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PubMed2003

Molecular imaging in prostate cancer.

Prostate cancer (PCa) is the most common non-cutaneous malignancy in men. New ways to diagnose this cancer in its early stages are needed. Unique genetic and biochemical changes in the cell pave the way for tumors to grow and metastasize. Novel imaging approaches attempt to detect pathological processes in cancer cells at the molecular level. This has led to the establishment and development of the field of molecular imaging. Positron emission tomography (PET), magnetic resonance spectroscopic imaging (MRSI), magnetic resonance imaging (MRI), and radiolabeled antibodies are a few of the modalities that can detect abnormal tumor metabolic processes in the clinical setting. Other imaging techniques are still in their early phase of development but hold promise for the future, including bioluminescence imaging (BLI), measurement of tumor oxygenation, and measurement of uptake of iodine by tumors. These techniques are non-invasive and can spare the patient undue morbidity, while potentially providing early diagnosis, accurate follow-up and, finally, valuable prognostic information.

Animals↗

PubMedDate not supplied

[Current multidisciplinary treatment of metastatic prostatic cancer].

Prostate cancer is one of the commonest causes of cancer-related death in the western world. The morbi-mortality associated is usually a direct consequence of metastatic spread to bone, in up to 50% of patients at first presentation. The aim of treatment of metastatic patients is to alleviate and to prevent the distressing symptoms. The approach include hormone-therapy, radiotherapy, radio-nuclides, surgery, chemotherapy, bisphosphonates and new drugs (agents that inhibit angiogenesis, immunotherapy and therapies that affect the differentiation). Decisions about therapy must also take into consideration the androgen-dependent or independent, so hormone-therapy is the first step of the treatment; the number and location of bone metastases; the severity of symptoms; the available of therapies; the status performance of patient; the prognosis and the cost-effect relationship. Some treatments have established indications whereas others are still in process of study in order to determinate their efficacy, their model of treatment and their indications. This article revises and updates these treatments.

Antineoplastic Agents↗

PubMed2002

The role of androgens and the androgen receptor in prostate cancer.

Prostate cancer (PCa) is the leading diagnosed malignancy in men in western countries. The relationship between androgens and the androgen receptor (AR) has been studied extensively in PCa. Plasma levels of androgens show variations between different populations, and in many cases this correlates with PCa susceptibility. Indeed, exposure of the fetus to higher androgen concentrations appears to be a risk factor for PCa. The AR is present in the majority of PCa, and its activation by androgens leads to different proliferative, apoptotic and angiogenic events. These events are in turn mediated by dysregulation of cyclin-dependent kinases, apoptotic factors and even mutations in the AR. Although androgen ablation has been the mainstay non-surgical treatment for this disease, most tumors will eventually become refractory to treatment. Different cellular mechanisms appear to be involved in the androgen-independent progression of PCa, including cytokine and growth factor-mediated activation of the AR as well as neuroendocrine differentiation. Thus, an understanding of the cellular mechanisms involved in androgen action may lead to better therapeutic targets for PCa.

Androgens↗

PubMed1990

Update in the management of prostate cancer.

Prostate cancer remains one of the commonest malignancies in our community, and it appears that its incidence is rising because of the increasing proportion of the aged population. Improved technology, including the development of new tumour markers and tumour imaging techniques, and a gradually increasing community awareness of this disease, may allow earlier diagnosis. In turn, as the proportion of patients presenting with early stage disease increases, improved approaches to the treatment of localized cancer may thus yield increased community cure rates. The mainstay of treatment of advanced disease remains hormonal manipulation. The introduction of the LHRH agonists has provided an alternative to surgical castration, but has not resulted in an improved response rate or survival from first-line therapy. We believe that these agents do not offer a major benefit, when compared with the simple procedure of orchidectomy, notwithstanding the psychological sequelae of castration. With a median survival of less than five years after hormonal manipulation, many patients still require salvage treatment after relapse. New hormonal therapies yield objective and subjective response rates of approximately 15% and 30%, respectively, but the median survival from the time of hormonal failure remains less than one year. Cytotoxic chemotherapy has not provided a panacea, but has shown definite evidence of antitumour activity in this disease. The use of relatively non-toxic single cytotoxic drugs can provide effective palliation of symptoms in up to 40% of patients and may even prolong survival in some patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗

PubMed2003

Metallothionein 2A interacts with the kinase domain of PKCmu in prostate cancer.

