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PubMed1999

Selenium and prostate cancer prevention.

Prostate cancer is the second leading cause of cancer deaths in men, therefore it is increasingly important to understand its biology and epidemiology. New approaches for the primary and secondary prevention of prostate cancer are needed, including innovative uses of chemoprevention. This review provides an overview of the epidemiological data suggesting that higher intakes of selenium may reduce the risk of prostate cancer. In addition, a discussion of preclinical data is presented. Special emphasis is placed on the following areas: (1) chemical forms of selenium and antitumorigenic activity, (2) in vitro effects of selenite versus monomethylated selenium, and (3) current clinical intervention trials with selenium in prostate cancer. Chemoprevention, especially with dietary forms of selenium, is a promising new approach that presently is undergoing intensive investigation.

Cell Division↗

PubMedDate not supplied

Diet, androgens, oxidative stress and prostate cancer susceptibility.

Prostate cancer is the most common human malignancy and the second leading cause of cancer deaths among men in Western nations. Descriptive epidemiologic data suggest that androgens and/or environmental exposures, such as diet (in particular, dietary fat), play an important role in prostatic carcinogenesis. One plausible link between diet and prostate cancer is oxidative stress. This process refers to the generation of reactive oxygen species, which can then trigger a host of pro-carcinogenic processes. Recent studies also indicate that androgens increase oxidative stress within human prostate cancer cell lines. Recent data from our institution indicate that oxidative stress is higher within the benign epithelium of prostate cancer patients than men without the disease. This confirms our hypothesis and suggests that antioxidants such as lycopene, vitamin E, and selenium may play an important role in preventing disease progression. Large-scale clinical trials with some of these agents are currently in the design phase.

Carotenoids↗

PubMed2003

Apolipoprotein E expression in localized prostate cancers.

Although prostate cancer has become the most common solid tumor diagnosed in men and the second leading cause of death due to malignancy, the progression of the disease is still somewhat unpredictable, until it becomes locally advanced or metastatic. The clinical problem to distinguish between dormant and progressive cancers is essential to patient care, as surgical and medical therapies have significant risk of morbidity and disability. Multiple gene expression in prostate cancer was surveyed by differential display cloning between the undifferentiated hormone refractory human prostate cancer cell line PC-3 (highly tumorigenic in nude mice) the hormone responsive LNCaP cell line (weakly tumorigenic in nude mice), and the poorly differentiated DU-145 cell line (moderately tumorigenic). ApoE mRNA was found to be highly expressed only in PC-3 cell-line. We further examined its protein expression by immunohistochemistry in 20 prostatectomy specimens and an association between Gleason score for each sample and ApoE expression was determined. ApoE expression correlates directly with the Gleason score in tissue sections, hormone independence as well as local and distant invasiveness. Prostatic intraepithelial neoplasias (PINs) adjacent to clinically manifested cancer were positive whereas more distant PINs were negative for ApoE. ApoE may represent a marker of more aggressive cells in human prostate cancers.

Aged↗

PubMed2005

Can we prevent prostate cancer?

BACKGROUND: Prostate cancer is the second leading cause of cancer deaths among men. It is common in Australia, New Zealand, North America and North West Europe, but rare in Asia, Africa and South America. OBJECTIVE: This article reviews the role of chemopreventive agents for prostate cancer. The available evidence strongly suggests that dietary changes and supplementation with a variety of micronutrients, vitamins and trace elements may reduce the incidence and mortality of prostate cancer. DISCUSSION: Epidemiologic observations reveal lower cancer rates in those with diets rich in fruits, vegetables, vitamins, and a number of specific foods. This available data is adequate to clinically apply the role of various factors to possibly reduce the incidence of prostate cancer.

Adult↗

PubMed2003

The combination of antiangiogenic and cytotoxic agents in the treatment of prostate cancer.

Metastatic prostate cancer is one of the leading causes of cancer death in men. Although initially responsive to hormone therapy, it eventually progresses in almost all patients. For this reason, there has been a search for novel agents to use in the fight against androgen-independent prostate cancer. Antiangiogenesis is a relatively new antitumor strategy that has been employed in the treatments of many malignancies. As prostate cancer is likely dependent on angiogenesis for its growth and progression, it would logically serve as a good target for this modality. Initially met with great enthusiasm, antiangiogenic drugs have seen only limited success when used as single agents. This has been attributed to many possible etiologies including lack of cytotoxicity and use in situations of large tumor burden. In order to overcome these problems, many investigators are combining antiangiogenic agents with more traditional cytotoxic chemotherapy regimens in hope of augmenting the effects of either drug alone. This article will review the background of angiogenesis inhibition and the use of such combinations in metastatic prostate cancer.

