SEARCH · PubMed Health

Results for “Prostate Cancer”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources

PubMed1998

Monograph series on aging-related diseases: X. Prostate cancer.

Prostate cancer is the most commonly diagnosed cancer among Canadian men, excluding non-melanoma skin cancer. Prostate cancer incidence increases almost exponentially with age; most cases are diagnosed in men aged 65 years or older. With the possible exception of animal fat consumption, no known widespread modifiable risk factors have been identified. Although the prognosis is good if appropriate treatment occurs in the early stages of disease, the ability of existing early detection techniques to decrease mortality has not yet been demonstrated. The considerable economic and societal burden of prostate cancer and its treatment, coupled with the projected large increase in the number of new prostate cancer cases as the population ages, make this disease a very important public health issue.

Aged↗

PubMed1992

Quality of life and psychosocial status in stage D prostate cancer. Zoladex Prostate Cancer Study Group.

Inasmuch as treatments for advanced prostate cancer may have identical clinical outcomes but very different meanings to patients, we sought to compare the impact of surgical and medical castration (orchiectomy versus injected goserelin acetate Zoladex) on quality of life and psychosocial status. A total of 147 men with Stage D prostate cancer participated in the study: 115 selected treatment with goserelin acetate, and 32 chose orchiectomy. Quality of life, as measured by the Functional Living Index: Cancer (FLIC), improved at both the 3 and the 6 month follow-up in the goserelin acetate group (p = 0.0001), but did not change from baseline at 6 months in the orchiectomy group (p = 0.54). These findings were paralleled by improvement from baseline in psychosocial status, as measured by the Profile of Mood States (POMS), at 6 month follow-up (p = 0.01 in the goserelin acetate group versus p = 0.60 in the orchiectomy group). This investigation, which is among the first to evaluate patients' appraisals of their lives following treatment choices for advanced prostatic cancer, argues compellingly for including quality of life in assessments of therapy.

Activities of Daily Living↗

PubMedDate not supplied

A qualitative analysis of interviews of men with early stage prostate cancer: the Prostate Cancer Lifestyle Trial.

We conducted interviews with a subsample of men (n = 26) participating in the Prostate Cancer Lifestyle Trial (PCLT), who had biopsy-proven prostate cancer (Gleason grade <7; prostate-specific antigen 4-10 ng/mL) and chose "watchful waiting" after diagnosis. The PCLT aimed at improving diet, exercise, stress management practices, and group support within a peer community setting. The aims of this study were to examine psychological, emotional, spiritual, and social reactions to (a) a diagnosis of early stage prostate cancer and (b) participation in the PCLT. Qualitative analyses were completed using MAXqda. Results indicated that the cancer diagnosis was met with anxiety, distress, and denial, or a "bump in the road" attitude. There was some indication that conflict with partners was exacerbated by the diagnosis. A significant component of the lifestyle intervention was involvement in the peer community. This community provided opportunities to experience connections with others facing similar health difficulties. Men generally expressed positive attitudes (emotionally, physically, and spiritually) about the lifestyle change, and felt that their participation in the program contributed to feelings of hope, optimism, and fighting spirit. Additionally, participants frequently mentioned increased comfort with emotional expression.

Adaptation, Psychological↗

PubMed2002

Parenteral estrogen versus combined androgen deprivation in the treatment of metastatic prostatic cancer -- Scandinavian Prostatic Cancer Group (SPCG) Study No. 5.

OBJECTIVE: In the mid-1980s, interest in parenteral estrogen therapy for prostate cancer was renewed when it was found that it influenced liver metabolism only marginally and had very few cardiovascular side-effects. In this study high-dose polyestradiol phosphate (PEP; Estradurin) was compared to combined androgen deprivation (CAD) for the treatment of patients with metastatic prostate cancer. The aim of the study was to compare anticancer efficacy and adverse events, especially cardiovascular side-effects. MATERIAL AND METHODS: A total of 917 patients with T0-4, NX, M1, G1-3 prostate cancer and an Eastern Cooperative Oncology Group performance status of 0-2 were randomized to treatment with either PEP 240 mg i.m. twice a month for 2 months and thereafter once a month or flutamide (Eulexin) 250 mg t.i.d. per os in combination with either triptorelin (Decapeptyl) 3.75 mg per month i.m. or, on an optional basis, bilateral orchidectomy. A total of 556 patients had died at the time of this analysis. RESULTS: There was no difference between the treatment arms in terms of time to biochemical or clinical progression and overall or disease-specific survival. There was no increase in cardiovascular mortality in the PEP arm. The PEP group had a higher prevalence of cardiovascular disease prior to the study and a significantly higher incidence of non-fatal ischemic heart events and heart decompensation during the study. CONCLUSIONS: PEP has an equal anticancer efficacy to CAD and does not increase cardiovascular mortality. Final evaluation of cardiovascular morbidity is awaiting further analysis and follow-up. PEP is considerably cheaper than CAD.

