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PubMed1993

Combined role of transrectal ultrasonography, Gleason score, and prostate-specific antigen in predicting organ-confined prostate cancer.

Prostate cancer staging is frequently inaccurate. By combining transrectal ultrasonography (TRUS) with a retrospectively derived grade-stratified prostate-specific antigen (PSA-GS) scale, we demonstrated 77 percent staging accuracy in 155 men with clinically localized prostate cancer undergoing radical prostatectomy. When used as the first step in a staging algorithm, PSA-GS (Score > or = 7: PSA > or = 4.0 ng/mL, uncontained; Score = 5 or 6: PSA > or = 8.0 ng/mL, uncontained; Score < or = 4: PSA > or = 16.0 ng/mL, uncontained) had a sensitivity of 75 percent and a specificity of 72 percent. The addition of TRUS to the staging algorithm, necessary only in patients with negative predictions by PSA-GS (46%), increased the sensitivity to 86 percent and the negative predictive value to 79 percent, while positive predictive value was unchanged at 77 percent. The combination of TRUS with PSA < 4 ng/mL or > or = 16 ng/mL identified subsets of patients with 85 percent and 88 percent likelihood of contained and uncontained disease, respectively. Our algorithm minimizes operator dependency by requiring TRUS in less than half of the patients. It produced improved staging, but the overall results were inaccurate in 23 percent of patients. Further refinements in prostate cancer staging are still necessary.

Aged↗

PubMed2005

Docetaxel for the treatment of prostate cancer.

Prostate cancer accounts for 12% of male cancer deaths, amounting to almost 10,000 deaths per year in the UK. Patients that develop metastatic disease may have their prostate cancer controlled for approximately 2 years with androgen deprivation but invariably progress to a castrate-independent state and succumb to metastatic disease. The previous experience of cytotoxic chemotherapy in hormone-refractory prostate cancer has yielded modest improvements in quality of life, with mitoxantrone in widest use. However, following encouraging Phase II data, two Phase III trials have demonstrated a survival advantage associated with the use of the synthetic taxoid cytotoxic docetaxel (Taxotere) over mitoxantrone and prednisolone. Moreover, this treatment was well tolerated. Therefore, docetaxel is set to be the standard by which future interventions are judged and a platform for future trials containing novel molecular therapies.

Antineoplastic Agents, Phytogenic↗

PubMed2006

Protective effects of green tea against prostate cancer.

Prostate cancer has the third highest incidence of all cancers in men worldwide with incidence and mortality being particularly high in affluent, developed countries. Tea, especially green tea, has demonstrated promise in the prevention of several cancers. Green tea contains several components including catechins, a category of polyphenols that have chemopreventive properties. Although evidence from epidemiological studies is not comprehensive, it is strengthened by animal and in vitro evidence suggesting that consumption of tea is associated with decreased risk or progression of prostate cancer. Emerging evidence and potential biological mechanisms for the role of green tea in prostate cancer prevention are presented in this review.

Animals↗

PubMed2001

Complementary and alternative medicine in prostate cancer.

Prostate cancer patients, like other cancer patients as well as the general population, are increasingly exploring the use of complementary and alternative medicine (CAM). This paper describes the use of CAM in this patient population and the evidence regarding some CAM treatments in the setting of prostate cancer. Some herbal agents and micronutrients have demonstrated biologic activity that may benefit patients with prostate cancer. The clinical effects of these and others and the potential interactions among CAM treatments and with conventional treatment remain an appropriate target for further investigation.

Complementary Therapies↗

PubMed2002

A Nod Scid mouse model to study human prostate cancer.

Prostate cancer is the second cause of cancer mortality in men in Western countries. To study new therapeutic approaches such as gene therapy, animal models of human prostate cancer with metastatic behavior are mandatory. We used the Nod Scid mouse strain to develop an orthotopic animal model. Two androgen-independent cell lines (PC-3 and DU 145) were used. Local tumor growth and metastases were analyzed. The tumor take rates were close to those reported in the literature. However, a high frequency of various metastatic sites has been observed (liver, lung, spleen, adrenal, kidney, lymph node, and diaphragm). It can be concluded that the Nod Scid mouse is a relevant preclinical animal model to study human prostate cancer. Metastatic sites seem more numerous in comparison to other orthotopic mice models described.