Angiogenesis Inhibitors↗

PubMed1998

Expression of the extracellular matrix signaling molecule Cyr61 is downregulated in prostate cancer.

BACKGROUND: Prostate cancer (CaP) is one of the most common neoplasms in the USA and Europe. We used differential display PCR (DD-PCR) to identify genes related to the development of prostate cancer. METHODS: The RNA of 4 patients with untreated CaP was analyzed for differentially expressed genes. Using DD-PCR, we identified a downregulated cDNA-fragment in these prostate cancer cells. This fragment (N7) was cloned and further analyzed by CMRT-PCR, Northern-blot analysis, and in situ hybridization. RESULTS: Sequence analysis revealed that N7 is identical to the 3'-untranslated region of the recently described immediate early gene Cyr61. Comparative multiplex RT-PCR with sequence specific primers showed that Cyr61 is downregulated in the tumor tissue of 7 out of 13 patients. By in situ hybridization we could demonstrate that the expression of Cyr61 is restricted to the epithelium of the prostate. Immunohistochemical analysis showed that Cyr61 protein could be found in the epithelium of normal prostatic tissue, whereas prostate cancer tissue showed a marked decrease of Cyr61 protein expression. CONCLUSIONS: Cyr61 is a member of the emerging family of extracellular signaling proteins and enhances the effect of bFGF. The changed pattern of expression Cyr61 might therefore contribute to the altered interactions between epithelial and stromal cells in prostate carcinoma.

Animals↗

PubMed2003

Populations at high risk for prostate cancer.

Although prostate cancer tends to be a slow-growing neoplasm affecting older men, there is clearly a subset of patients at high risk for developing early and possibly more aggressive disease. This group of high-risk patients includes men with a family history of prostate cancer and various histologic features such as PIN and ASAP identified on an initial biopsy. Black American men have a much higher risk of developing prostate cancer when compared with white men and especially Asian men. This finding may reflect both genetic and environmental factors. Screening men at increased risk of developing prostate cancer appears to be a logical strategy, especially in light of recent reports that suggest a benefit to aggressive treatment.

Diet↗

PubMed2006

Knowledge of epigenetic influence for prostate cancer therapy.

Prostate cancer is one of the most prevalent cancers in men in many countries, increasing in frequency with age through the most advanced years. The standard treatment for newly diagnosed metastatic tumors is androgen ablation. However, advanced prostate cancer nevertheless often develops in many cases. Although hormonal manipulation and chemotherapy have uncertain value for advanced lesions, especially androgen-independent, recent studies of docetaxel-based chemotherapy in men with androgen-independent prostate cancer have shown a survival benefit. Intensive investigations have shown that aberrant epigenetic features. including aberrant DNA methylation, make an important contribution to carcinogenesis as well as genetic alterations. Hypermethylation of CpG islands in promoter regions can lead to silencing of tumor-suppressor genes, while hypomethylation of the genome leads to instability. This review attempts to provide up-to-date information regarding the significance of epigenetics for human prostate cancer, with aberrations offering dues to therapy and possibly also providing targets for anticancer drugs.

Animals↗

PubMed2004

Therapeutic potential of curcumin in prostate cancer--V: Interference with the osteomimetic properties of hormone refractory C4-2B prostate cancer cells.