Aged↗

PubMed2005

Assessing benefit and risk in the prevention of prostate cancer: the prostate cancer prevention trial revisited.

PURPOSE: The Prostate Cancer Prevention Trial demonstrated a 25% reduction in period prevalence of prostate cancer in men randomly assigned to 5 mg/d of finasteride. However, widespread use of finasteride for prevention is inhibited by the observed increased risk of high-grade disease. We present a model of risk and benefit that estimates the potential effects of histologic artifact in the assignment of excess risk for high-grade disease and the possible effect of overdetection bias introduced by finasteride-induced volume reduction. METHODS: The absolute benefit/absolute risk ratio of finasteride use was estimated by calculating the ratio of absolute risk reduction in the finasteride arm to the absolute risk of excess high-grade cancers. This ratio was recalculated for assumptions that 10%, 25%, or 50% of the excess high-grade cancers were due to histologic artifact, and that there was a 25% overdetection bias in the finasteride arm. RESULTS: For all cancers the absolute benefit/absolute risk ratio increased from 4.6:1 to 5.1:1, 6.2:1, and 9.2:1 for assumptions of 10%, 25%, or 50% histologic artifact, respectively. The ratio increased from 4.6:1 to 8.2:1 for the assumption of 25% overdetection bias, and to 9.1:1, 10.9:1, and 16.3:1 for combined assumptions of 25% overdetection bias and 10%, 25%, or 50% histologic artifact, respectively. CONCLUSION: The adoption of a prevention strategy hinges on potential benefits weighed against potential risks. This model demonstrates the magnitude of effect for a hypothesized range of histologic artifact and overdetection bias on the assessment of risk versus benefit for finasteride.

Adenocarcinoma↗

PubMedDate not supplied

Derivation of MPR and TRAMP models of prostate cancer and prostate cancer metastasis for evaluation of therapeutic strategies.

Pre-clinical models of primary and metastatic prostate cancer are increasingly needed to evaluate efficacy of the new therapeutic strategies currently under investigation. The androgen-independent RM1 and androgen-dependent TR cell lines derived from transgenic mouse models of prostate cancer were examined in this regard. Following implantation in immune competent mice, the RM1 cell line was able to generate extremely fast growing s.c. and iprost tumors and metastatic lung lesions providing a time period of approximately 14-17 days from the time of tumor establishment to animal sacrifice to assess therapies. Implantation of TR cell lines resulted in more slowly growing s.c. and iprost tumors and metastatic lung lesions that exhibited highly variable incidence and growth. These models represent the best available means to evaluate therapeutics in primary and metastatic prostate cancer variants in an intact immune system.

Animals↗

PubMed2006

A prospective study of calcium intake and incident and fatal prostate cancer.

