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PubMed2003

The role of PTEN in the progression and survival of prostate cancer.

PTEN (phosphatase and tensin homologue deleted on chromosome-10), a dual specificity phosphatase, is a tumor suppressor gene whose inactivation has been associated with many different types of cancer including prostate cancer. Prostate adenocarcinoma is one of the most commonly diagnosed malignancies afflicting the male population in both the United States and Europe. The frequency of PTEN inactivation appears to increase during the progression of prostatic cancer. The physical loss of the PTEN genetic locus in prostate cancer progression has been well characterized, however the molecular implication of this loss of PTEN remains enigmatic. The purpose of this review is to describe the functional role of PTEN in the molecular pathogenesis of prostatic disease. We review the function of PTEN discussing its association with the phosphoinositol 3-kinase (PI3K) and mitogen activated protein kinase (MAPK) signal transduction pathways. Additionally, we discuss the role of PTEN in the regulation of apoptotic pathways involving the anti-apoptotic gene bcl-2 and the pro-apoptotic ligand TRAIL. We also review the mechanisms that can lead to the loss of PTEN function. We describe genetic inactivation including loss of heterozygosity, haploinsufficiency and mutation. We conclude by outlining epigenetic loss including methylation, post-translational modifications and oxidative stress.

Gene Silencing↗

PubMed2006

Protein tyrosine phosphatase PTP1B is involved in neuroendocrine differentiation of prostate cancer.

BACKGROUND: Prostate cancer (PC) contains a minor component of neuroendocrine (NE) cells that may stimulate androgen-independent growth of the tumor. The mechanism of neuroendocrine differentiation remains unknown. METHODS: The expression of PTP1B, a protein tyrosine phosphatase, was studied in LNCaP cells induced to show neuroendocrine phenotype by androgen withdrawal. Wild-type PTP1B and its dominant-negative mutant were transfected into LNCaP cells to study their effects on neuroendocrine differentiation. In vivo expression of PTP1B in human prostate cancer was studied by immunohistochemistry. RESULTS: Androgen withdrawal of LNCaP cells led to increased expression of PTP1B with a corresponding increase in its tyrosine phosphatase activity. Overexpression of PTP1B in LNCaP cells led to neuroendocrine differentiation while expression of its dominant-negative mutant inhibited neuroendocrine differentiation. Immunohistochemical study showed that PTP1B was exclusively expressed in neuroendocrine cells of human prostate cancer tissue. CONCLUSION: Our findings suggest that PTP1B plays an important role in neuroendocrine differentiation, and therefore, may possibly be involved in the progression of prostate cancer.

Androgens↗

PubMed2004

The ceramide analog, B13, induces apoptosis in prostate cancer cell lines and inhibits tumor growth in prostate cancer xenografts.

BACKGROUND: Apoptosis is a therapeutic target for the elimination of cancer cells. As elevations in ceramide levels induce apoptosis, there is much excitement about the use of agents that elevate ceramide levels as novel chemotherapeutic agents. Ceramidases are enzymes involved in degradation of ceramide and inhibition of ceramidase has been proposed as a mechanism to increase ceramide levels. This study provides the first insight into the effect of B13, an inhibitor of acid ceramidase, on human prostate cancer cell lines and xenografts. METHODS: Cell death was evaluated by the trypan blue assay; apoptosis by the Apo2.7 apoptosis assay; and glutathione levels by HPLC. Tumors were irradiated with a dose of 5 Gy of X-rays (250 kVp, 15 mA, 2 Gy/min) and tumor volume was measured during the course of the experiment. At the conclusion of the experiment, tumor weight was determined and the tumors were evaluated histologically. RESULTS: B13 is an inducer of cell death, by apoptosis, in cultured prostate cancer cells. LNCaP and PC3 cells have different responsiveness to the enantiomers of B13. In LNCaP cells, the R enantiomer of B13 (10 microM) was significantly more effective than the S enantiomer at inducing cell death as determined by the trypan blue assay, culminating in approximately 90% cell death at 48 hr. In contrast, the same concentration of B13S induced <20% cell death at 48 hr. In PC3 cells, the S enantiomer was a more effective inducer of cell death, culminating in approximately 30% cell death, relative to 14% for B13R in this model. Evaluation of induction of apoptosis by the Apo2.7 mitochondrial assay confirmed that this induction of cell death was by apoptosis. Concurrent with induction of apoptosis, glutathione levels drop in response to B13. Specifically, B13R caused a significant drop in glutathione levels in LNCaP cells, culminating in a reduction to 40% control values at 48 hr. In PC3 cells, in contrast, the drop in glutathione levels was more dramatic, culminating in a drop to 12% control values in response to B13S at 48 hr. The effects of B13R, however, were not significantly different from control values. In in vivo studies using a model of xenografted androgen-insensitive prostate cancer, B13 sensitized the tumors to the effects of radiation, resulting in a significant reduction in tumor volume and weight after treatment with the combination of B13 and radiation. Microscopic evaluation of the tumors indicated that apoptosis was the primary mechanism of this effect. CONCLUSIONS: Targeting ceramide pathways may be a novel treatment strategy for hormone refractory prostate cancer.

