of advanced prostate cancer and high-risk localized disease. The benefits of ADT in other settings need to be weighed carefully against substantial risks and adverse effects on quality of life.

Androgen Antagonists↗

PubMed2003

Predictors of prostate cancer on repeat prostatic biopsy in men with serum total prostate-specific antigen between 4.1 and 10 ng/mL.

OBJECTIVES: We determine whether the different molecular forms of prostate-specific antigen (PSA) and other PSA variables can predict prostate cancer in men undergoing repeat prostate needle biopsy. METHODS: Between 1997 and 2001, repeat biopsy was performed in 97 patients who had undergone prior negative prostate biopsy. The ability of total PSA (tPSA), complexed PSA (cPSA), free PSA (fPSA), free-to-total PSA (fPSA/tPSA), free-to-complexed PSA (fPSA/cPSA), complexed-to-total PSA (cPSA/tPSA), tPSA density (tPSAD), cPSA density (cPSAD), transition zone tPSA density (tPSATZ) and transition zone cPSA density (cPSATZ) was assessed by univariate and multivariate analyzes as well as receiver operating characteristics (ROC) curves. RESULTS: Prostate cancer on repeat biopsy was detected in 24% of subjects (23 of 97) who had a negative initial biopsy. The PSA parameters cut-off to ensure a 96% sensitivity of cancer detection, were 29% using fPSA/tPSA, 32% using fPSA/cPSA, 0.18 ng/mL/cc using tPSATZ and 0.16 ng/mL/cc using cPSATZ. The fPSA/tPSA would have prevented 32% of negative biopsies, the fPSA/cPSA 28%, the tPSATZ 23% and the cPSATZ 30%. ROC curve analysis fPSA/tPSA, fPSA/cPSA ratios, tPSATZ and cPSATZ were significantly better predictors of repeat biopsy results than tPSA or cPSA, but there was no significant difference in the ROC curves among these four PSA parameters. In the multivariate logistic regression analysis these four PSA parameters were significant predictors for cancer detection in the repeat biopsy group (P < 0.001). CONCLUSION: fPSA/tPSA ratio, fPSA/cPSA ratio, tPSATZ and cPSATZ enhance the specificity of PSA testing compared to tPSA or cPSA when determining which patients should undergo repeat biopsy.

Aged↗

PubMed1994

Meta-analysis of the literature: guideline development for prostate cancer treatment. American Urological Association Prostate Cancer Guideline Panel.

Medical interventions are identified to be in need of practice guidelines based on several criteria, including uncertainty of therapeutic benefit, economic impact, variation in practice patterns and lack of objective data for new developments. Treatment of localized adenocarcinoma of the prostate meets these criteria and has been identified as an issue in need of practice guideline development. The American Urological Association began working toward establishing prostate cancer treatment guidelines in 1989. An explicit method based on collection of scientific data was adopted, which requires complete review of the literature and analysis of the evidence collected. An update on the progress toward this data analysis and guideline document is presented.

Adenocarcinoma↗

PubMed2006

New insights into prostate cancer biology.

Prostate cancer is common, biologically heterogeneous, and protean in its clinical manifestations. Through the use and analysis of isogenic cell lines, xeno-grafts, transgenic mice, and human tumors, one begins to deconvolute the precise biologic mechanisms that combine to create the native complexity and heterogeneity of this disease. In this article, the authors have underscored compelling recent discoveries in prostate cancer so as to provide the reader with molecular paradigms with which to interpret future insights into its biology. Although it was inevitably necessary to omit a significant amount of important research in prostate cancer, the work discussed here is exemplary of current prostate cancer research. Looking forward, it is hoped that the collective work of mapping genetic and biologic interactions among key regulators of prostate epithelial cells, epithelial-stromal interactions, host immune system, and host genetics will eventually result in a comprehensive understanding of prostate cancer. Although it is likely that the molecular characteristics of an individual's prostate cancer will be analyzed using limited molecular tools in the near future, eventual application of genomic technologies and nanotechnology offers the promise of robust future characterization. Such a characterization is likely to be required to maximize our ability to optimize and individualize preventive and treatment strategies.

Genomics↗

PubMed1998

Hereditary prostate cancer and other genetic predispositions to prostate cancer.

The incidence of prostate cancer (CaP) and its increase in the last 10 years vary both from country to country and according to the ethnic group, with the highest incidence reported for Afro-Americans and the lowest for Asian men. To date, only three risk factors have been established for CaP: age; familial aggregation of CaP, and ethnic origins. No dietary or environment-related cause has been established. However, some variations in endogenous genetic factors may help explain differences in risk among ethnic groups or geographic areas. Similarly, certain genetic polymorphisms of genes encoding for 5alpha-reductase, androgen receptor or vitamin D, have been associated with different levels of CaP risk, and could explain the variations observed between populations. Different studies support the view that familial CaP may truly be hereditary, and not due to a similar lifestyle. Thus, familial inheritance is a parameter that needs to be considered in recommending screening for high-risk families. Indeed, when 1, 2, and 3 first-degree relatives are affected, the relative risk of first-degree relatives of CaP patients may increase to 2, 5, and 11%, respectively. Some familial forms appear to be associated with transmission of a rare putative dominant gene with a high penetrance (88% at age 85), with the cumulative proportion of CaP attributable to this gene being more marked for younger patients (a 43 versus a 34% risk of CaP appearing before the age of 55 versus 70 years). Using this transmission model and linkage analysis, a predisposing locus on chromosome 1q24-25 (HPC-1) has been described. Moreover, recessive and X-linked transmission has been suggested, showing that a large proportion of familial CaP may not be due to segregation of a few major gene mutations, but rather to familial sharing of alleles at many loci, each contributing to a small increase in cancer risk. Candidate genes may be the same suppressor genes that are involved in other cancers and in sporadic CaP.

