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PubMed1997

Cancer immunotherapy for prostate cancer.

Our approach to prostate cancer immunotherapy involves two components dendritic cells as antigen-presenting cells; and the antigen used to target T-cell attack, HLA-A0201-associated peptides from prostate specific membrane antigen (PSMA). We have conducted a phase I dose-ranging study in 51 men with advanced prostate cancer, using dendritic cells pulsed with a PSMA peptide. no significant toxicity was observed. In that study, T-cell response was enhanced, with seven men meeting NCPC and PSA criteria for partial response. We are now conducting a phase II study with 67 men, who will receive 6 infusions of dendritic cells that have been pulsed with 2 PSMA peptides, at 6-week intervals. The phase II study design and rationale is described in this paper.

Journal Article↗

PubMed2005

Signal transduction in prostate cancer progression.

Prostate cancer is the most frequently diagnosed cancer among men and the second leading cause of male cancer deaths in the United States. When prostate cancer initially presents in the clinic, the tumour is dependent on androgen for growth and, therefore, responsive to the surgical or pharmacological ablation of circulating androgens. However, there is a high rate of treatment failure because the disease often recurs as androgen-independent metastases. Surprisingly, this late-stage androgen-independent prostate cancer almost always retains expression of the AR (androgen receptor), despite the near absence of circulating androgens. Although late-stage prostate cancer is androgen-independent, the AR still seems to play a role in cancer cell growth at this stage of disease. Therefore a key to understanding hormone-independent prostate cancer is to determine the mechanism(s) by which the AR can function even in the absence of physiological levels of circulating androgen. This review will focus on the role of growth factor signalling in prostate cancer progression to androgen independence and thus outline potential molecular areas of intervention to treat prostate cancer progression.

Disease Progression↗

PubMed1993

Elderly men with cancer: social work interventions in prostate cancer.

Prostate cancer requires the attention of social workers in health care for three reasons: the growing elderly population which will increase the number diagnosed, the recent introduction of new treatments and the lack of social acceptability for this condition. Interventions for prostate cancer are specific to the stage of the disease. These individual, family and group interventions are a model for social work services to elderly men with other forms of cancer. Social workers have opportunity to research quality of life and decision-making issues to enhance medical practise in prostate cancer.

Adaptation, Psychological↗

PubMed1988

Echograms of prostate cancer: inside echo patterns of localized prostate cancer.

Transrectal ultrasonography has been considered useful for the diagnosis of prostate cancer. There have been few reports on localized cancer in the prostate diagnosed by echogram. In this paper, we discuss echograms of the prostate in cases of localized cancer, advanced cancer and well-controlled cancer. Hypoechoic lesions seem to suggest prostate cancer.

Adenocarcinoma↗

PubMed1999

Osteomimetic properties of prostate cancer cells: a hypothesis supporting the predilection of prostate cancer metastasis and growth in the bone environment.

BACKGROUND: Unlike most other malignancies, prostate cancer metastasizes preferentially to the skeleton and elicits osteoblastic reactions. METHODS: We present a hypothesis, based upon results obtained from our laboratory and others, on the nature of progression of prostate cancer cells and their predilection to growth and metastasis in the bone microenvironment. We propose the hypothesis that osseous metastatic prostate cancer cells must be osteomimetic in order to metastasize, grow, and survive in the skeleton. The reciprocal interaction between prostate cancer and bone stromal growth factors, including basic fibroblast growth factor (bFGF), hepatocyte growth factor/scatter factor (HGF/SF), and especially the insulin growth factor (IGF) axis initiates bone tropism, and is enhanced by prostate secreted endothelin-1 (ET-1) and urokinase-type plasminogen activator (uPA). Growth factors and peptides that have differentiating activity, such as transforming growth factor beta (TGF-beta), parathyroid hormone-related protein (PTH-rp), and the bone morphogenetic proteins (BMPs), can shift local homeostasis to produce the characteristic blastic phenotype, via interaction with prostate-secreted human kalikrein 2 (hK2), and prostate-specific antigen (PSA). This proposal asserts that altering the expression of certain critical transcription factors, such as Cbfa and MSX in prostate cancer cells, which presumably are under the inductive influences of prostate or bone stromal cells, can confer profiles of gene expression, such as osteopontin (OPN), osteocalcin (OC), and bone sialoprotein (BSP), that mimic that of osteoblasts. RESULTS AND CONCLUSIONS: Elucidation of common proteins, presumably driven by the same promoters, expressed by both prostate cancer and bone stromal cells, could result in the development of novel preventive and therapeutic strategies for the treatment of prostate cancer skeletal metastasis. Agents developed using these strategies could have the potential advantage of interfering with growth and enhancing apoptosis in both prostate cancer and bone stromal compartments. The selective application of gene therapy strategy, driven by tissue-specific and tumor-restricted promoters for the safe delivery and expression of therapeutic genes in experimental models of prostate cancer metastasis, is discussed.