Amides↗

PubMed2001

Randomized, controlled chemoprevention trials in populations at very high risk for prostate cancer: Elevated prostate-specific antigen and high-grade prostatic intraepithelial neoplasia.

This is a report of research efforts underway at the Arizona Cancer Center. These efforts build upon Larry Clark's unanticipated clinical prevention trial results: those results indicated that 200 microg/day of selenium in selenized yeast decreased prostate cancer risk by almost 60%. The trials underway address various phases of the possible preventive activity of selenium. The first of these, for men who are suspected to have prostate cancer but who have had a biopsy revealing no evidence of cancer, will test the ability of selenium to prevent the development of clinical prostate cancer. The second is for men with high-grade prostatic intraepithelial neoplasia; the trial will test whether selenium will prevent the development of prostatic cancer in this high-risk group. The third trial is for men who have been diagnosed with prostate cancer and are scheduled for prostatectomy: the trial is designed to test whether evidence of selenium-linked changes can be identified in the tissue removed at prostatectomy. The fourth trial is for men who have been diagnosed with prostate cancer but who have chosen neither surgery nor irradiation; this trial will evaluate whether treatment with selenium will inhibit the progress of prostate cancer. Together, these trials will provide important information as to the prostate cancer chemopreventive potential of selenium.

Anticarcinogenic Agents↗

PubMed1999

A case-cohort study on prostate cancer risk in relation to family history of prostate cancer.

We investigated the risk of prostate cancer in relation to a family history of prostate cancer in 58,279 men ages 55-69 years. We found 704 incident cases after 6.3 years of follow-up. Rate ratios and 95% confidence intervals for having an affected vs nonaffected father and brother were, respectively 1.44 (0.80-2.58) and 5.57 (1.61-19.26). We found no evidence for an increasing risk with an increasing percentage of affected family members. The associations we observed were stronger for cases diagnosed before age 70 compared with cases diagnosed after age 70 and for advanced compared with localized tumors.

Aged↗

PubMedDate not supplied

Delivering prostate cancer prevention messages to the public: how the National Cancer Institute (NCI) effectively spread the word about the Prostate Cancer Prevention Trial (PCPT) results.

The Prostate Cancer Prevention Trial was the first clinical trial to show that a direct intervention (5 mg of finasteride daily for 7 years) could reduce a man's risk of developing prostate cancer. Initial results also suggested that men taking finasteride had an increased risk of developing what appeared to be higher-grade disease (Gleason score 7-10). The National Cancer Institute has a congressional mandate to communicate health information to the public and has established methods to reach the public directly and to reach information intermediaries in the media, professional societies, and advocacy groups. The groundbreaking yet complicated results of the Prostate Cancer Prevention Trial were widely disseminated by National Cancer Institute using the social marketing and public-relations strategies and tactics detailed here.

Clinical Trials as Topic↗

PubMed1997

Detection of micrometastatic prostate cancer cells in the bone marrow of patients with prostate cancer.