Prostate cancer (PC) patients die from progression to androgen independence (AI) and chemoresistance (CR). Protein kinase Cmu (PKCmu) a novel member of the PKC family of signal transduction proteins is downregulated in AI PC. Studying PKCmu interactors in the yeast two-hybrid system identified metallothionein 2A (MT 2A) as an interactor of PKCmu kinase domain (KD) in PC, which was quantified by beta-gal assay, confirmed in PC cells by immunoprecipitation, and PKCmu-MT 2A co-localization in vivo by immunofluorescence studies. PKCmu domain interaction studies revealed that MT 2A interacted strongly with KD, relatively weakly with C1, and failed to interact with C2, PH or kinase mutant domains. Peptide library and in silico analysis strongly suggest that MT 2A is a novel substrate of PKCmu and our data indicate that the PKCmu-MT 2A interaction depends on PKCmu kinase activity. Because metallothioneins are associated with cell proliferation and CR, the PKCmu-MT 2A interaction may contribute to CR and/or AI in PC.

Androgens↗

PubMed2001

Signal transduction targets in androgen-independent prostate cancer.

Prostate cancer (PCa) first manifests as an androgen-dependent disease. Thus, androgen-deprivation therapy is a standard regimen for patients with metastatic PCa. Despite the initial success of androgen-deprivation therapy, PCa inevitably progresses from being androgen dependent (AD) to androgen independent (AI), and this marks the poor prognosis of this disease. Relapse of AIPCa becomes life threatening and accounts for the majority of mortality of PCa patients. Currently, no effective therapy is available for controlling AIPCa. Therefore, the challenge in providing a new intervention is to understand the fundamental changes that occur in AIPCa. Increasing evidence indicates that, under androgen-deprived milieu, several signal networks elicited by peptide growth factors dictate the AI phenotype of PCa. This review covers the latest studies investigating the potential involvement of autocrine growth factors in cell proliferation, survival, metastasis, and the reciprocal interaction with the androgen receptor pathway. In addition, loss of the negative feedback mechanism of the signal cascade further amplifies the effect of growth factors, and thus contributes significantly to the onset of AIPCa. The understanding of the signal target(s) in AIPCa should provide the new markers for prognosis and a new strategy for prevention and therapy.

Adenocarcinoma↗

PubMed2004

[Docetaxel and prostate cancer].

Prostate cancer is currently the most-frequency malignancy in men, and the second cause of death from cancer in the Western world. Once the disease has metastasized, palliative treatment is the rule. First-sine therapy consists in surgical or chemical castration, associated or not with anti-androgens. This treatment approach is active in 80% cases but failures occur within 12-18 months. When the disease becomes refractory to hormone therapy, few alternatives are available. The combination of mitoxantrone-steroids improves clinical symptoms, namely by reducing pain, but does not improve patient survival. Both docetaxel and estramustine act through microtubules and synergistic interactions have been shown between these two compounds. Recently, several studies have demonstrated the efficacy of a combination of estramustine and taxanes, and in particular docetaxel. Phase II trials using docetaxel monotherapy have demonstrated responses rates concerning PSA of 45 to 58% and objective response of 33% and 40%. Combination with estramustine increases the biochemical response rate from 45% and 74%. A randomized phase II trial revealed the superiority of this combination compared to mitoxantrone in terms of response rate and clinical benefit. The results of phase III trials are still not available, in particular as concerns survival, but the combination docetaxel-estramustine appears very promising, even though the ideal therapeutic protocol is still under evaluation.

Antineoplastic Agents, Phytogenic↗

PubMed1995

[Usefulness of hyper sensitive PSA assay kits for determination on low range of prostate specific antigen in prostate cancer].

