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PubMed2005

EphB4 expression and biological significance in prostate cancer.

Prostate cancer is the most common cancer in men. Advanced prostate cancer spreading beyond the gland is incurable. Identifying factors that regulate the spread of tumor into the regional nodes and distant sites would guide the development of novel diagnostic, prognostic, and therapeutic targets. The aim of our study was to examine the expression and biological role of EphB4 in prostate cancer. EphB4 mRNA is expressed in 64 of 72 (89%) prostate tumor tissues assessed. EphB4 protein expression is found in the majority (41 of 62, 66%) of tumors, and 3 of 20 (15%) normal prostate tissues. Little or no expression was observed in benign prostate epithelial cell line, but EphB4 was expressed in all prostate cancer cell lines to varying degrees. EphB4 protein levels are high in the PC3 prostate cancer cell line and several folds higher in a metastatic clone of PC3 (PC3M) where overexpression was accompanied by EphB4 gene amplification. EphB4 expression is induced by loss of PTEN, p53, and induced by epidermal growth factor/epidermal growth factor receptor and insulin-like growth factor-I/insulin-like growth factor-IR. Knockdown of the EphB4 protein using EphB4 short interfering RNA or antisense oligodeoxynucleotide significantly inhibits cell growth/viability, migration, and invasion, and induces apoptosis in prostate cancer cell lines. Antisense oligodeoxynucleotide targeting EphB4 in vivo showed antitumor activity in murine human tumor xenograft model. These data show a role for EphB4 in prostate cancer and provide a rationale to study EphB4 for diagnostic, prognostic, and therapeutic applications.

Animals↗

PubMed1997

Prostatic intraepithelial neoplasia in dogs with spontaneous prostate cancer.

Prostatic intraepithelial neoplasia (PIN) is the most likely precursor of human prostate cancer. The prevalence and immunophenotype of PIN in dogs with spontaneous prostate cancer has not been previously described. To investigate the association between PIN and prostate cancer, we evaluated the prostates of dogs with spontaneous prostate carcinoma. The prevalence of PIN was determined in formalin-fixed prostates from 29 dogs with spontaneous prostate cancer. Using immunoperoxidase techniques, we compared basal cell layer integrity (high molecular weight keratin 34 beta-E12), proliferative index (MIB-1), and microvessel density (Factor VIII-related antigen) in 14 prostates which contained benign epithelium, PIN, and carcinoma. PIN was present in 19 of 29 (66%) prostates from dogs with spontaneous prostate cancer. The basal cell layer was intact in benign epithelium, disrupted in 72% of acini with PIN, and absent in carcinoma. The mean proliferative index was 17%, 25%, and 40% for benign epithelium, PIN, and carcinoma, respectively, and these differences were significant. The mean microvessel density in foci of PIN and carcinoma (32 and 39 vessels per mm2, respectively) was greater than in benign epithelium (23 vessels per mm2). High-grade PIN is common in the prostates of dogs with spontaneous carcinoma. The basal cell layer is partially disrupted in PIN, whereas it is absent in prostate cancer. The proliferative index and microvessel density of PIN are intermediate between benign epithelium and cancer. These results are similar to those reported for human PIN and prostate cancer, and indicate that PIN is part of a morphologic continuum in the progression of prostate cancer. To our knowledge, this is the first description of high-grade PIN spontaneously occurring in animals. The canine prostate may serve as a useful model for examining factors that modulate PIN and prostate cancer progression.

Animals↗

PubMed1989

Early detection of prostate cancer.

Prostate cancer is the second most common malignancy in American males and the third leading cause of cancer deaths in this population. There are no symptoms that are unique to early prostate cancer, and nearly one-half of patients will have metastatic disease at diagnosis. Because of its tremendous impact upon the health and well-being of the American male population, and the importance of early diagnosis in curability, there is keen interest in the development of effective screening procedures that are highly sensitive, specific, and cost-effective. Rectal examination serves as the historical control. The serum tumor markers of prostate cancer, prostatic acid phosphatase (PAP), and prostate-specific antigen (PSA), are sensitive but relatively nonspecific in the diagnosis of prostate cancer. The use of transrectal ultrasound as a screening tool is highly controversial but suffers from a similar lack of specificity. As yet, no diagnostic tests, alone or in combination, have proven to be of practical value in screening for prostate cancer. Fundamental but unanswered questions about the natural history and the high incidence of "latent" disease also obscure the issue of early diagnosis of prostate cancer and its impact on survival.