Prostate cancer is the most common incident cancer and the second leading cause of cancer mortality in U.S. males. Higher milk intake has been relatively consistently associated with an increased risk of prostate cancer, especially advanced prostate cancer. Some data suggest that high intake of calcium might account for this association, but this relationship remains controversial. We hypothesized that high calcium intake, possibly by lowering 1,25(OH)2 vitamin D levels, is associated with poorer differentiation in prostate cancer and thereby with fatal prostate cancer. We examined calcium intake in relation to prostate cancer risk using data from the Health Professionals Follow-up Study, a prospective cohort study of 47,750 male health professionals with no history of cancer other than nonmelanoma skin cancer at baseline. We assessed total, dietary, and supplementary calcium intake in 1986, 1990, 1994, and 1998, using a validated food frequency questionnaire. We calculated the multivariable relative risk (RR) and 95% confidence intervals (95% CI) using Cox proportional hazards regression. Over 16 years of follow-up, we identified 3,544 total cases of prostate cancer, 523 advanced (extraprostatic) cases, and 312 fatal cases. Higher calcium intake was not appreciably associated with total or nonadvanced prostate cancer but was associated with a higher risk of advanced and fatal prostate cancer [for fatal prostate cancer, compared with men whose long-term calcium intake was 500-749 mg/d (excluding supplement use of <5 years); those with intakes of 1,500-1,999 mg/d had a RR, 1.87; 95% CI, 1.17-3.01; and those with > or = 2,000 mg/d had a RR, 2.43; 95% CI, 1.32-4.48; P(trend) = 0.003]. Dietary calcium and supplementary calcium were independently associated with an increased risk. For high-grade prostate cancer (Gleason > or = 7), an association was observed for high versus low calcium intake (RR, 1.89; 95% CI, 1.32-2.71; P(trend) = 0.005), but a nonsignificant, inverse association was observed for organ-confined, low-grade prostate cancer (RR, 0.79; 95% CI, 0.50-1.25; P(trend) = 0.09). In a sample of this cohort, higher calcium intake was associated with lower circulating 1,25(OH)2 vitamin D levels. Our findings suggest that calcium intakes exceeding 1,500 mg/d may be associated with a decrease in differentiation in prostate cancer and ultimately with a higher risk of advanced and fatal prostate cancer but not with well-differentiated, organ-confined cancers.

Adult↗

PubMed1996

Preclinical models of prostate cancer.

Prostate cancer is the most common non-skin malignancy, yet the biological and molecular characteristics of the disease remain only poorly understood. One of the many reasons for this is that there are so few animal or human laboratory models of prostate cancer. Prostate cancer rarely arises spontaneously in animals, and the human cancer is unusually hard to grow in culture or as xenografts even short-term. The prostate cancer models that do exist are basically rodent models, human cell lines, human xenografts, and gene transfer and transgenic models. Many laboratories have put great effort into developing prostate cancer models, without much success. These efforts recently have been forced to be curtailed, primarily due to a lack of funding. There is good reason to believe, however, that propagation of metastatic tissue will be much more successful. At the University of Washington, the Prostate Cancer Donor Program, organized in a manner similar to existing methods for cadaver organ harvest, has been instituted to help recruit patients for these approaches. Prospects for success of model development also have been improved because of advances in techniques for the maintenance of severe combined immunodeficiency disease mice or nude mice.

Animals↗

PubMed2005

Elevation of dipeptidylpeptidase iv activities in the prostate peripheral zone and prostatic secretions of men with prostate cancer: possible prostate cancer disease marker.

PURPOSE: Dipeptidylpeptidase IV (DPIV) is a multifunctional type II plasma membrane glycoprotein with serine-type exopeptidase activity that is secreted by the prostate and increased in prostate cancer. We determined whether changes in DPIV activities in prostatic tissue zones and expressed secretions were associated with the presence of cancer. MATERIALS AND METHODS: Expressed prostatic secretion (EPS), and biopsy of the transition (TZ) and peripheral (PZ) zones were collected from men undergoing ultrasound guided prostate biopsy. DPIV activities were measured by glypro-p-nitroanalide hydrolysis. RESULTS: DPIV activities were significantly higher in TZ than in PZ tissues in men with no evidence of malignancy. However, activities in EPS were negatively associated with TZ volume and positively associated with PZ volume. Mean and median DPIV activities in EPS from men with biopsy determined cancer were significantly higher than in men with no evidence of malignancy. DPIV activities in TZ and PZ biopsies were higher in men with cancer but most markedly in the PZ. CONCLUSIONS: These data indicate that secreted DPIV originates from the TZ and PZ. Increased DPIV activities in cancer are strongly associated with the PZ, which is the zone most commonly involved with cancer. Measuring DPIV levels in expressed EPS or post-digital rectal prostate examination urine may be useful for evaluating men for prostate cancer.

Adenosine Deaminase↗

PubMed2002

The polycomb group protein EZH2 is involved in progression of prostate cancer.