Thirty-five patients with prostate cancer were examined for micrometastases to the bone marrow using reverse transcription-polymerase chain reaction (RT-PCR) with primers specific for the prostate-specific antigen (PSA) gene. Of nine patients with bone metastases detectable by bone scan imaging, five patients had PSA mRNA expression in the bone marrow detectable by RT-PCR. Of 26 patients with negative bone scan findings, seven patients had PSA mRNA expression detectable in the bone marrow. RT-PCR could detect micrometastatic prostate cancer cells in the bone marrow that were not detectable by bone scan imaging. Of 16 patients with a serum PSA concentration of 25 ng ml(-1) or greater, only nine (56.3%) had bone metastases detected by bone scans. Of the remaining seven patients, five had micrometastases to the bone marrow detected by RT-PCR. Overall, 14 of 16 patients (87.5%) with a serum PSA concentration of 25 ng ml(-1) or greater had metastatic bone diseases including bone marrow micrometastases. Of 19 patients with a serum PSA concentration of less than 25 ng ml(-1), two (10.5%) had only micrometastatic disease detected by RT-PCR. A significant correlation was observed between the incidence of bone involvement and the serum PSA concentration. This study suggests that RT-PCR will potentially develop into a relevant tool to assess bone involvement including bone marrow micrometastases and establish a precise correlation between serum PSA concentration and metastatic bone disease in patients with prostate cancer.

Bone Marrow↗

PubMed1996

[Flow cytometry analysis of the DNA content of the prostate cancer--study on the tumor heterogeneity in prostate cancer].

PURPOSE: Clinical significance of DNA ploidy pattern and its DNA heterogeneity is examined in prostate cancer. METHODS: Fresh needle biopsy specimens were analyzed with flow cytometry and were compared with histopathological findings in 42 patients. RESULTS: Seven patients had stage B (1 case of B1, 6 cases of B2), 14 had stage C and 21 had stage D disease respectively. Histopathologically, 18 of the cases were well, 12 were moderately and 12 were poorly differentiated adenocarcinoma. Diploid was observed in 20, aneuploid in 22. Though 22 cases showed no DNA heterogeneity, 14 had type A heterogeneity with aneuploid in association with diploid pattern, and 6 cases had type B heterogeneity in which multiple aneuploid patterns with different D.I. values were observed. The heterogeneity was observed in 28% of well, 58% of moderately and 67% of poorly differentiated adenocarcinoma, respectively, and also in 14% of stage B, 50% of stage C and 57% of stage D patients, respectively. CONCLUSION: We conclude that DNA heterogeneity in prostate cancer is more frequently seen in poorer differentiated ones on histologic grade and in more advanced ones on clinical stage.

Adenocarcinoma↗

PubMed1999

Strategies for chemoprevention of prostate cancer.

Because prostate cancer has a long latency and high incidence, it is a good target for chemoprevention by agents such as retinoids, antiandrogens, antiestrogens, and vitamin D analogs. Phase II chemoprevention trials are frequently conducted on cohorts of patients with previous cancers or premalignant lesions who are scheduled for prostate cancer surgery; such trials are currently in progress with several agents. Prostatic intraepithelial neoplasia (PIN) can be used as a surrogate endpoint biomarker for prostate cancer incidence. Studies of men with high-grade PIN (HGPIN) are particularly useful in that they require a much smaller cohort of 200-400 patients instead of the 18 000 patients required for typical Phase III trials. Even with a smaller sample size, statistically significant evidence of cancer prevention is achieved due to the high probability of HGPIN progressing to cancer (35-55%). A Bayesian sequential monitoring system allows interim analysis of biomarker modulation as early as the completion of 30 patients. Putting all these strategies together will help inhibit, delay, or modulate the natural history of prostate carcinogenesis.

Journal Article↗

PubMed2003

BSP-PC (Bononian Satisfaction Profile--Prostate Cancer): development and validation of a "disease-specific" questionnaire for the evaluation of health-related quality of life in patients with prostate cancer.