Prostate specific antigen (PSA) levels after total prostatectomy or radiation therapy to localized prostate cancer and also during endocrine therapy are within normal range. Therefore, it is necessary to use hyper sensitive PSA assay kits for early detection of relapse. The present study was undertaken to evaluate two hyper sensitive assay kits (Delfia kit, lower limit 0.1 ng/ml, Kabi Pharmacia Diagnostics Co. and Markit M kit, 0.5 ng/ml, Dainippon Pharmaceutical Co.) and to compare them with conventional PSA kit (Eiken Chemical Co., 1.0 ng/ml). Total of 291 sera were examined: patients consisted of 10 total prostatectomy+endocrine therapy, 9 radiation therapy+endocrine therapy, 5 radiation therapy alone and 44 endocrine therapy alone. Values of endocrine therapy alone were divided into two groups according to duration after start of treatment; more or less than 5 years. The following results were obtained. 1. In non-relapse patients after total prostatectomy+endocrine therapy and radiation+endocrine therapy, PSA showed under lower limit with hyper sensitive kit. On the contrary, conventional kit indicated more than 1.0 ng/ml. 2. Radiation therapy alone kept PSA in detectable range with hyper sensitive kit in spite of no sign of relapse. 3. In non-relapsed patients under endocrine therapy alone, long duration (more than 5 years after start of treatment) decreased PSA in non detectable values with hyper sensitive kits. In this case, conventional kit still showed PSA as more than 1 ng/ml. 4. Doubling time at relapse was estimated similar with Delfia kit and Markit M kit, and much longer with conventional kit. It is concluded that hyper sensitive kit is more useful to manage patients after therapy than conventional kit.

Aged↗

PubMed1998

Clinical pharmacokinetics of the antiandrogens and their efficacy in prostate cancer.

Prostatic cancer is the second most common cause of cancer death in males. Treatment by radical prostatectomy and radiotherapy is useful in the early stages of the disease. Whenever metastases occur, patients are usually treated by surgical (orchidectomy) or medical [gonadotropin releasing hormone (GnRH) analogue] castration. This form of treatment is, however, associated with unwanted adverse effects, such as flushing, loss of libido and potency and all patients ultimately escape therapy after a delay of 1 to 2 years. For this reason antiandrogens have been developed as another means of endocrine ablation therapy. Antiandrogens fall in 2 groups of which the first group, the steroidal antiandrogens such as cyproterone acetate (CPA), have a direct blocking effect at the cellular level but also inhibit testosterone production by their additional gestagenic properties blocking gonadotropin secretion. Except in preventing the flare-up associated with the start of GnRH analogue therapy and in reducing flushing, no evidence exist of any superiority for CPA over classical therapy in terms of adverse effects and survival. The second group, the nonsteroidal or 'pure' antiandrogens, only block androgens at the cellular level without any central effects. In contrast with other forms of castration, patients on pure antiandrogens as monotherapy preserve their sexual function and potency, at the expense of a slightly inferior androgen blockade and gynecomastia. These latter effects are explained by a compensatory rise in androgens as a result of the blockade at the central level, which weakens the androgen blockade, and by peripheral aromatisation of the increased androgens to oestrogens. In addition, some evidence exist that pure antiandrogens improve survival if combined with other forms of castration as they also inhibit the adrenal androgens, the so-called maximal androgen blockade (MAB). If patients escape control under MAB, a trial of stopping the antiandrogen must always be considered, as some tumours have 'learned' to be activated by these drugs. At the moment it is not yet clear if antiandrogens are of any benefit in downstaging the extent of disease before prostatectomy and/or radiotherapy. Of the currently known pure antiandrogens, bicalutamide offers some advantages over flutamide as it possesses a much longer half-life, allowing a once daily regimen, and has advantages over nilutamide in terms of fewer adverse effects.

Androgen Antagonists↗

PubMed2005

The extent of lymphadenectomy for pTXNO prostate cancer does not affect prostate cancer outcome in the prostate specific antigen era.