BACKGROUND: There is increasing evidence that the stringent selective pressure imposed by androgen ablation therapy on the residual prostate cancer cells may actually accelerate the development of the hormone refractory and bone metastatic phenotype. The propensity of prostate cancer to establish osseous metastases is very likely mediated by the osteomimetic properties of the prostate cancer cells. Prostate cancer cells acquire these "bone-like" properties in order to survive in the bony microenvironment. This process is facilitated by common growth factor trophisms between the bone stromal cells, osteoblasts, and the prostate cancer cells wherein a number of growth factors and their receptors are involved. Thus, a general inhibition of the tyrosine kinase signaling pathways may have a therapeutic advantage in interfering with the metastatic potential of these prostate cancer cells. This study focuses on the potential of curcumin, a plant based non-toxic tyrosine kinase inhibitor in interfering with the development of bone like properties of C4-2B, a highly metastatic derivative of LNCaP prostate cancer cell line. METHODS: C4-2B prostate cancer cells were analyzed for their constitutive expression and ligand inducible activation of growth factor receptors such as EGF-R and CSF1-R. Expression of bone-specific transcription factors such as Cbfa-1 and the production of PTHRP were followed. The ability of the C4-2B cells to mineralize under specific conditions was analyzed. The activation status of the transcription factor NF-kappa B was also followed. RESULTS: Curcumin inhibited the ligand-stimulated autophosphorylation of EGF-R and CSF1-R that were crucially involved in the development of osteomimetic properties of C4-2B cells. When C4-2B cells were grown under promineralization conditions, curcumin prevented the formation of the mineralized nodules. It also inhibited the expression of the core-binding factor a-1 in C4-2B cells which was responsible for the expression of several bone-specific proteins. The IKK activity was severely impaired, showing marked NF-kappa B inhibition. The experiments indicate that curcumin can also interfere with the development of the osteoblast and the osteoclast-like properties by these prostate cancer cells. CONCLUSIONS: The highly metastatic C4-2B prostate cancer cell line is already "programmed" to exhibit the bone-like properties that would at least in part explain its affinity to set up osseous metastases. Curcumin is able to interfere with the osteoblastic component as well as the osteoclastic component of this phenotype, by interfering with the growth factor receptor pathways and by inhibiting the NF-kappa B activation process. It is concluded that curcumin may inhibit the growth factor collaboration between the prostate cancer cells and the osteoblast/stromal cells, thus exhibiting a potential to prevent the establishment of bony metastases.

Antineoplastic Agents↗

PubMed1996

Serum prostate-specific antigen and digital rectal examination for early detection of prostate cancer in a national community-based program. The Prostate Cancer Education Council.

OBJECTIVES: This study analyzed methods of prostate cancer early detection in community settings throughout the United States against standards and findings of earlier studies conducted at academic medical centers. METHODS: The study was conducted at 148 clinical centers during Prostate Cancer Awareness Week in September 1993 and continued through June 1994. A total of 31,953 eligible subjects were tested by both digital rectal examination (DRE) and prostate-specific antigen (PSA). PSA was tested with the Abbott IMx PSA assay and reported by Roche Biomedical, Inc. RESULTS: The study confirmed that elevated PSA levels (greater than 4.0 ng/mL) aid in the detection of organ-confined prostate cancer when used in conjunction with the DRE. Reflecting more conservative biopsy decision-making practices, study results nonetheless are comparable to earlier reports. Among 1307 subjects who underwent biopsy, 322 cancers were detected. The cancer detection rate was 3.6% for PSA, 3.0% for DRE, and 4.7% if either test result was positive. The positive predictive value (PPV) for elevated PSA levels (greater than 4.0 ng/mL) was 3l.6%, significantly better (P < 0.0001) than the PPV for abnormal DRE results (25.5%). Nearly 90% (88.9%) of staged cancers were diagnosed as localized. Elevated PSA levels detected more localized cancers (76 of 105 [72.4%]) than the DRE (72 of 105 [68.6%]). Of localized tumors, 33 (31.4%) were missed by DRE and detected solely by PSA, and 29 (27.6%) were missed by PSA and detected solely by DRE. The combined use of the two methods detected 33 additional localized tumors. CONCLUSIONS: Community practice throughout the United States demonstrates that PSA and DRE are consistently effective and efficient in the early detection of prostate cancer.

Aged↗

PubMed1994

Detection of prostate cancer in males with prostatism.