Biomarkers, Tumor↗

PubMed2001

Delineation of prognostic biomarkers in prostate cancer.

Prostate cancer is the most frequently diagnosed cancer in American men. Screening for prostate-specific antigen (PSA) has led to earlier detection of prostate cancer, but elevated serum PSA levels may be present in non-malignant conditions such as benign prostatic hyperlasia (BPH). Characterization of gene-expression profiles that molecularly distinguish prostatic neoplasms may identify genes involved in prostate carcinogenesis, elucidate clinical biomarkers, and lead to an improved classification of prostate cancer. Using microarrays of complementary DNA, we examined gene-expression profiles of more than 50 normal and neoplastic prostate specimens and three common prostate-cancer cell lines. Signature expression profiles of normal adjacent prostate (NAP), BPH, localized prostate cancer, and metastatic, hormone-refractory prostate cancer were determined. Here we establish many associations between genes and prostate cancer. We assessed two of these genes-hepsin, a transmembrane serine protease, and pim-1, a serine/threonine kinase-at the protein level using tissue microarrays consisting of over 700 clinically stratified prostate-cancer specimens. Expression of hepsin and pim-1 proteins was significantly correlated with measures of clinical outcome. Thus, the integration of cDNA microarray, high-density tissue microarray, and linked clinical and pathology data is a powerful approach to molecular profiling of human cancer.

Biomarkers, Tumor↗

PubMed2002

Gene expression analysis of prostate cancers.

Prostate cancer is a biologically heterogeneous disease with considerable variation in clinical aggressiveness. The behavior of prostate cancer can be considered a direct or indirect result of aberrant alterations of gene expression in prostate epithelial cells. Identification of the patterns of gene-expression alterations that are related to the aggressiveness of prostate cancers will greatly assist the development of tools for early detection of prostate cancers with poor clinical outcome and identification of targets for future therapeutic intervention. To detect the patterns of gene-expression alterations of prostate cancers, we performed a comprehensive gene-expression analysis on 30 prostate tissues of various levels of invasiveness (ranging from those confined to the organ to distant metastases) and Gleason grades (combined scores 4-9), using the Affymetrix chip set Hu35k (A-D) and U95a. Following three sequential selection screens, we identified 84 largely novel genes and expressed sequence tag (EST) sequences whose expression levels were altered significantly in prostate cancer samples compared with control normal tissues. In addition, the expression levels of a group of 12 genes and EST sequences was found to be altered significantly in aggressive type of prostate cancers but not in organ-confined prostate cancers. Cluster analysis using the 84-gene list showed that the highly aggressive prostate cancers contained gene-expression patterns that were distinct from organ-confined prostate cancers.

Cluster Analysis↗

PubMed1996

Immunohistochemical detection of a fatty acid synthase (OA-519) as a predictor of progression of prostate cancer.

Prostate cancer is the most common newly diagnosed non-skin cancer and the second leading cause of cancer death in men. It is a unique neoplasm because of the large discrepancy between its clinical incidence and the much higher incidence of latent cancer. Predicting the prognosis of prostate cancer, especially the cancers detected incidentally or by screening, remains a clinically important problem. Immunoreactivity for Onco-antigen 519 (OA-519), a recently described fatty acid synthase (FAS), has been associated with poor prognosis in breast cancers. The authors have previously shown that its detection in prostate cancer correlated with high-grade, large volume, and advanced stage tumors. This study examines the association between OA-519 immunoreactivity in primary prostate cancer and disease progression. The authors used immunohistochemistry with an affinity-purified anti-OA-519 antibody and examined primary prostate cancers (stages A1 to D1) from 99 men with a mean follow-up of 4 years (range = 2 to 9.3). Survival analysis was used to evaluate differences in progression-free survival. OA-519 immunoreactivity was seen in 56 (57%) of the 99 primary prostate cancers examined. OA-519-positive cancers were more likely to progress than the OA-519-negative cancers (P < .04). Univariate survival analysis showed that OA-519 (FAS), histological grade (Gleason score), and clinical stage were significant predictors of disease progression. Multivariate analyses of all cases showed that only histological grade was significant. However, multivariate analysis of the 85 cancers with Gleason scores 2-7 (ie, low to intermediate grade) showed OA-519 (FAS) immunoreactivity to be the only statistically significant predictor of cancer progression (P < .02). Expression of the fatty acid synthase OA-519 by prostate cancers is potentially a clinically useful predictor of disease progression. It appears to be independent of histological grade (Gleason score), at least in cancers with low to intermediate grades. Further studies are needed to evaluate the role of fatty acid synthase in malignancy and the potential therapeutic implications of enzyme blockers.