OBJECTIVES: Prostate cancer (PC) is the most common neoplasia in men over 50 years of age in western countries. Nowadays, since there are several alternative medical-surgical treatments for this cancer, health-related quality of life (HQoL) evaluation has become very important. The present study deals with the development and the validation of a questionnaire (BSP-PC), considering the HQoL in prostate cancer patients. The BSP-PC items are mainly related to the subjects' satisfaction. As far as we know, it does not exist any disease specific instrument based on such aspect. MATERIALS AND METHODS: Questionnaire development: During three different meetings, with ten experts and twenty patients, we have defined the life aspects which are the most affected by prostate cancer. Subsequently we have created a first 40-item version of the BSP-PC. Patients were asked to fill in this particular questionnaire in addition to a generic and validated one (the EuroQol). A final 24 item questionnaire version, was finally achieved by other statistical analysis and meetings with experts. Questionnaire validation: the BSP-PC was filled in by 261 patients divided into 3 groups: "healthy" (57), "prostate cancer" (103), "other diseases" (100). RESULTS: Questionnaire development: participants' mean age was 59 years (N=71); 46% had prostate cancer, while 53% of the sample did not report notable diseases. The 24 items were selected on the basis of the following criteria: a) r>0.50, p<0.05 (correlation test re-test), b) p<0.05 (ANOVA presence vs absence of PC), c) r>0.50, p<0.05 (correlation with EuroQol). Questionnaire validation: participants' mean age was 68 years (N=261). Four factors were identified: 1) satisfaction about physical functionality (Crombach alpha=0.95), 2) satisfaction about sexual functionality (alpha=0.94), 3) satisfaction about social functionality (alpha=0.77), 4) satisfaction about urinary functionality (alpha=0.89); total Crombach alpha was 0.94. CONCLUSIONS: The BSP-PC questionnaire can be used as an instrument in the evaluation of HQoL in PC patients by principally considering their subjective satisfaction.

Activities of Daily Living↗

PubMed2005

Biochemical recurrence after definitive prostate cancer therapy. Part II: treatment strategies for biochemical recurrence of prostate cancer.

PURPOSE OF REVIEW: Through the prostate-specific antigen era, the proportion of men less than 55 years old with newly diagnosed prostate cancer more than doubled to almost 15%. As increasing numbers of men are living longer with prostate cancer, larger proportions will eventually present to our collective practices with rising prostate-specific antigen levels. Such prostate-specific antigen relapses, conservatively estimated to affect approximately 50 000 men each year, have become the most common form of advanced prostate cancer in the current period. RECENT FINDINGS: Increasing evidence suggests that early hormonal therapy improves progression-free survival and may alter the cancer-specific survival. However, there is a cost to pay in side-effects when androgen deprivation is administered over prolonged periods. The non-steroidal anti-androgen bicalutamide may offer an equivalent progression-free survival to castration without the complications of androgen deprivation. Observational data seem to indicate that high-risk individuals (i.e. those with high-grade, high-stage disease or a prostate-specific antigen doubling time less than 12 months) may also receive benefit from early therapy. SUMMARY: The definition of advanced prostate cancer has changed. Multimodal therapy improves cancer-specific outcomes especially in men with high-risk disease. The potential opportunities for novel therapeutic agents with low associated morbidity are great.

Androgen Antagonists↗

PubMed2005

Detection of prostate cancer: the impact of the European Randomized Study of Screening for Prostate Cancer (ERSPC).

The European Randomized Study of Screening for Prostate Cancer (ERSPC) is a large, randomized controlled trial of screening versus control, conducted in eight European countries (Belgium, Finland, France, Italy, the Netherlands, Spain, Sweden, and Switzerland). This article focuses on important aspects relating to recent findings from the ERSPC about two topics: first, leadtime and overdiagnosis, and second, prostate-specific antigen (PSA) as a test for repeated screening. The ERSPC together with the prostate cancer arm of the Prostate, Lung, Colon and Ovary (PLCO) screening trial of the National Cancer Institute in the United States are set to show or exclude an effect of screening on prostate cancer mortality. Both studies are progressing according to plan. Definitive endpoint-related data can be expected between 2005 and 2010 depending on the difference in prostate cancer mortality that may be shown between the screening and control arms. The ERSPC will allow a risk-to-benefit analysis including parameters of quality of life and cost. Overdiagnosis with present prostate cancer screening regimens is high. This amount of overdiagnosis is likely to be unacceptable for most healthcare policy makers and providers. Addressing overdiagnosis will be a major research task for urologists for the years to come. Present screening needs to be more "selective" for cases that have aggressive patterns and are likely to lead to clinical diagnosis of prostate cancer and/or death. The test characteristics of prostate-specific antigen (PSA) change after one use. The positive relation between PSA levels and positive predictive value (PPV) and detection rates in first screening rounds are lost. This may be compatible with the observation that tumor volumes in second round screening are smaller, and larger tumors are harvested. Tumor volume becomes a negative predictor in round 2, indicating that a large proportion of elevated PSA values are caused by benign prostatic hyperplasia (BPH) rather than by prostate cancer. While the outcome of the ongoing randomized studies is uncertain, screening tests cannot be refused to men who are well-informed and accept to take the risk of experiencing more harm than benefit as a result of a positive screening test result.