Prostate cancer is a leading cause of cancer-related death in males and is second only to lung cancer. Although effective surgical and radiation treatments exist for clinically localized prostate cancer, metastatic prostate cancer remains essentially incurable. Here we show, through gene expression profiling, that the polycomb group protein enhancer of zeste homolog 2 (EZH2) is overexpressed in hormone-refractory, metastatic prostate cancer. Small interfering RNA (siRNA) duplexes targeted against EZH2 reduce the amounts of EZH2 protein present in prostate cells and also inhibit cell proliferation in vitro. Ectopic expression of EZH2 in prostate cells induces transcriptional repression of a specific cohort of genes. Gene silencing mediated by EZH2 requires the SET domain and is attenuated by inhibiting histone deacetylase activity. Amounts of both EZH2 messenger RNA and EZH2 protein are increased in metastatic prostate cancer; in addition, clinically localized prostate cancers that express higher concentrations of EZH2 show a poorer prognosis. Thus, dysregulated expression of EZH2 may be involved in the progression of prostate cancer, as well as being a marker that distinguishes indolent prostate cancer from those at risk of lethal progression.

Biomarkers, Tumor↗

PubMed1995

Prostate cancer risk in U.S. blacks and whites with a family history of cancer.

Prostate cancer occurs more frequently in U.S. blacks than whites. A population-based case-control study which investigated the association with family history of cancer was carried out among 981 men (479 black, 502 white) with pathologically confirmed prostate cancer, diagnosed between August 1, 1986, and April 30, 1989, and 1,315 controls (594 black, 721 white). Study subjects, aged 40-79, resided in Atlanta, Detroit, and 10 counties in New Jersey, geographic areas covered by population-based cancer registries. Prostate cancer risk was significantly elevated among those who reported a history of prostate cancer in first-degree relatives (O.R. = 3.2; 95% C.I.: 2.0-5.0), with blacks and whites having similarly elevated risks. These risks were unchanged by statistical adjustment for job-related socio-economic status, education, income, and marital status. Overall, the ORs associated with history of prostate cancer in fathers and brothers were 2.5 (95% C.I.: 1.5-4.2) and 5.3 (95% C.I.: 2.3-12.5), respectively. Risks associated with a family history of prostate cancer were consistently elevated among younger and older subjects. Only small non-significant excesses of prostate cancer risk were associated with a family history of breast, colorectal, or other cancers. While familial occurrence is a key risk factor for prostate cancer and likely to be genetically based, the similar familial risks among blacks and whites suggest that the ethnic disparity in incidence is influenced by environmental factors.

Adult↗

PubMed2006

Nomogram prediction for prostate cancer and aggressive prostate cancer at time of biopsy: utilizing all risk factors and tumor markers for prostate cancer.

BACKGROUND: There is a large amount of confusion in interpreting prostate specific antigen (PSA) values for prostate cancer. More precise risk assessments for prostate cancer detection are needed for men faced with an abnormal PSA. METHODS: We studied a sample of 2,637 men who underwent a prostate biopsy for an abnormal digital rectal exam (DRE) or PSA. Using factors including age, ethnicity, family history of prostate cancer, previous negative biopsy, presence of voiding symptoms, prostate volume, DRE and PSA, we constructed nomograms to predict the probability of prostate cancer at biopsy. RESULTS: Of the 2,637 men, 1,282 men (48.6%) had prostate cancer detected. Age, ethnicity, family history of prostate cancer, a previous negative biopsy, prostate volume, DRE and PSA were all significant predictors of prostate cancer. Nomograms were constructed based on these factors to predict the risk of prostate cancer and of aggressive prostate cancer (defined as a Gleason Score 7 or more). The positive predictive value varied from 5% to 95% based on the nomograms. The nomograms were validated using bootstrapping methods and the expected and observed proportions were found to be highly concordant. CONCLUSIONS: For men with an abnormal PSA or DRE, the risk for prostate cancer can be accurately estimated using a nomogram based on age, ethnicity, family history of prostate cancer, previous negative biopsy, presence of voiding symptoms, prostate volume, DRE and PSA. This tool will aid physicians and patients in determining the need for prostate biopsy.

Adult↗

PubMed2004

The role of fibroblast growth factors and their receptors in prostate cancer.