Aged↗

PubMed2005

Assessment of a fragment of e-cadherin as a serum biomarker with predictive value for prostate cancer.

In prostate cancer, biomarkers may provide additional value above standard clinical and pathology parameters to predict outcome after specific therapy. The purpose of this study is to evaluate an 80 kDa fragment of the cell adhesion molecule e-cadherin as a serum biomarker. A broad spectrum of prostate cancer serum samples, representing different stages of prostate cancer disease, including benign prostatic hyperplasia (BPH), localised (Loc PCA) and metastatic prostate cancer (Met PCA), was examined for the cleaved product. There is a significant difference in the expression level of the 80 kDa fragment in the serum of healthy individuals vs patients with BPH and between BPH vs Loc PCA and Met PCA (P<0.001). Highest expression levels are observed in advanced metastatic disease. In the cohort of Loc PCA cases, there was no association between the 80 kDa serum concentration and clinical parameters. Interestingly, patients with an 80 kDa level of >7.9 microg l(-1) at the time of diagnosis have a 55-fold higher risk of biochemical failure after surgery compared to those with lower levels. This is the first report of the application of an 80 kDa fragment of e-cadherin as a serum biomarker in a broad spectrum of prostate cancer cases. At an optimised cutoff, high expression at the time of diagnosis is associated with a significantly increased risk of biochemical failure, potentially supporting its use for a tailored follow-up protocol for those patients.

Aged↗

PubMed2005

Adiponectin as a growth inhibitor in prostate cancer cells.

Prostate cancer is associated with obesity. However, the molecular basis of this association is not well known. Adiponectin is a major adipose cytokine that decreases in circulation in obesity and ameliorates obesity. Here, we identify adiponectin as a novel inhibitor in prostate cancer cell growth. Adiponectin occurs in non-proteolytic (full-length adiponectin: f-adiponectin) and proteolytic (globular adiponectin) forms in various oligomeric states (trimer, hexamer, and high molecular weight complex). The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay demonstrates that f-adiponectin inhibits prostate cancer cell growth drastically at subphysiological concentrations. Furthermore, velocity sedimentation analysis shows that the high molecular weight complex of f-adiponectin is the inhibitory form. Moreover, f-adiponectin suppresses leptin- and/or insulin-like growth factor-I (IGF-I)-stimulated, androgen-independent DU145 cell growth, and dihydrotestosterone-stimulated, androgen-dependent LNCaP-FGC cell growth. In addition, f-adiponectin enhances doxorubicin inhibition of prostate cancer cell growth. Therefore, f-adiponectin is a molecular mediator between prostate cancer and obesity, and may be therapeutic to prostate cancer.

Adipocytes↗

PubMed2001

Loss of heterozygosity of the putative prostate cancer susceptibility gene HPC2/ELAC2 is uncommon in sporadic and familial prostate cancer.

The recognition that prostate cancer clusters within families has led to the search for prostate cancer susceptibility genes. Recently, the HPC2/ELAC2 gene on chromosome 17p has been identified as a potential prostate cancer predisposition gene using both family based as well as case-control studies. Many cancer susceptibility genes act as tumor suppressor genes in which inactivation of one allele in the tumor can be detected via loss of heterozygosity (LOH). To determine whether the HPC2/ELAC2 gene demonstrates significant LOH in sporadic and familial prostate cancers, paired tumor and normal DNA samples were isolated using microdissection techniques from 44 radical prostatectomy specimens. Cases were analyzed using a panel of markers in the following order: TP53-D17S969-D17S947-(HPC2/ELAC2)-D17S799-D17S936. LOH was observed in < 10% of cases using the four markers that map to the HPC2/ELAC2 region. However, allelic loss was observed at the TP53 gene in 25% of informative cases. Taken together, inactivation of the HPC2/ELAC2 gene via LOH is a relatively uncommon event in prostate cancer. Future studies will determine whether 17p LOH occurs in the subset of patients with an inherited mutation in HPC2/ELAC2.

Adult↗

PubMedDate not supplied

Identification of metastasis-associated genes in prostate cancer by genetic profiling of human prostate cancer cell lines.