PURPOSE: Recent data suggest that extended lymph node dissection in prostate cancer may be necessary for accurate staging. With limited lymph node dissection apparently node negative cases might be under staged. We determined the impact that the number of lymph nodes removed at radical retropubic prostatectomy (RRP) has on cancer progression and cause specific survival in pTXNO cases. MATERIALS AND METHODS: We reviewed the RRP prostate cancer database on 7,036 patients with clinical T1 to T3 disease, no adjuvant therapy and node negative disease in the prostate specific antigen (PSA) era from 1987 to 2000. Factors evaluated were the number of lymph nodes obtained at RRP, preoperative PSA, clinical and pathological stage and grade, margin status, year of surgery and specific surgeon for 5 surgeons who operated throughout the period and performed more than 500 RRPs. Cox analysis was done to determine the RR of progression (PSA or systemic) and prostate cancer death for the number of lymph nodes excised. RESULTS: Median patient age was 65 years and median preoperative PSA was 6.6 ng/ml. At pathological evaluation 5,379 tumors (77%) were organ confined, 4,491 (65%) were Gleason score 5 to 6 and 2,027 (29%) were Gleason score 7 to 10. The median number of nodes obtained significantly decreased from 14 in 1987 to 1989 to 5 in 1999 to 2000 (p <0.001). Ten years after RRP Kaplan-Meier estimates were 63% of cases free of PSA progression, 95% free of systemic progression and 98% free of prostate cancer related death. Median followup was 5.9 years. After adjusting for pathological factors (PSA, grade, stage, margin status and surgical date) the number of lymph nodes obtained at lymphadenectomy was not significantly associated with PSA progression (for each additional node (RR 0.99, 95% CI 0.98 to 1.02, p = 0.90), systemic progression (RR 0.99, 95% CI 0.96 to 1.03, p = 0.68) or cause specific survival (RR 1.01, 95% CI 0.96 to 1.06, p = 0.75). CONCLUSIONS: The extent of lymphadenectomy does not appear to affect prostate cancer outcome in lymph node negative cases. This includes patients with high preoperative PSA, high pathological grade and extracapsular disease. These results suggest that under staging is not present in apparently node negative cases with limited lymphadenectomy and, even if present, its impact on outcome is likely to be negligible.

Adult↗

PubMed1994

Prostate cancer.

Prostate carcinoma is a growing concern in our aging society. While the disease often follows a indolent course, it is the second leading cause of cancer-related deaths in males. Prostate cancer screening is promising but remains unproven and controversial. The therapy of prostate cancer has changed little over the past 10 years. The tumor remains refractory to conventional chemotherapeutic agents. True containment of this disease will require novel strategies of diagnosis, biologic assessment, and therapy.

Humans↗

PubMed1994

Cost-effective prostate cancer detection. Reduction of low-yield biopsies. Investigators of the American Cancer Society National Prostate Cancer Detection Project.

BACKGROUND: In hopes of limiting low-yield prostate biopsies, results of digital rectal examination (DRE), transrectal ultrasound (TRUS), prostate specific antigen (PSA) and age-related PSA values, gland-volume-adjusted PSA levels, and longitudinal PSA changes were analyzed to identify their cost-effectiveness as prognostic indicators in screening, biopsy, and follow-up of patients with prostate cancer. METHODS: Twenty-nine hundred men with complete data sets from an initial cohort of 2999 men with an annual follow-up for up to 5 years were examined. Intrapatient PSA and gland-volume variability, optimal PSA operating points (o.p.), and test performance scores were determined for each parameter. Decision analysis was then applied retrospectively to each parameter to determine the cancer detection yield, biopsy requirements, and costs for commonly used detection strategies. RESULTS: For the initial screening decision, the optimal PSA o.p. was 3.0 ng/ml but increased to 5.0 ng/ml in combination with DRE, whereas age-related PSA performed no better than did PSA. The mean intrapatient variability in TRUS gland volume (+5.5 cc) relative to mean volume (34 cc) was 16%, which was less than the 28% (0.64/2.3 ng/ml) relative variability for PSA. For biopsy decisions, using PSA density (PSAD) with a level of 0.12 ng/ml/cc there was no significant difference in accuracy compared with the systematic biopsy of all patients with elevated PSA or age-related PSA levels. Rather than perform systematic biopsy on all patients with PSA levels greater than 4 ng/ml, decision analysis showed that a 16-55% reduction in biopsies could be achieved with a respective cancer loss of 4-25% by limiting biopsy to patients with an increased PSAD level and/or abnormal results of DRE. Using age-related PSA criteria in combination with DRE reduced biopsies by 12% but resulted in minimal cost reductions. The greatest biopsy reduction relative to cancer yield and lowest cost per cancer detected occurred with PSAD-driven biopsy strategies. During follow-up, longitudinal changes in absolute PSA and PSAD levels were significantly better (P < 0.05) than the percentage change in PSA levels per year. CONCLUSIONS: Cost-effective prostate cancer detection with PSA as a parameter is better achieved if screening and biopsy decisions are not linked intimately. A tailored-biopsy approach for patients with disproportionately elevated PSA levels of suspicious DRE results in the greatest biopsy reduction by selecting lower risk groups for more conservative follow-up.