Adenocarcinoma↗

PubMed2003

Docetaxel and thalidomide as a treatment option for androgen- independent, nonmetastatic prostate cancer.

Prostate cancer usually presents with early-stage disease, yet a significant proportion of patients present or will progress to androgen-independent, nonmetastatic prostate cancer (AIPC). Chemotherapy has demonstrated statistically significant improvements in palliation of AIPC. Docetaxel in particular has demonstrated high response rates as a single agent. Thalidomide is effective in treating many malignancies, including prostate cancer. Thalidomide may act synergistically with docetaxel through their antiangiogenic effects. We performed a phase II trial of docetaxel with or without thalidomide in patients with AIPC and demonstrated encouraging response rates with combination therapy. We advocate further investigation of this promising combination regimen.

Journal Article↗

PubMed2001

Identification of differentially expressed genes by serial analysis of gene expression in human prostate cancer.

Prostate cancer is the leading cause of cancer death in American males. To better understand the genetic bases of this disease, we have generated a comprehensive molecular profile of human prostate. The gene expression pattern in normal and prostate cancer tissues was analyzed by serial analysis of gene expression (SAGE). A total of 133,217 transcripts were analyzed, and 35,185 distinct SAGE tags were identified representing 19,287 genes. Comparison of the transcripts in normal and tumor tissue revealed 156 differentially expressed genes (P < 0.05), of which 88 genes were up-regulated and 68 genes were down-regulated in the tumor tissue. Based on SAGE data, we estimate that the transcriptome for human prostate is approximately 37,000. Several differentially expressed genes identified by SAGE were selected for confirmation using immunohistochemistry. Some genes (e.g., E2F4) were overexpressed in tumor epithelial cells and some (e.g., Daxx) were increased in tumor stroma. Further characterization of the role of E2F4 and Daxx as well as other differentially expressed genes may provide useful insights into the mechanism of prostate cancer development.

Dihydrotestosterone↗

PubMedDate not supplied

Racial differences in prostate-specific antigen levels in patients with local-regional prostate cancer.

Prostate cancer is a significant health problem for blacks. The incidence and mortality rates are higher in blacks than in whites; blacks often present with a higher stage. Prostate-specific antigen (PSA) is a very useful serum marker in prostate cancer. We analyzed data from a cohort of 161 patients to determine whether there were any racial differences in PSA levels prior to treatment in local-regional prostate cancer. The immunoradiometric method was used to determine the PSA values. The mean PSA levels were significantly higher in blacks than in whites (P = 0.022), and the difference remained significant in multivariate analysis after adjusting for stage and grade (P = 0.020). However, when analyzed further, the difference was statistically significant in one hospital (P = 0.001) and not in another (P = 0.493). Thus, our results are not unequivocal, but our data do suggest that racial differences in PSA levels not accounted for by tumor stage or grade may exist. Assuming that the data truly reflect a racial difference, the cause(s) of this difference remains to be determined. It may exist because, within each clinical stage, blacks are presenting with a higher tumor cell burden, or it may be indicative of more aggressive biological behavior. The possibility that racial differences are due to socioeconomic factors was considered by estimating median income level from zip code of residence; although a correlation between socioeconomic status and PSA level was found, racial differences remained borderline significant (P = 0.055) after adjusting for income level (in addition to stage and grade).

Black or African American↗

PubMed2005

[Prevention of prostate cancer].

Prostate cancer has become the most frequently diagnosed male cancer next to non-melanotic skin cancer in the Western world. Preventive measures would therefore have important potential effects on the incidence and prevalence of this disease. A potential for effective prevention of prostate cancer is currently seen in dietary changes and perhaps in dietary supplementation with vitamins D and E or selenium. Pharmacological prevention seems a possibility with drugs acting on intraprostatic testosterone metabolism. Several large randomised trials are ongoing to clarify the potential for successful prostate cancer prevention.