Bone Neoplasms↗

PubMed1998

A case of small cell lung cancer metastasizing to prostatic cancer.

Although the fact that the presence of two or more malignancies in a single patient is not a rare occurrence, metastasis of cancer to cancer is rare. Generally the most frequent donor tumor is a lung cancer, and the most common recipient tumor is a renal cell carcinoma. A rare case of lung cancer with metastasis to prostatic cancer is described. To our knowledge, this report represents the first case of a small cell lung cancer metastasizing to a prostatic cancer.

Adenocarcinoma↗

PubMed2005

[Preclinical models of prostate cancer].

Although prostate cancer is a major cause of cancer death and morbidity in Western countries, one major hindrance in the study of the biology of prostate cancer has been the limited number of laboratory models, compared with the number of models available for other neoplasms. For a long time, only three cell lines, namely LNCaP, PC3, and DU145, were routinely used to study prostate cancer in the lab. The success rate to establish cell lines from human prostate cancer tissues is low, in the 1% range. Currently, only about 10 prostate cancer cell lines are available, and many of them do not reproduce typical features of the human disease, like androgen receptor expression or prostate specific antigen (PSA) secretion. Spontaneous models in animals (including rat and dog) are practically not convenient for research purposes. Several in vivo models were artificially established by transforming prostate cells by potent oncogenes. Other models were developed by injecting prostate cancer cell lines into the prostate (orthotopic model), the vessel, or the bones of immuno-deficient mice, to mimic localized and metastatic prostate cancer. This was successfully done with the MDA PCa2b cell line. This cell line was also used to generate an in vitro model of bone metastases by a co-culture system with osteoblasts. This model allows to study the paracrine cross-talk between the two cell compartments and the resulting molecular modifications. The objective of the present article is to review the currently available model systems of prostate cancer.

Animals↗

PubMed2001

New serum tests for the diagnosis of prostate cancer.

Prostate-specific antigen (PSA) has had a profound impact on the early diagnosis, treatment and follow-up of prostate cancer, the most common malignancy in men. However, it is not only a marker for prostate cancer but is also often expressed in benign conditions such as benign prostatic hyperplasia, prostatitis and other inflammatory disorders. For early detection of prostate cancer, limitations of the use of PSA become obvious; its widespread use has led to extensive expensive and often unnecessary diagnostic procedures associated with significant morbidity. New serum tests derived from total PSA may play a key role in enhancing the accuracy of prostate cancer diagnosis. The ratio of free to total PSA improves specificity while maintaining a high sensitivity for prostate cancer detection for men with a total PSA of 2.5-10 ng/ml who also have a normal digital rectal examination. Human glandular kallikrein 2 also has the potential to be a valuable tool in combination with both total and free PSA for the early diagnosis of prostate cancer. However, the optimal clinical use of human glandular kallikrein 2 still remains to be clarified. Complex PSA seems to be a reliable tool and equivalent alternative to total PSA to improve specificity at high sensitivity levels in men with suspected prostate cancer, mainly for PSA levels below 4 ng/ml. Several newly discovered isoforms of free PSA (bPSA, [-2]pPSA and inactive intact PSA) may also impact the early detection of prostate cancer, with encouraging preliminary results that warrant further clinical investigation. (c) 2001 Prous Science. All rights reserved.

Journal Article↗

PubMed1987

Vasectomy and the risk of prostatic cancer and benign prostatic hypertrophy.