Aged↗

PubMed2003

Searching for the gatekeeper oncogene of prostate cancer.

Prostate cancer is a common malignancy that has a heterogeneous etiology and a variable outcome. Nearly all prostatic adenocarcinoma results from androgen-dependent tumor promotion. However, the cause of prostate cancer initiation is not well understood and only a few of the target oncogenes activated during prostate cancer initiation have been identified. Prostate cancer risk is strongly influenced by family history. Several genetic loci have been found to cosegregate with prostate cancer occurrence in high-risk families. Some candidate oncogenes that map to these loci have been implicated by the identification of mutations in high-risk kindreds. However, the roles of the putative oncogene products in the biochemical pathways that mediate carcinogenesis remain obscure and their influence on cancer etiology has yet to be supported by gene targeting experiments in mice. Moreover, the genes that have been implicated in hereditary prostate cancers do not appear to be mutated in sporadic cancers. Karyotypic and loss of heterozygosity analysis of sporadic prostate cancers have identified 8p, 10q, and 17p as the loci most often disrupted. Candidate oncogenes have been identified at each of these regions. Additional genes with pathogenic significance in prostate cancer have been identified by analysis of cDNA microarrays comparing benign and malignant prostate tissue, by differential genetic analysis of benign and malignant prostatic epithelium, and by induction of experimental prostate cancer in genetically engineered mice.

Adenocarcinoma↗

PubMed1995

Prostate-specific antigen: its clinical use and application in screening for prostate cancer.

Prostate cancer in most European countries is the second most frequent cancer in males and the second most frequent cause of cancer death. Prostate specific antigen (PSA) is an important tumour marker, which relates to many aspects of this disease. It has been shown that PSA is helpful in the early diagnosis of prostate cancer and in this respect is superior to other available tests like rectal examination and transrectal ultrasonography. PSA is also helpful in staging of locally confined disease. It can be used to identify or exclude local extension of disease, if combined with T category and grade of differentiation determined on biopsy. The same parameters also give an indication of the presence of lymph node metastases, which may prevent unnecessary and invasive staging procedures in certain groups of patients with favourable prognostic factors and a low PSA value. PSA is less suitable as a marker for metastatic disease. Progression of untreated prostate cancer in various stages can be monitored by PSA. The true value of the marker in this respect is still underexplored. It may be possible that PSA will be shown to differentiate effectively between aggressive and non-progressive disease. In this respect, it could become an essential tool to identify those patients that may not require treatment at all. PSA is also a useful marker for therapy response. An elevation of PSA after radical prostatectomy indicates local or metastatic progression, which will occur within 1-2 years. PSA is an androgen dependent enzyme and decreases under endocrine treatment. It is unexplained why in spite of its endocrine dependent character, PSA rises with endocrine independent progression of prostate cancer.

Humans↗

PubMed2001

Myopodin, a synaptopodin homologue, is frequently deleted in invasive prostate cancers.

Prostate cancer is one of the leading causes of cancer-related deaths for men in the United States. Like other malignancies, prostate cancer is underscored by a variety of aberrant genetic alterations during its development. Although loss of heterozygosity or allelic loss is frequently identified among prostate cancers, few genes have been identified thus far as critical to the development of invasive prostate cancers. In this report, we used the recently developed technology, the "differential subtraction chain," to perform a genome-wide search for sequences that are deleted in an aggressive prostate cancer. Among the deleted sequences, we found that one sequence was deleted in >50% of prostate cancers we tested. We mapped this sequence to chromosome 4q25 by screening the Genebridge 4 hamster radiation panel with primers specific to this probe, and subsequently identify a 54-kb minimal common deletion region that contains the sequence encoding myopodin. Sequence analysis indicates that myopodin shares significant homology with synaptopodin, a protein closely associated with podocyte and neuron differentiation. Further study shows that frequent complete or partial deletions of the myopodin gene occurred among invasive prostate cancer cases (25 of 31 cases, or 80%). Statistical analysis indicates that deletion of myopodin is highly correlated with the invasiveness of prostate cancers, and thus may hold promise as an important prognostic marker for prostate cancers.