Age Factors↗

PubMed1997

Frequency and clinical significance of transition zone cancer in prostate cancer screening.

Approximately 20% of prostate cancers originate in the transition zone (TZ). Although transrectal ultrasound (TRUS) and systematic biopsies have improved peripheral zone (PZ) cancer diagnosis, additional biopsies directed into the TZ may further improve cancer detection. To evaluate the frequency and clinical significance of TZ cancers, we added two TZ biopsies to the routinely performed sextant biopsies. Three hundred forty patients (aged 45-75) from our prostate-specific antigen (PSA) screening study (21,078 volunteers) with negative rectal examination findings underwent systematic and TZ biopsies with three-dimensional ultrasound equipment. All patients had elevated PSA levels according to age-specific reference ranges. Ninety-eight of 340 men (28.5%) had biopsies positive for cancer. Of these 98 cancers, 28 (28%) originated in the TZ only and 5 (5%) were located in the TZ as well as the PZ. Eight men showed TZ abnormalities on ultrasound images, of whom four had biopsies positive for TZ cancer. The TZ cancers detected were pathologically significant in 96% (27 of 28). Seventy-one percent (20 of 28) of pathologically staged cancers were found to be organ confined and all combined TZ and PZ cancers were advanced tumors. We conclude that TZ biopsies enhance the cancer detection rate in prostate cancer screening and should therefore be added to the routinely done sextant biopsies in men with PSA elevation and normal digital rectal examination findings.

Aged↗

PubMed2001

[The epidemiology of prostate cancer--recent trends in prostate cancer incidence and mortality].

Prostate cancer is one of the major malignant diseases in Western countries. In Japan, the incidence and mortality of prostate cancer is not so high, but is continuously increasing. The recent drastic increase in incidence has been attributed to the growth of the elderly population, a westernized diet in daily life, widespread environmental contamination, and improved screening techniques such as the serum PSA test. The epidemiology of prostate cancer hints that its etiology is both environmental and genetic. Androgenic stimulation over time, perhaps due to a high fat diet, has been suggested as a cause of prostate cancer. Dietary factors such as phytoestrogens, vitamins and trace elements are suggested to have a protective effect against prostate cancer, and encourage us to search for means of prevention. Some have suggested that certain polymorphisms increase the risk of prostate cancer, whereas others are searching for genetic mutations that may also increase prostate cancer risk. The cause of prostate cancer is likely to be a combination of environmental and genetic factors.

Adult↗

PubMed2004

Prostate stem cell antigen (PSCA) expression in human prostate cancer tissues: implications for prostate carcinogenesis and progression of prostate cancer.

OBJECTIVE: Prostate stem cell antigen (PSCA) is a recently defined homolog of the Thy-1/Ly-6 family of glycosylphosphatidylinositol (GPI)-anchored cell surface antigens. The objective of the present study was to examine the expression status of PSCA protein and mRNA in clinical specimens of human prostate cancer (PCa) and to validate it as a potential molecular target for diagnosis and treatment of PCa. METHODS: Immunohistochemical (IHC) and in situ hybridization (ISH) analyses of PSCA expression were simultaneously performed on paraffin-embedded sections of 20 benign prostatic hyperplasia (BPH), 20 prostatic intraepithelial neoplasm (PIN) and 48 prostate cancer (PCa) tissues, including 9 androgen-independent prostate cancers. The level of PSCA expression was semiquantitatively scored by assessing both the percentage and intensity of PSCA-positive staining cells in the specimens. We then compared the PSCA expression between BPH, PIN and PCa tissues and analyzed the correlations of PSCA expression level with pathological grade, clinical stage and progression to androgen-independence in PCa. RESULTS: In BPH and low grade PIN, PSCA protein and mRNA staining were weak or negative and less intense and uniform than that observed in high grade PIN (HGPIN) and PCa. Moderate to strong PSCA protein and mRNA expression were noted in 8 of 11 (72.7%) HGPIN and in 40 of 48 (83.4%) PCa specimens examined by IHC and ISH analyses, and their statistical significance was compared with BPH (20%) and low-grade PIN (22.2%) specimens (P < 0.05). The expression level of PSCA increased with a higher Gleason grade, advanced stage and progression to androgen-independence (P < 0.05). In addition, IHC and ISH staining revealed a high degree of correlation between PSCA protein and mRNA overexpression. CONCLUSIONS: Our data demonstrate that PSCA as a new cell surface marker is overexpressed in a majority of cases of human PCa. PSCA expression correlates positively with adverse tumor characteristics, such as increasing pathological grade (poor cell differentiation), worsening clinical stage and androgen-independence and speculatively with prostate carcinogenesis. PSCA may possess prognostic utility and may be a promising molecular target for diagnosis and treatment of PCa.