5-alpha Reductase Inhibitors↗

PubMed2004

Conditional deletion of Rb causes early stage prostate cancer.

Prostate cancer remains the second leading cause of cancer-related death for men in the United States. Mutations in tumor suppressor genes including retinoblastoma (Rb), p53, and PTEN have been linked to the development of prostate cancer in man and mouse models, and loss of heterozygosity of the Rb locus has been observed in up to 60% of clinical cases. In this study we demonstrate that conditional somatic deletion of even a single Rb allele in the epithelial cells of the mouse prostate causes focal hyperplasia, thereby establishing a causal relationship between Rb loss and development of early stage prostate cancer. As a consequence of Rb ablation we observed increased expression of E2F target genes and a concomitant increase in proliferation in the epithelial compartment. However, by 52 weeks of age these lesions had not become malignant and represent an early stage of the disease. Nevertheless, the multifocal nature of the phenotype in the mice closely resembled multifocality of clinical disease. Taken together, our data demonstrated that loss of pRB-mediated cell cycle control directly caused the initiation of proliferative prostate disease but was insufficient to cause malignancy. Establishment of this early initiation model will aid efforts to thoroughly characterize early prostate disease as well as the elucidation of molecular mechanisms that cooperate with Rb loss to facilitate progression and metastasis.

Animals↗

PubMed2005

Secondary hormonal manipulations in the management of advanced prostate cancer.

Prostate cancer is a heterogeneous disease and clinical outcomes vary considerably after failure of primary androgen ablation. With the development of new therapeutics the management of patients with androgen independent prostate cancer has changed considerably over the last few years. Multiple secondary hormonal manipulations are available and may lead to prolonged periods of clinical response. These maneuvers include the use of oral antiandrogens, antiandrogen withdrawal, ketoconazole, aminoglutethimide, corticosteroids and use of estrogenic compounds. This article reviews the clinical activity of these agents in management of patients with advanced prostate cancer.

Androgens↗

PubMed2001

[Consumption coagulopathy disclosing prostatic cancer].

Prostate cancer can be complicated by disseminated intravascular coagulation. The severity of this complication justifies rapid medical treatment. The authors describe the case of a man in his seventies presenting with disseminated purpuric lesions due to disseminated intravascular coagulation. Prostate cancer was documented concomitantly. The clinical course was rapidly unfavourable despite endocrine therapy and blood transfusions. The mechanism of disseminated intravascular coagulation in prostate cancer has not been clearly elucidated, but appears to be related to release of procoagulant substances during certain diagnostic or therapeutic procedures. The severity of the prognosis justifies rapid introduction of endocrine therapy, which is not immediately effective. It can help to achieve a period of remission if the haemorrhagic syndrome is controlled. Further studies may help to improve therapeutic management.

Aged↗

PubMed1999

Treatment of prostate cancer.

Prostate cancer is the leading cause of cancer death among older men in western countries. However, controversy surrounds many issues related to this disease, particularly its most appropriate treatment, with a wide spectrum of opinions ranging from watchful waiting to aggressive therapy. Patients with newly diagnosed prostate cancer, as well as their doctors, will have to make difficult decisions regarding treatment of this disease. In this article we discuss the current available treatment options and some novel therapeutic approaches to tackling the patient with prostate cancer.

Combined Modality Therapy↗

PubMed2006

Chemoprevention of prostate cancer.

Prostate cancer is a common malignancy with multiple potential opportunities for cancer prevention. As the genetic basis of this malignancy is further understood, prevention strategies will be developed for individual patients based on specific risk factors and pathways of carcinogenesis. The PCPT has conclusively proven that prostate cancer prevention is possible. The results of the SELECT should be available within several years. An enormous challenge for the medical community will be the development of an efficient strategy to evaluate the substantial number of dietary, behavioral, and pharmacologic prevention opportunities. Ultimately, the goal of prostate can-cer prevention is to (1) identify men who are destined to develop clinically significant prostate cancer, and (2) provide individualized agents to prevent disease development.