The present study was designed to compare the prostate cancer detection rate, sensitivity, specificity, and positive predictive value of digital rectal examination (DRE) and serum prostatic specific antigen (PSA) in a consecutive cohort of males presenting to a single institution with clinically significant prostatism. The study population was comprised of 224 consecutive males with clinically significant prostatism referred to the Prostate Center at the Medical College of Wisconsin between June 1990 and December 1991. Subjects were considered to have clinically significant prostatism if they elected to pursue medical or surgical therapy following exclusion of carcinoma of the prostate. The initial examination consisted of a Boyarsky symptom score assessment, DRE, uroflowmetry, postvoid residual determination, serum PSA level, and transrectal prostatic ultrasonography. Subjects with an abnormality on DRE or serum PSA > 4 ng/dl were advised to undergo transrectal prostatic biopsy. Of the 224 subjects, 40 (17.9%) had an abnormal DRE and 57 (25.4%) had an elevated serum PSA > 4 ng/dl. The overall detection rate of prostate cancer in the study population was 6.7%. The prostate cancer detection rates for PSA alone and DRE alone were 5.8% and 5.3%, respectively. The sensitivity, specificity, and positive predictive values of PSA alone were 86.7%, 80.9%, and 25.0% and of DRE alone 80.0%, 86.3%, and 30.0%, respectively. Receiver operator characteristic (ROC) curves were constructed for the entire study population in order to compare the screening measures serum PSA and PSA density. The area under the curves was 0.88 for both tests, indicating that these screening tests for prostate cancer were not significantly different. The present study demonstrated that males with clinically significant prostatism represent a high risk cohort for detecting prostate cancer. DRE and PSA are equally effective measures for detecting prostate cancer. PSA density does not offer any advantage over serum PSA in screening for prostate cancer, except in the subset of patients with a normal DRE and serum PSA levels between 4.0 and 9.9 ng/dl.

Adult↗

PubMed2006

A recombinant PSMA-specific single-chain immunotoxin has potent and selective toxicity against prostate cancer cells.

Prostate cancer is the most commonly diagnosed form of cancer and the second leading cancer-related death among men in the Western civilization. Since no effective therapy exists for this tumor after progression beyond resectable boundaries, there is an urgent need for new treatment strategies. Prostate specific membrane antigen (PSMA) represents an excellent target on prostate cancer cells, and therefore specific immunotherapy may be a novel therapeutic option for the management of this tumor. We constructed a fully recombinant immunotoxin (A5-PE40) from a single-chain antibody fragment (scFv) against cell-adherent PSMA and a truncated form of Pseudomonas exotoxin A (PE40) lacking its natural binding domain Ia. The scFv A5 was obtained from a mAb elicited with native PSMA by phage display technology and direct selection on cells carrying the antigen. The bacterially expressed and purified immunotoxin A5-PE40 specifically binds to PSMA-positive prostate cancer cells and induces a 50% reduction of viability (IC50) at a concentration of 20 pM, while PSMA-negative cells remain unaffected. Due to its high and specific toxicity this recombinant immunotoxin is a promising candidate for therapeutic applications in patients with prostate cancer.

ADP Ribose Transferases↗

PubMed2001

Activator protein 2alpha transcription factor expression is associated with luminal differentiation and is lost in prostate cancer.

PURPOSE: Prostate cancer progression is associated with deregulation of genes like E-cadherin, p21/WAF1, MMP-2, VEGF, and IGF-binding protein, 3 and 5, all of which are target genes for the transcription factor activator protein 2alpha (AP-2alpha). We, therefore, hypothesize that the development/progression of prostate cancer is associated with changes in the expression of AP-2alpha. EXPERIMENTAL DESIGN: We used immunofluorescent staining to assess the presence of AP-2alpha in normal, benign, and malignant human prostate tissues and to correlate its expression with tumor grade and stage. RESULTS: We found that although AP-2alpha was expressed in normal prostate epithelium, it was not expressed in 30 prostate cancer specimens of different Gleason scores. Moreover, AP-2alpha protein was present in the luminal cell layer but not in the basal cell layer of the normal epithelium, which indicated that the loss of AP-2alpha staining in the prostate cancer specimens was not attributable to a lack of AP-2alpha-expressing cells. Further analysis demonstrated the presence of AP-2alpha in 2 (40%) of 5 atrophic normal epithelium, in 4 (24%) of 17 cases of benign prostatic hyperplasia, and in 2 (13%) of 13 cases of high-grade prostatic intraepithelial neoplasia. Loss or reduction in AP-2alpha expression was also observed in LNCaP, LNCaP-LN3, and PC3M-LN4 cell lines. CONCLUSIONS: Our data demonstrate that AP-2alpha expression is associated with normal luminal differentiation and that a loss of AP-2alpha expression occurs early in the development of prostate adenocarcinoma. Loss of AP-2alpha may lead to deregulation in AP-2alpha target genes that normally regulate cellular growth and differentiation.

Biomarkers, Tumor↗

PubMed2006

Chemotherapy for hormone-refractory prostate cancer.