Aged↗

PubMed2006

Obesity, diabetes, and risk of prostate cancer: results from the prostate cancer prevention trial.

Studies on the relationship between obesity and prostate cancer incidence are inconsistent. In part, this inconsistency may be due to a differential effect of obesity on low-grade and high-grade cancer or confounding of the association of obesity with prostate cancer risk by diabetes. We investigated the associations of obesity and diabetes with low-grade and high-grade prostate cancer risk. Data were from 10,258 participants (1,936 prostate cancers) in the Prostate Cancer Prevention Trial who all had cancer presence or absence determined by prostate biopsy. Multiple logistic regression was used to model the risk of total prostate cancer, and polytomous logistic regression was used to model the risk of low-grade and high-grade prostate cancer. Compared with men with body mass index < 25, obese men (body mass index > or =30) had an 18% [odds ratio (OR), 0.82; 95% confidence interval (95% CI), 0.69-0.98] decreased risk of low-grade prostate cancer (Gleason <7) and a 29% (OR, 1.29; 95% CI, 1.01-1.67) increased risk of high-grade prostate cancer (Gleason > or =7) or, alternatively, a 78% (OR, 1.78; 95% CI, 1.10-2.87) increased risk defining high-grade cancer as Gleason sum 8 to 10. Diabetes was associated with a 47% (OR, 0.53; 95% CI, 0.34-0.83) reduced risk of low-grade prostate cancer and a 28% (OR, 0.72; 95% CI, 0.55-0.94) reduced risk of high-grade prostate cancer. Associations of obesity or diabetes with cancer risk were not substantially changed by mutually statistical controlling for each other. Obesity increases the risk of high-grade but decreases the risk of low-grade prostate cancer, and this relationship is independent of the lower risk for prostate cancer among men with diabetes.

Adenocarcinoma↗

PubMedDate not supplied

E-cadherin and associated molecules in the invasion and progression of prostate cancer.

Prostatic carcinoma is the most common type of male cancer found in the Western world and its distant metastasis becomes a life threatening event in tumour bearing patients. However, the biology of prostate cancer and metastasis is poorly understood. We review the progress made in the last decade on the molecular and cellular biology of cell-cell adhesion molecules in the invasion and progression of prostate cancer, with emphasis being placed on E-cadherin and its associated molecules.

Cadherins↗

PubMed2002

Expression of Ki-67 and PCNA as proliferating markers in prostate cancer.

Prostate carcinoma (PCa) is the most common male cancer in industrialized societies and represents a serious public health problem. The aim of our study was the immunohistochemical evaluation of Ki-67 and proliferating cell nuclear antigen (PCNA) expression in prostate cancer (PCa) following radical prostatectomy and analysis of its relationship to chosen anatomo-clinical and morfological parameters of the tumours. Archival sections from 28 PCas were immunostained with monoclonal antibodies against Ki-67, and proliferating cell nuclear antigen (PCNA). Immunolocalization of Ki-67 and PCNA was performed using LSAB method. No statistically significant correlation was found between the expression of Ki-67, PCNA and preoperative PSA level, lymph node metastases, capsular penetration, seminal vesicle invasive and positive or negative surgical resection margins. However, a strong statistically significant correlation between Ki-67 positive and T stage was found. We also found relationship between Gleason score 7 or above and high expression of Ki-67 and PCNA in prostate cancers (p < 0.004, p < 0.02 respectively). These results suggest that PCNA and especially Ki-67 may be useful as tumour markers in prostate carcinoma, but further studies on larger group are required.

Adenocarcinoma↗