Age Distribution↗

PubMed1999

Prospective evaluation of prostate cancer detection by prostate-specific antigen-related parameters.

BACKGROUND: The diagnostic value of prostate-specific antigen (PSA) for differentiating prostate cancer from benign prostatic conditions is limited by its lack of specificity. Several PSA-related parameters have been suggested as enhancing the discriminatory power of total PSA values, but their clinical utility should be considered preliminary until established in a prospectively evaluated cohort. METHODS: In a prospective cohort study, results of ultrasound-guided biopsy and/or transurethral resection of the prostate gland were assessed in 706 consecutive Japanese men. The clinical usefulness of total PSA, free PSA, percentage of free PSA, PSA density (PSAD), PSA density for transition zone (PSADT) and gland volume for predicting prostate cancer was investigated using receiver operating characteristic (ROC) curve analysis in 16 different patient subgroups. RESULTS: Overall, 150 of the 706 patients (21.2%) had prostate carcinoma. The ROC curve analysis showed that PSAD and PSADT were more powerful predictors of prostate cancer than total PSA in most of the 16 patient subgroups tested. The improvement in performance was modest, however. No substantial difference was noted between PSAD and PSADT. Total gland volume did not significantly affect the performance of these parameters. The use of a PSAD threshold value of 0.11-10.15 ng/mL per cm3 (or a PSADT value of 0.23-0.27 ng/mL per cm3) would have avoided 24-48% (or, for PSADT, 34-40%) of unnecessary biopsies at the cost of missing 5-10% of detectable cancers in a patient subgroup with intermediate total PSA levels. The performance of free PSA and percentage of free PSA was worse than that of any other test in this study. This may be due to inappropriate handling of sera prior to measurement. CONCLUSIONS: The discriminatory potential of total PSA for predicting prostate cancer was modestly improved by the use of PSAD and PSADT. No substantial advantage of PSADT over PSAD could be demonstrated. Stringent and standardized storage conditions should always be maintained when applying free PSA-related parameters.

Aged↗

PubMed2000

The immunotherapy of prostate cancer.

Advanced prostate cancer remains incurable with standard treatment options. Immunotherapy may be a realistic alternative given the growing evidence that the immune response can affect the growth of other solid tumours and the regulation of both specific and shared prostate cancer antigens. Early studies suggest that both non-specific and specific vaccines can effect relevant animal models and clinical trials based on these observations are now in progress. A number of other approaches including gene therapy with HSVtk are already undergoing clinical studies (Herman et al. Hum Gene Ther 1999; 10: 1239-1249). Prostate Cancer and Prostatic Diseases (2000) 3, 303-307

Journal Article↗

PubMed2004

Intraosseous growth of human prostate cancer in implanted adult human bone: relationship of prostate cancer cells to osteoclasts in osteoblastic metastatic lesions.

BACKGROUND: More than 80% of patients with advanced prostate cancer have skeletal involvement, but the biology of bone metastasis is poorly understood. This study investigated the in vivo formation and progression of bone metastases under conditions that resembled the human bone environment as closely as possible. METHODS: Adult human bone fragments were implanted subcutaneously into 120 male NOD/SCID mice. Four weeks later, 1 x 10(7) LNCaP prostate cancer cells or phosphate-buffered saline were injected intravenously into 80 or 40 mice, respectively. The implanted bone fragments were removed from 20 to 10 mice in each group at 2, 4, 6, and 8 weeks after injection. RESULTS: LNCaP colonized the bone marrow blood vessels within 2 weeks, and then gradually expanded into the entire medullary cavity. An osteoblastic response often occurred at the edges of metastatic foci (intertrabecular bone metaplasia). In addition, new bone formation was observed adjacent to mature lamellar bone (appositional bone formation). These two processes appeared to occur through different mechanisms, but might similarly cause osteosclerosis. Osteoclasts showed a marked increase in numbers at sites of early tumor invasion, whereas few osteoclasts were observed at sites where tumor invasion was complete. CONCLUSIONS: The predominance of osteoblastic change with resorption may lead to bone remodeling in metastatic lesions, and osteoclasts may play an important role in bone metastasis from prostate cancer.

Animals↗

PubMed2003

Use of neoadjuvant and adjuvant therapy to prevent or delay recurrence of prostate cancer in patients undergoing radiation treatment for prostate cancer.