Amino Acid Sequence↗

PubMed1990

Zoladex plus flutamide vs. orchidectomy for advanced prostatic cancer. Danish Prostatic Cancer Group (DAPROCA).

The study comprised 262 patients with previously untreated advanced carcinoma of the prostate. Patients were randomized either to undergo orchidectomy or to receive combined treatment with Zoladex, 3.6 mg every 4 weeks, plus flutamide, 250 mg t.i.d. At present the median follow-up is 39 months. The objective response to therapy was better in the Zoladex plus flutamide group, but no differences in subjective response, time to disease progression, or survival have been demonstrated between the 2 groups. Adverse effects were more common in the Zoladex plus flutamide group. Thus, 'total androgen blockade' with Zoladex plus flutamide was not clinically superior to orchidectomy in the treatment of patients with advanced prostatic cancer.

Aged↗

PubMed1994

Cadmium and prostate cancer.

Prostatic cancer is a common and frequently lethal malignant disease. In the United States and other countries the incidence and mortality rate of prostate cancer continue to rise. Cancer of the prostate has an extremely complex etiology and appears dependent on a variety of factors, making linkage to a single factor very difficult to detect. Cadmium is a metallic toxin of great environmental and occupational concern. Cadmium exposure has been associated with human prostatic cancer in some, but not all, epidemiologic studies. Some studies indicate that tissue levels of cadmium in the human prostate correlate with malignant disease. Any association between cadmium and prostatic cancer has been controversial, in large part because of a previous lack of relevant animal models. However, several chronic studies in rats revealing a correlation between cadmium exposure and prostatic tumors have been published over the last several years. These include a study of oral cadmium exposure, a route extremely relevant to human exposure. Several of these chronic studies indicate a hormonal dependence of cadmium-induced prostate cancer. Other supportive work continues to accumulate, such as studies showing in vitro malignant transformation of prostatic epithelial cells with cadmium exposure. In addition, there are indications that the primary biologic tolerance system for cadmium (i.e., the metallothionein gene) may be only poorly active in the specific lobes of the rat prostate in which cadmium induces tumors. The induction in rats of prostate cancer by cadmium treatment clearly supports, but does not definitively establish, a possible role for cadmium as an etiological agent in human prostate cancer. Further research, however, will be required to establish the precise role of cadmium in this important human malignancy.

Animals↗

PubMed2005

Prostate-specific antigen doubling time as a prognostic marker in prostate cancer.

Prostate cancer has a varied natural history. Men with similar serum prostate-specific antigen (PSA) levels, clinical stages, and histologic features in their tissue specimens can have markedly different outcomes. While prostate cancer is lethal in some patients, most men die with cancer rather than because of it. Moreover, histologically apparent cancer can be found in the prostate glands of approximately 42% of men over 50 years of age who die from other causes, but the lifetime risk that a man in the US will be diagnosed with prostate cancer is estimated to be 11% and the risk of dying from the disease is only 3.1%. Consequently, appropriate disease management requires risk assessment. How likely is it that a given man's cancer will progress or metastasize over his remaining lifetime? What is the probability of successful treatment? What are the risks of adverse effects and complications of each treatment? Physicians use a variety of clinical and pathologic parameters to assess the risk that a given cancer poses to an individual patient. In addition to the accepted parameters of serum PSA level, clinical staging, and pathologic grading and staging, PSA doubling time has emerged as an important factor in the evaluation of men with newly diagnosed prostate cancer or prostate cancer that recurs after treatment. PSA doubling time can also be used as a surrogate marker for prostate cancer-specific death. This review summarizes current knowledge regarding the role of PSA doubling time as a prognostic marker in men with prostate cancer.

Algorithms↗

PubMed2006

Insulin-like growth factor I secreted from prostate stromal cells mediates tumor-stromal cell interactions of prostate cancer.