Prostate cancer is the most common malignancy in men in the USA and the second leading cause of cancer deaths. Fibroblast growth factors (FGFs), including FGF1 (acidic FGF), FGF2 (basic FGF), FGF6 and FGF8 are all expressed at increased levels in prostate cancer as paracrine and/or autocrine growth factors for the prostate cancer cells. In addition, increased mobilization of FGFs from the extracellular matrix in cancer tissues can increase the availability of FGFs to cancer cells. Prostate cancer epithelial cells express all four types of FGF receptors (FGFR-1 to -4) at variable frequencies. Expression of FGFR-1 and FGFR-4 is most closely linked to prostate cancer progression, while the role of FGFR-2 remains controversial. Activation of FGF receptors can activate multiple signal transduction pathways including the phospholipase Cgamma, phosphatidyl inositol 3-kinase, mitogen-activated protein kinase and signal transducers and activators of transcription (STAT) pathways, all of which play a role in prostate cancer progression. Sprouty proteins can negatively regulate FGF signal transduction, potentially limiting the impact of FGF signaling in prostate cancer, but in a significant fraction of prostate cancers there is decreased expression of Sprouty1 mRNA and protein. The effects of increased FGF receptor signaling are wide ranging and involve both the cancer cells and surrounding stroma, including the vasculature. The net result of increased FGF signaling includes enhanced proliferation, resistance to cell death, increased motility and invasiveness, increased angiogenesis, enhanced metastasis, resistance to chemotherapy and radiation and androgen independence, all of which can enhance tumor progression and clinical aggressiveness. For this reason, the FGF signaling system it is an attractive therapeutic target, particularly since therapies targeting FGF receptors and/or FGF signaling can affect both the tumor cells directly and tumor angiogenesis. A number of approaches that could target FGF receptors and/or FGF receptor signaling in prostate cancer are currently being developed.

Antineoplastic Agents↗

PubMed1993

[Usefulness of prostate specific antigen/gamma-seminoprotein ratio for diagnosis of prostate cancer].

Prostate specific antigen (PSA) and gamma-seminoprotein (gamma-Sm) are used as tumor markers of the prostate cancer. However, the serum concentrations of PSA and gamma-Sm are frequently increased in patients with benign prostatic hypertrophy (BPH). We measured the ratio of serum PSA to gamma-Sm concentration (P/S ratio), and evaluated its usefulness for diagnosis of prostate cancers. Between April 1988 and July 1992, 162 men underwent prostatic biopsy and/or TUR-P, and were diagnosed pathologically. Of 162 patients, 112 were diagnosed as BPH and 50 were diagnosed as prostate cancer. Of 24 patients with serum PSA level of > 20 ng/ml, 23 (95.8%) were prostate cancer, while, of 79 patients with serum PSA level of 3.0-20 ng/ml, 23 (29.1%) were prostate cancer. The sensitivity and the specificity for PSA were 92.0% and 49.1%, respectively. Of 85 patients with serum gamma-Sm level of > 4.0 ng/ml, 30 (35.3%) were prostate cancer. The sensitivity and the specificity for gamma-Sm were 60.0% and 50.9%, respectively. A mean +/- SD of P/S ratio in 112 patients with BPH was 0.954 +/- 0.591. While, the mean +/- SD of P/S ratio was 16.295 +/- 58.584 in all prostate cancer patients, and 2.031 +/- 0.654 in 27 prostate cancer patients with serum PSA level of < or = 20 ng/ml. P/S Ratio in prostate cancer patients with serum PSA of < or = 20 ng/ml as well as in all prostate cancer patients were significantly higher than P/S Ratio of BPH patients (p < 0.0001). Of 55 patients with P/S Ratio of > or = 1.50, 45 (81.8%) were prostate cancer and 10 (18.2%) were BPH. While, of 107 patients with P/S Ratio of < 1.50, 102 (95.3%) were BPH and 5 (4.7%) were prostate cancer. The sensitivity and the specificity for P/S Ratio were 90.0% and 91.1%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗

PubMed2006

[Nutrition and pharmacological treatment for prevention of prostate cancer].