OBJECTIVES: Prostate cancer (PCa) is a heterogeneous tumour entity with known interindividual differences in biological behaviour regarding tumour aggressiveness and metastatic potentiaL To date, the prediction of the metastatic status of patients with PCa has not been possible. To identify the molecular causes behind these differences, the gene expression profiles of two cell lines (LNCaP and LNCaP C4-2) with different metastatic potentials were examined using DNA microarray technology. MATERIALS AND METHODS: LNCaP and LNCaP C4-2 cells were cultured under standard conditions. RNA was isolated using Trizol extraction. After processing the total RNA according to the manufacturer's instructions, we performed Affymetrix GeneChip analysis with HG-U133A chips. Data analysis was performed using NetAffx, dChip, GenMAPP and OMIM software. RESULTS: After statistical evaluation of the raw data, we obtained a set of 158 differently expressed probe sets in the LNCaP and LNCaP C4-2 cells. The search for genes associated with proliferation, cell metabolism, growth factors, metastatic potential and tumour progression in this list revealed a number of 42 differently expressed probe sets. The comparison of this list of probe sets with the literature resulted in a list of 14 differently expressed genes which could well contribute to the metastatic potential and progression of PCa. Of these 14 genes only 6 (Cip1, IGF-1, NK4, CXCL 12, ILGF2R, RHOE) have already been associated with PCa, whereas the other 8 genes (FSTL-1, SOCS-2, Midkine, Thrombospondin 1, Secretory leukocyte protease inhibitor, Desmoglein 2, MLT 1, PTPRF) had not been previously related to PCa. CONCLUSION: DNA microarray technology offers the possibility of screening a large number of genes with regard to alterations in the expression level or mutations. In this study, we identified 14 genes that are most probably associated with the higher metastatic potential of LNCaP C4-2 cells as compared to LNCaP cells. Eight of these 14 genes are potential new molecular markers for assessing the metastatic potential of PCa, or may serve as therapeutical targets.

Apoptosis↗

PubMed1998

Expression of gonadotropin-releasing hormone (GnRH) and GnRH receptor mRNA in prostate cancer cells and effect of GnRH on the proliferation of prostate cancer cells.

The purpose of this study was to determine the production of gonadotropin-releasing hormone (GnRH), the co-occurrence of GnRH receptors in prostate cancer cells, and the effect of GnRH on prostate cancer cell proliferation. Four human prostate cancer cell lines were studied. LNCaP is an androgen sensitive prostate cancer cell line, DU-145 and PC-3 are androgen resistant, and TSU-Pr1 is uncharacterized. The expression of GnRH and GnRH receptor mRNAs were assessed by in situ hybridization and the effect of exogenous GnRH on proliferation of prostate cancer cells was measured by thymidine incorporation assay. GnRH mRNA expression, determined by in situ hybridization, was found in 83.48% of the LNCaP, 89.7% of the TSU-Pr1, 86.2% of the PC-3 and 95.3% of the DU-145. Signals of GnRH receptor mRNA were detected in more than 95% of the cells of all four cell lines. The proliferation of the prostate cancer cells grown in media supplemented with peptide hormone lacking charcoal-stripped serum was significantly (P < 0.05) suppressed. No significant effect of GnRH on the proliferation of all four prostate cancer cells was observed. In summary, prostate cancer cells produced GnRH and its receptors, and exogenous GnRH treatment did not affect the prostate cancer cell proliferation. The existence of GnRH and GnRH receptor mRNA in the same cell suggests that the role of GnRH produced by prostate cancer cells would be autocrine.

Cell Division↗

PubMedDate not supplied

Novel polymorphisms in prostate specific antigen gene and its association with prostate cancer.

Prostate-specific antigen (PSA) is now used widely for the diagnosis and monitoring of patients with prostate cancer. The PSA gene is a target of the androgen receptor (AR) which interacts with androgen response elements (AREs) in the PSA gene promoter. Recently, we identified two novel polymorphisms in the PSA promoter ARE2 region in breast cancer. We hypothesized that some genetic variations might also exist in the AREs of prostate cancer, and that feature might correlate with cancer development and/or progression. To test this hypothesis, three AREs of the PSA gene promoter were characterized for 47 prostate cancer cases and 105 controls from the Japanese population. We demonstrated the presence of two polymorphisms at positions -252 (G or A) and -205 (A or AA), which were the same as those we have found in breast cancer. Interestingly, the -252 A was linked with the presence of -205 AA, and the -252 G was always linked with the presence of -205 A. Therefore, only A-AA and G-A (-252--205) alleles were present in the Japanese population. The proportion of patients who were either heterozygotes or homozygotes for the A-AA allele was not significantly different from that observed among 105 individuals without cancer (p = 0.726). However, comparing with G-A allele homozygotes, prostate cancer patients carrying at least 1 A-AA alleles tended to exhibit high serum PSA levels (p = 0.0002), poor differentiation (p = 0.0149) and advanced clinical stage (p = 0.0077). These results suggest that the novel polymorphisms identified in the PSA gene promoter may affect transcriptional activity of the PSA gene, and an excess of PSA production may enhance rapid progression of prostate cancer.

Aged↗