Prostate cancer shows high expression of type I insulin-like growth factor (IGF-I) receptor (IGF-IR) and prostate stromal cells (PrSC) produce IGF-I. Although high plasma level of IGF-I is a risk factor of prostate cancer, the significance of the prostate stromal IGF-I in the regulation of prostate cancer remains elusive. Here we show that the stromal IGF-I certainly regulates the development of prostate cancer. Coinoculation of PrSC increased the growth of human prostate cancer LNCaP and DU-145 tumors in severe combined immunodeficient mice. The conditioned medium of PrSC, as well as IGF-I, induced phosphorylation of IGF-IR and increased the growth of LNCaP and DU-145 cells. PrSC, but not LNCaP and DU-145 cells, secreted significant amounts of IGF-I. Coculture with PrSC increased the growth of DU-145 cells in vitro but the pretreatment of PrSC with small interfering RNA of IGF-I did not enhance it. Furthermore, various chemical inhibitors consisting of 79 compounds with approximately 60 different targets led to the finding that only IGF-IR inhibitor suppressed the PrSC-induced growth enhancement of DU-145 cells. Thus, these results show that the prostate stromal IGF-I mediates tumor-stromal cell interactions of prostate cancer to accelerate tumor growth, supporting the idea that the IGF-I signaling is a valuable target for the treatment of prostate cancer.

Cell Communication↗

PubMed2000

Vitamin D receptor polymorphisms and prostate cancer.

Prostate cancer is a common disease, yet determinants of prostate cancer risk remain largely unidentified. Low circulating levels of 1, 25-dihydroxy vitamin D (1,25-D) have been implicated as a risk factor for prostate cancer. In addition, 1,25-D exhibits significant antineoplastic properties both in vitro and in vivo, and these antiproliferative effects appear to be mediated through the vitamin D receptor (VDR). The VDR has a number of common polymorphisms, including a TaqI restriction fragment length polymorphism in exon 9 and a poly(A) length polymorphism in the 3'-untranslated region. Previous studies have found an association between the TaqI T allele or poly(A) L allele and prostate cancer. To further investigate the putative link between VDR polymorphisms and prostate cancer, we conducted a case-control study of prostate cancer patients from the Piedmont region of North Carolina. Using polymerase chain reaction-based techniques on DNA extracted from peripheral blood, we genotyped 77 cases (70 white, seven black) and 183 controls (169 white, 14 black) for the TaqI and poly(A) alleles. We report here an overall lack of association between either the TaqI or poly(A) genotype and prostate cancer odds ratio (OR)=1.4, 95% confidence interval (CI)=0.7-2.8; and OR=1.2, 95% CI=0.6-2.5, respectively). Using a case-case analysis, we tested whether these polymorphisms might be associated with more advanced disease but found no statistically significant association for the TaqI T or poly(A) L allele (OR=2.5, 95% CI=0.3-21.7; OR=2.8, 95% CI=0.3-23.8, respectively). We report strong evidence of linkage disequilibrium between the TaqI and poly(A) polymorphisms (P < 0.0001), with whites demonstrating stronger linkage disequilibrium than blacks (D=0.24 vs. D=0.18).

Aged↗

PubMed2004

The role of alpha-blockers in the management of prostate cancer.

Prostate cancer is the second most common cause of cancer death in men in the US. Patients with prostate cancer are initially treated with surgical resection, radiation or antiandrogen therapy. After an initial remission, however, the majority of prostate tumours evolve into a highly aggressive, metastatic androgen-independent state, for which successful therapy has not yet been established. During the past few years, new perspectives have emerged towards the development of preventive and therapeutic approaches for prostate cancer. Quinazoline-based alpha(1)-blockers have been shown to have antitumour efficacy against prostate cancer cells in inducing apoptosis and anoikis via an alpha(1)-adrenoceptor-independent mechanism. Specifically, doxazosin and terazosin can induce apoptosis, inhibit invasion and migration of prostate cancer and endothelial cells, and reduce their adhesion potential to extracellular matrix components, thus enhancing their susceptibility to anoikis. This review discusses recent evidence suggesting the apoptotic efficacy of quinazoline-based alpha(1)-adrenoceptor antagonists, doxazosin and terazosin and speculates on the therapeutic promise of these drugs as novel antitumour agents against prostate cancer. From a drug discovery perspective, separation of the effect of doxazosin on apoptosis in prostate cancer cells from its original pharmacological activity in normal prostate cells, will provide a molecular basis in developing a novel class of apoptosis-inducing agents through lead optimisation.

Adrenergic alpha-1 Receptor Antagonists↗

PubMed2004

Exercise and prostate cancer.