Multiple oncologic treatment modalities are often integrated into the curative treatment approach for the patient with a newly established diagnosis of cancer. The combination of neoadjuvant and adjuvant therapies with radiotherapy for the care of the patient with prostate cancer is no exception. There is clear evidence that neoadjuvant androgen suppression reduces the volume of tumor in preparation for radiotherapy, and it is an effective addition to conventional-dose external radiotherapy in patients with large-volume primary prostatic tumors. Adjuvant androgen suppression improves local and systemic tumor control and improves survival duration compared with radiotherapy alone for patients with locally advanced or node-positive prostate cancer, particularly in those with high-grade disease. The role of neoadjuvant and adjuvant therapies is under intense scrutiny as several randomized clinical trials seek to optimize the combination of androgen suppression, chemotherapy, and radiotherapy. The historical precedent for combining androgen suppression with radiotherapy is described, as are the results of prior definitive trials and ongoing studies in this setting.

Adenocarcinoma↗

PubMed2007

Global update on defining and treating high-risk localized prostate cancer with leuprorelin: a USA perspective--identifying men at diagnosis who are at high risk of prostate cancer death after surgery or radiation therapy.

Prostate-specific antigen doubling time (PSA-DT) after surgery or radiotherapy (RT) is known to be a predictive factor for death from prostate cancer (prostate cancer-specific mortality, PCSM). An analysis of two multi-institutional databases, including 8669 men with prostate cancer treated with surgery or RT, found that a PSA-DT of <3 months, and the specific value of the PSA-DT when > or = 3 months, appeared to be surrogate endpoints for PCSM after surgery or RT. While many PSA failures occur after local therapy for localized prostate cancer, few of these patients go on to die from their disease, so it is important to identify other factors associated with PCSM, so that the subgroup of high-risk patients can be identified. An analysis was undertaken to determine whether patients at risk of PCSM could be identified using information available at diagnosis. The results showed that risk factors for PCSM were a PSA velocity of >2.0 ng/mL/year, a Gleason score of 8-10 and an increasing PSA level. However, the most important risk factor that had an impact on both PCSM and all-cause mortality was a PSA velocity of >2.0 ng/mL/year. PSA kinetics are being increasingly used in the setting of rising PSA levels after radical prostatectomy or RT, and several studies showed that the rate of increase in PSA level at the time of recurrence is closely associated with time to cancer death. A PSA-DT of <3 months is associated with a poor prognosis, and represents 15-20% of PSA failures in the general population and 6-7% of PSA failures in a screened population, such as those included in clinical trials. Better risk-assessment models are needed to help to identify at an early stage men who are at high risk of prostate cancer death and those who are at low risk, so that each subgroup can receive the most appropriate therapy for their disease.

Aged↗

PubMed1999

Early results of radical prostatectomy and adjuvant endocrine therapy for prostate cancer with or without preoperative androgen deprivation. The Prostate Cancer Study Group.

BACKGROUND: The effects of preoperative androgen deprivation were explored in the patients who received radical prostatectomy and subsequent adjuvant endocrine therapy for prostate cancer. METHODS: Stage A2, B or C prostate cancers were randomized to one of two groups: (i) group I (n=90), who received androgen deprivation (leuploride and chlormadinone acetate) for 3 months preoperatively followed by radical prostatectomy and adjuvant endocrine therapy (leuploride only); and (ii) group II (n=86), who underwent the surgery followed by 3 month androgen deprivation and subsequent adjuvant endocrine therapy. The effects of preoperative androgen deprivation on clinical relapse (serum prostate specific antigen (PSA) > 1.98 ng/mL, local recurrence or distant metastasis) and PSA relapse (PSA >0.2ng/mL) were evaluated at 2 years after randomization. RESULTS: There was no significant difference in clinical or PSA relapse-free survival and quality of life measures between the two groups, although relapses occurred significantly more frequently in patients who had more advanced stages, higher pretreatment PSA values or lower histologic differentiation in either group. Subgroup analysis indicated that clinical relapse-free survival in stage C cancer tended to be better in patients with preoperative androgen deprivation than in those patients without it (P< 0.1). CONCLUSIONS: Preoperative androgen deprivation may be beneficial for stage C prostate cancer patients receiving radical prostatectomy and adjuvant endocrine therapy over the 2 year observation period. A longer follow up is needed to clarify the exact extent of benefit in terms of survival and quality of life.

Aged↗