Prostate cancer is the most common neoplasm and the second cause of cancer death. It is an excellent target for primary chemopreventive strategies for the following reasons: it is highly prevalent and has a long latency period, there are identifiable risk factors and a precursor lesion and it produces a biochemical marker (serum PSA) which can serve as an intermediate end point in chemoprevention studies. The goal of primary prevention strategies is to prevent development of clinical life-threatening neoplasms in asymptomatic patients with no evidence of clinical disease. Identification of populations at risk for developing cancer is the cornerstone of chemoprevention. Well-established risk factors for prostate cancer include African-American race, older age and family history. Data on diet and obesity are less clearly defined. Since high grade prostatic intraepithelial neoplasia (PIN) is an early predictor of prostate cancer, preventive strategies focusing on men with high grade PIN are being explored. It was demonstrated that finasteride could significantly reduce prostate cancer in asymptomatic men with normal PSA and no abnormalities on rectal examination. Elevated prostaglandin levels, and upregulation of cyclooxygenase-2 (COX-2) are found in prostate cancer cell lines. There is some epidemiologic evidence that regular use of NSAIDs, which inhibit COX-2, may be associated with a lower risk of prostate cancer. In the field of nutrition, data from prospective large-scale studies demonstrated that increased consumption of lycopene-rich tomato-based foods referred to a reduction in the risk for prostate cancer. Vitamin E was also found to reduce prostate cancer risk. Prospective data showed that vitamin D has an inhibitory effect on prostate cancer development while increased calcium consumption, independent from dietary intake, might increase the risk. Dietary fat intake, particularly from animal sources, may also increase the risk for prostate cancer. Whether this effect is strictly due to the already identified compounds or to other compounds, remains to be explored. Further study will hopefully help to establish a core set of nutritional and dietary factors that can positively or negatively affect prostate cancer development, as well as a set of pharmacologic agents that can reduce the risk of prostate cancer development and/or progression in selected patients.

Anticarcinogenic Agents↗

PubMed2003

Therapeutic targets for metastatic prostate cancer.

Prostate cancer is the most commonly diagnosed non-cutaneous cancer in adult males. Although prostate cancer that is confined to the gland can be cured in many patients using surgery or radiation, these treatments are only effective for localized tumors and the long-term failure rates for these treatments suggests that prostate cancer can metastasize relatively early in the course of the disease. Once prostate cancer has metastasized there are no curative therapies. The greatest challenge in the treatment of advanced prostate cancer is to access and eliminate metastatic cells. Therefore, effective prostate cancer therapy will require novel strategies to target cancer cells both at the site of the primary tumor and at distant metastatic sites. In this article we review several therapeutic targets and approaches that may provide new treatments for metastatic prostate cancer. We discuss the use of small molecules to target specific molecular events associated with metastatic prostate cancer, the use of specific antibodies that target unique metastasis associated molecules and the use of various gene therapy strategies to achieve anti-metastatic activities.

Animals↗

PubMed1995

Prostate-specific antigen testing to screen for prostate cancer.

Prostate cancer is a common cause of cancer-related morbidity and mortality in men. Prostate-specific antigen (PSA) measurement to screen for prostate cancer has been promoted as a way to reduce morbidity and mortality from prostate cancer. This paper examines the usefulness of PSA screening for asymptomatic prostate cancer, focusing on outcomes for all patients screened. The sensitivity and specificity of PSA testing for prostate cancer are low and have not been studied properly in asymptomatic men being screened for prostate cancer. PSA screening detects localized prostate cancer undetected by digital rectal examination in fewer than 1% of men screened. The effectiveness of early treatment of prostate cancer, compared with deferral of treatment until symptoms develop, is unproven, and good survival rates have been reported among patients who defer aggressive treatment. Complications of treating prostate cancer with radical prostatectomy or radiation treatment include death, impotence, urethral stricture, incontinence, and rectal injury. At the present time, there is insufficient evidence to support a policy of PSA screening, and its use should be discouraged until randomized controlled trials demonstrate benefit from PSA screening.

Humans↗

PubMed2007

Does PSA play a role as a promoting agent during the initiation and/or progression of prostate cancer?

Prostate cancer cells, like normal prostate epithelial cells, produce high levels of the differentiation marker and serine protease prostate-specific antigen (PSA). PSA is used extensively as a biomarker to screen for prostate cancer, to detect recurrence following local therapies, and to follow response to systemic therapies for metastatic disease. While much is known about PSA's role as a biomarker, only a relatively few studies address the role played by PSA in the pathobiology of prostate cancer. Autopsy studies have documented that not only do prostate cancer cells maintain production of high amounts of PSA but they also maintain the enzymatic machinery required to process PSA to an enzymatically active form. A variety studies performed over the last 10 years have hinted at a role for PSA in growth, progression, and metastases of prostate cancer. A fuller understanding of PSA's functional role in prostate cancer biology, however, has been hampered by the lack of appropriate models and tools. Therefore, the purpose of this review is not to address issues related to PSA as a biomarker. Instead, by reviewing what is known about the genetics, biochemistry, and biology of PSA in normal and malignant prostate tissue, insights may be gained into the role PSA may be playing in the pathobiology of prostate cancer that can connect measurement of this biomarker to an understanding of the underlying etiology and progression of the disease.

Adult↗