Prostate cancer is a leading cause of cancer morbidity and mortality in men. In addition to improved treatments, strategies to reduce disease risk are urgently required. This review summarises the literature that examines the association between exercise and prostate cancer risk. Between 1989 and 2001, 13 cohort studies were conducted in the US and internationally. Of these, nine showed an association between exercise and decreased prostate cancer risk. Five of 11 case-control studies conducted between 1988 and 2002 reported an association between decreased risk of prostate cancer and high activity levels. Considering all studies performed between 1976 and 2002, 16 out of 27 studies reported reduced risk in men who were most active; in nine out of 16 studies the reduction in risk was statistically significant. Average risk reduction ranged from 10-30%. In aggregate, this evidence suggests a probable link between increased physical exercise and decreased prostate cancer risk. The ability of exercise to modulate hormone levels, prevent obesity, enhance immune function and reduce oxidative stress have all been postulated as mechanisms that may underlie the protective effect of exercise. Exercise may also be of benefit in men undergoing treatment for prostate cancer. Overall, study design and control of potential confounding factors varied greatly among studies, possibly contributing to the variation in results. Epidemiological studies that are better controlled, larger in scale and more carefully designed may help to more fully clarify the relationship between exercise and prostate cancer. In addition, intervention trials that test whether exercise programmes can reduce prostate cancer risk are currently underway to rigorously test the ability of exercise to reduce prostate cancer incidence.

Bone Density↗

PubMed2000

Prostate stem cell antigen (PSCA) expression increases with high gleason score, advanced stage and bone metastasis in prostate cancer.

Prostate stem cell antigen (PSCA) is a recently defined homologue of the Thy-1/Ly-6 family of glycosylphosphatidylinositol (GPI)-anchored cell surface antigens. PSCA mRNA is expressed in the basal cells of normal prostate and in more than 80% of prostate cancers. The purpose of the present study was to examine PSCA protein expression in clinical specimens of human prostate cancer. Five monoclonal antibodies were raised against a PSCA-GST fusion protein and screened for their ability to recognize PSCA on the cell surface of human prostate cancer cells. Immunohistochemical analysis of PSCA expression was performed on paraffin-embedded sections from 25 normal tissues, 112 primary prostate cancers and nine prostate cancers metastatic to bone. The level of PSCA expression in prostate tumors was quantified and compared with expression in adjacent normal glands. The antibodies detect PSCA expression on the cell surface of normal and malignant prostate cells and distinguish three extracellular epitopes on PSCA. Prostate and transitional epithelium reacted strongly with PSCA. PSCA staining was also seen in placental trophoblasts, renal collecting ducts and neuroendocrine cells in the stomach and colon. All other normal tissues tested were negative. PSCA protein expression was identified in 105/112 (94%) primary prostate tumors and 9/9 (100%) bone metastases. The level of PSCA expression increased with higher Gleason score (P=0.016), higher tumor stage (P=0.010) and progression to androgen-independence (P=0. 021). Intense, homogeneous staining was seen in all nine bone metastases. PSCA is a cell surface protein with limited expression in extraprostatic normal tissues. PSCA expression correlates with tumor stage, grade and androgen independence and may have prognostic utility. Because expression on the surface of prostate cancer cells increases with tumor progression, PSCA may be a useful molecular target in advanced prostate cancer.

Antibodies, Monoclonal↗

PubMed2000

In vitro human cell culture models for the study of prostate cancer.

Prostate cancer is the most commonly diagnosed malignancy in the American men and the second leading cause of male cancer death in the United States. Despite its high incidence, the molecular and genetic events involved in prostate cancer progression remain poorly understood. A hurdle in understanding the molecular genetic changes in prostate cancer has been the difficulty in establishing premalignant lesions and primary prostate tumors as in vitro cell cultures. Primary epithelial cells grow for a finite life span and then senesce. Immortalization is defined by continuous growth of otherwise senescing cells and is believed to represent an early stage in tumor progression. In order to examine these early stages, we and others have developed in vitro models of prostate epithelial cell immortalization. Because prostate cancer is a multistep, progressive disease with a typical onset later in life and with an unusually high number of latent cases that do not develop into clinically manifest cancer, the steps in the progression to malignancy are of particular interest. To understand the many factors that are suspected to contribute to the development of this malignancy, there is a need for an in vitro multistep human prostate epithelial (HPE) culture system. These models have been extremely important in identifying genetic and molecular changes involved in prostate cancer progression. Prostate Cancer and Prostatic Diseases (2000) 3, 229-235

Journal Article↗