BACKGROUND: Prostate cancer mainly affects elderly men, and its incidence has steadily increased over the last decade. The management of this disease is replete with controversy. In men with advanced, metastatic prostate cancer, hormone therapy is almost universally accepted as the initial treatment of choice and produces good responses in most patients. However, many patients will relapse and become resistant to further hormone manipulation; the outlook for these patients is poor. Many have disease extending to the skeleton, which is associated with severe pain. Therapies for these men include chemotherapy, bisphosphonates, palliative radiotherapy, and radioisotopes. Systemic chemotherapy has been evaluated in men with hormone-refractory prostate cancer (HRPC) for many years, with disappointing results. However, more recent studies with newer agents have shown encouraging results. There is therefore a need to explore the value of chemotherapy in this disease. OBJECTIVES: The present review aims to assess the role of chemotherapy in men with metastatic HRPC. The major outcome was overall survival. Secondary objectives include the effect of chemotherapy on pain relief, prostate-specific antigen (PSA) response, quality of life, and treatment-related toxicity. SEARCH STRATEGY: Trials were identified by searching electronic databases, such as MEDLINE, and handsearching of relevant journals and conference proceedings. There was no restriction of language or location. SELECTION CRITERIA: Only published randomised trials of chemotherapy in HRPC patients were eligible for inclusion in this review. Randomised comparisons of different chemotherapeutic regimens, chemotherapy versus best standard of care or placebo, were relevant to this review. Randomised, dose-escalation studies were not included in this review. DATA COLLECTION AND ANALYSIS: Data extraction tables were designed specifically for this review to aid data collection. Data from relevant studies were extracted and included information on trial design, participants, and outcomes. Trial quality was also assessed using a scoring system for randomisation, blinding, and description of patient withdrawal. MAIN RESULTS: Out of 107 randomised trials of chemotherapy in advanced prostate cancer identified by the search strategy, 47 were included in this review and represented 6929 patients with HRPC. Only two trials compared the same chemotherapeutic interventions and therefore a meta-analysis was considered inappropriate. The quality of some trials was poor because of poor reporting, low-patient recruitment, or poor trial design. For clarity, trials were categorised according to the major drug used, but this was not a definitive grouping, since many trials used several agents and would be eligible for inclusion in a number of categories. Drug categories included estramustine, 5-fluorouracil, cyclophosphamide, doxorubicin, mitoxantrone, and docetaxel. Only studies using docetaxel reported a significant improvement in overall survival compared to best standard of care, although the increase was small (< 2.5 months). The mean percentage of patients achieving at least a 50% reduction in PSA compared to baseline was as follows: estramustine 48%; 5-fluorouracil 20%; doxorubicin 50% (one study only); mitoxantrone 33%; and docetaxel 52%. Pain relief was reported in 35% to 76% of patients receiving either single agents or combination regimens. A three weekly regime of docetaxel significantly improved pain relief compared to mitoxantrone plus prednisone (the latter regimen approved as standard therapy for HRPC in the USA). All chemotherapeutics, either as single agents or in combination, were associated with toxicity; the major ones being myelosuppression, gastrointestinal toxicity, cardiac toxicity, neuropathy, and alopecia. Quality of life was significantly improved with docetaxel compared to mitoxantrone plus prednisone. AUTHORS' CONCLUSIONS: Patients with HRPC have not traditionally been offered chemotherapy as a routine treatment because of treatment-related toxicity and poor responses. Recent data from randomised studies, in particular those using docetaxel, have provided encouraging improvements in overall survival, palliation of symptoms, and improvements in quality of life. Chemotherapy should be considered as a treatment option for patients with HRPC. However, patients should make an informed decision based on the risks and benefits of chemotherapy.

Aged↗

PubMed2004

An evaluation of bicalutamide in the treatment of prostate cancer.

Although prostate cancer is traditionally considered a disease of old age, improved diagnostic techniques have resulted in early diagnosis, and many men are now treated while still physically and sexually active. Current therapies for prostate cancer often include medical or surgical castration, which cause adverse effects on physical and sexual function; therefore, greater attention has been focused on quality of life. The nonsteroidal antiandrogen bicalutamide is an effective agent with a favorable tolerability profile and, in some settings, represents an alternative to castration. Mature survival data reveal that bicalutamide monotherapy provides survival benefits for untreated locally advanced disease that do not differ significantly from those of castration and maintains better physical capacity and sexual interest. Recent data from a prospective randomized trial demonstrate that bicalutamide given as immediate therapy, either alone or as adjuvant to therapy of curative intent, significantly reduces the risk of objective disease progression in patients with localized or locally advanced prostate cancer. Antiandrogens are also used in combination with castration, a treatment known as combined androgen blockade (CAB), for advanced disease. A randomized trial demonstrated that CAB with bicalutamide is associated with similar survival outcome to CAB with flutamide and is better tolerated. Current evidence demonstrates that bicalutamide currently has a favorable risk-benefit ratio in several stages of prostate cancer and that the role of bicalutamide will be further defined by ongoing studies.