Anticarcinogenic Agents↗

PubMed1985

[Clinical evaluation of prostate antigen (PA) in prostate cancer].

Prostate antigen (PA) which was isolated at 1979 and may have a probability to be a tumor marker of prostate cancer has been evaluated clinically using an EIA for detection method. From mean +3 S.D. of normal male subjects, upper cut-off values of Americans and Japanese have been decided as 2.5 and 1.2 ng/ml, respectively. Of a total of 1,109 assayed serum PA, positive rate in prostate cancer were 78% in Americans (n = 570) and 61% in Japanese (n = 45), whereas false positive rate was lower in Japanese. Serum PA values could be used for speculation of patients' prognosis and monitoring in prostate cancer.

Acid Phosphatase↗

PubMed2004

Novel therapeutic strategies in prostate cancer.

Prostate cancer is the most common noncutaneous cancer in American men and the second most common cause of death. It is estimated that in 2003, 220,900 new cases will be diagnosed and 28,900 men will die from the disease.1 Hormonal therapy via surgical or chemical castration is the mainstay of treatment for metastatic prostate cancer. While this is quite effective initially, with time patients become refractory to this treatment and may require additional therapy. There have been a substantial number of novel agents that have been developed in the last 10 years that show promise in the treatment of patients with prostate cancer, when used alone or when combined with current approaches (Table 1).

Angiogenesis Inhibitors↗

PubMed2006

Combinatorial androgen receptor targeted therapy for prostate cancer.

Prostatic carcinogenesis is associated with changes in the androgen receptor (AR) axis converting it from a paracrine dependence upon stromal signaling to an autocrine-initiated signaling for proliferation and survival of prostatic cancer cells. This malignant conversion is due to gain of function changes in which the AR activates novel genomic (i.e. transcriptional) and non-genomic signaling pathways, which are not present in normal prostate epithelial cells. During further progression, additional molecular changes occur which allow these unique malignancy-dependent AR signaling pathways to be activated even in the low androgen ligand environment present following androgen ablation therapy. These signaling pathways are the result of partnering the AR with a series of other genomic (e.g. transcriptional co-activators) or non-genomic (e.g. steroid receptor co-activator (Src) kinase) signaling molecules. Thus, a combinatorial androgen receptor targeted therapy (termed CART therapy) inhibiting several points in the AR signaling cascade is needed to prevent the approximately 30,000 US males per year dying subsequent to failure of standard androgen ablation therapy. To develop such CART therapy, a series of agents targeted at specific points in the AR cascade should be used in combination with standard androgen ablative therapy to define the fewest number of agents needed to produce the maximal therapeutic anti-prostate cancer effect. As an initial approach for developing such CART therapy, a variety of new agents could be combined with luteinizing hormone-releasing hormone analogs. These include: (1) 5alpha-reductase inhibitors to inhibit the conversion of testosterone to the more potent androgen, dihydrotestosterone; (2) geldanamycin analogs to downregulate AR protein in prostate cancer cells, (3) 'bulky' steroid analogs, which can bind to AR and prevent its partnering with other co-activators/signaling molecules, and (4) small molecule kinase inhibitors to inhibit MEK, which is activated as part of the malignant AR signaling cascade.

Antineoplastic Agents↗

PubMed2004

[Early diagnosis and surgical management of prostate cancer].

Prostate cancer is a significant cause of morbidity and mortality in the United States and Europe. The natural ageing of the population as well as the continued and widespread use of diagnostic tests such as prostate specific antigen (PSA), has led to an increase in the numbers of men diagnosed with localised prostate cancer. Screening to identify organ-confined disease has provoked much public and scientific attention, but remains controversial. Radical prostatectomy is one of the most challenging urological procedures performed. Improvements in technique due to better understanding of pelvic anatomy have reduced complications, with acceptable standards and excellent results in high-volume institutions. Continual refinements in technique and the recent introduction of laparoscopic radical prostatectomy are likely to improve functional outcome further. However the effectiveness of surgery in improving survival and quality of life, in men with early prostate cancer remains to be determined. The results from large randomised controlled trials are eagerly awaited.

Diagnosis, Differential↗