Anilides↗

PubMed2005

Hyperthermia-induced proteasome inhibition and loss of androgen receptor expression in human prostate cancer cells.

Prostate cancer is the second leading cause of death in men in western countries and is usually treated by surgery and/or radiotherapy. More recently, hyperthermia has been introduced into clinical trials investigating a possible effect in the first-line treatment of prostate cancer. However, the molecular mechanisms of hyperthermia are not completely understood. In this study, we investigated the effects of hyperthermia on proteasome function and its significance for signal transduction, cell death and androgen receptor (AR) expression in PC-3, LnCaP, and DU-145 human and TRAMP-C2 murine prostate cancer cells. Hyperthermia caused apoptosis and radiosensitization and decreased 26S proteasome activity in all three human cell lines to about 40% of untreated control cells. 20S proteasome activity was not affected by heat. Heat treatment inhibited constitutive and radiation-induced activation of nuclear factor kappaB caused by stabilization of IkappaB. Although stabilization of AR by proteasome inhibitors has been reported previously, AR protein levels in LnCaP cells decreased dramatically after heat. Our data suggest that inhibition of proteasome function and dependent signal transduction pathways might be a major molecular mechanisms of heat-induced apoptosis and radiosensitization. Hyperthermia abrogates AR expression in androgen-dependent cells and might thus promote malignant progression of prostate cancer.

Animals↗

PubMed2005

A SOCS-1 peptide mimetic inhibits both constitutive and IL-6 induced activation of STAT3 in prostate cancer cells.

Prostate cancer is the second highest cause of cancer-related deaths of men in the US. Signal transducers and activators of transcription (STATs) proteins are a small family of latent cytoplasmic transcription factors that act downstream of Janus kinase (JAK) activation and mediate intracellular signaling from a wide variety of cytokines, growth factors, and hormones. Aberrant activation of STAT3 has been implicated in the progression of many human carcinomas, including prostate cancer. Previously, we have characterized a novel tyrosine kinase inhibitor peptide, Tkip, that is a mimetic of suppressor of cytokine signaling 1 (SOCS-1). Similar to SOCS-1, Tkip binds to the autophosphorylation site of JAK2 and inhibits phosphorylation of STAT1alpha. In this study, we determined the inhibitory effects of Tkip on the human prostate cancer cell lines DU145 and LNCaP. Tkip inhibited cellular proliferation of both DU145 and LNCaP cells, with a slightly greater antiproliferative effect on DU145 cells. Cell cycle analysis using flow cytometry showed Tkip blockage of progression into the S phase of the cell cycle. Tkip also inhibited constitutive (DU145) and IL-6-induced (LNCaP) activation of STAT3, consistent with the fact that STAT3 activation is mediated by JAK2. Tkip also slightly reduced the levels of cyclin D1, an important regulator of cell cycle progression into S phase, in DU145 and LNCaP cancer cell lines. These data describe a potentially important therapeutic that targets both constitutive and IL-6-induced STAT3 activation in human prostate cancer cell lines.

Amino Acid Sequence↗

PubMed2001

Prostate cancer chemoprevention agents exhibit selective activity against early stage prostate cancer cells.

Preclinical models for the identification of prostate cancer chemoprevention agents are lacking. Based upon the notion that clinically useful chemoprevention agents should exhibit selective activity against early stage disease, studies were undertaken to assess whether chemoprevention agents selectively inhibited the growth of early stage prostate cancer, as compared to late stage cancer. First, a series of cell and molecular studies were performed, which, when taken together, validated the use of a panel of prostate cell lines as a model of the different stages of carcinogenesis. Next, therapeutic responsiveness to ten different cytotoxic or chemoprevention agents was evaluated. Chemoprevention agents exhibited selective activity against normal and early transformed prostate tissue, whereas cytotoxic agents were non-specific. Selective activity against early versus advanced prostate cancer cells is identified as a potential screening method for chemoprevention agents.Prostate Cancer and Prostatic Diseases (2001) 4, 81-91

Journal Article↗