The incidence of prostatic disease (prostatic cancer and benign prostatic hypertrophy) was studied in a cohort of 5,332 vasectomized Kaiser Permanente Health Plan members, each matched with 3 nonvasectomized comparison subjects. Relative risks of 1.0 for prostatic cancer (68 cases, 95 per cent confidence limits 0.6 and 1.7) and 1.2 for benign prostatic hypertrophy (90 cases, 95 per cent confidence limits 0.7 and 1.8) were associated with vasectomy. In this study group the risk of prostatic disease was not altered by a history of vasectomy.

Adult↗

PubMed2002

A randomised comparison of bicalutamide ('Casodex') 150 mg versus placebo as immediate therapy either alone or as adjuvant to standard care for early non-metastatic prostate cancer. First report from the Scandinavian Prostatic Cancer Group Study No. 6.

OBJECTIVES: To assess the efficacy and tolerability of bicalutamide 150 mg ('Casodex'(1)) as immediate therapy, either alone or as adjuvant to treatment of curative intent, in patients with early (T1b-T4, any N, M0) prostate cancer. METHODS: This randomised, double-blind study was conducted in the Nordic countries as part of the 'Casodex' Early Prostate Cancer programme. Patients received bicalutamide 150 mg (n=607) or placebo (n=611) in addition to standard care. RESULTS: More than 80% of patients had not received therapy of primary curative intent. Median follow-up in both groups was 3 years. Median exposure to study treatment in the bicalutamide and standard care alone groups was 2.5 and 2.3 years, respectively. Bicalutamide reduced the risk of objective disease progression by 57% compared with standard care alone (HR 0.43; 95% CI 0.34, 0.55; p<<0.0001). Survival data were immature (11.4% deaths) with no difference between the two treatment groups. CONCLUSIONS: Bicalutamide 150 mg as immediate therapy, either alone or as adjuvant to treatment of curative intent, significantly reduces the risk of disease progression in patients with early prostate cancer. The trial is ongoing to assess whether the reduction in risk of objective progression translates into an overall survival benefit.

Aged↗

PubMed1995

Combination of screening and preoperative endocrine therapy: the potential for an important decrease in prostate cancer mortality.

Prostate cancer is the second cause of cancer death in men in the Western world; its medical and social impact is comparable to that of breast cancer in women. Although it is well recognized that early treatment is the only possibility for reducing the high rate of death from prostate cancer, screening and even early treatment are controversial issues due mainly to arguments based upon old literature and lack of awareness of the significant advances recently made in this field. As it is well known that surgical removal of organ-confined prostate cancer cures the disease, and it has been demonstrated that annual screening with prostate-specific antigen coupled with digital rectal examination followed, when indicated, by transrectal ultrasonography of the prostate more than doubles the proportion of organ-confined disease, screening alone offers the possibility of at least doubling the number of patients curable from prostate cancer or the potential for a cure to an estimated 45% of prostate cancer patients compared to a maximum of 20% in the absence of screening. It is important to mention that screening does not detect small and insignificant cancers, especially when random biopsies are not performed routinely. The critical volume of prostate cancer is estimated at 0.3 cm or a tumor 7.5 mm in diameter, if spherical. Such a tumor should increase serum prostate-specific antigen by 0.5 ng/mL. Contrary to the belief that screening detects cancers that are too small, the fact is that screening detects prostate cancer too late or nonorgan- or nonspecimen-confined cancer in 35-50% of cases. There is, thus, a narrow window when prostate cancer can be detected at a curable stage, and even the best available screening techniques cannot succeed in all cases. It should be mentioned that the recent improvements of the technique of radical prostatectomy have markedly improved the acceptability of surgery. Concerning the recent publicity related to watchful waiting, it is essential to indicate that all such reports support the notion that prostate cancer grows slowly, but steadily and irremediably, with increasing malignancy and risk of distant metastases and death if sufficient time is allowed. Another serious limitation of watchful waiting is that the available prognostic factors have a large margin of error and cannot predict with certainty the rate of progression of the tumor.(ABSTRACT TRUNCATED AT 400 WORDS)

Androgen Antagonists↗

PubMed2002

Bicalutamide as immediate therapy either alone or as adjuvant to standard care of patients with localized or locally advanced prostate cancer: first analysis of the early prostate cancer program.

PURPOSE: We determine the efficacy and tolerability of bicalutamide as immediate therapy, either alone or as adjuvant to treatment of curative intent, in patients with clinically localized or locally advanced prostate cancer. MATERIALS AND METHODS: This international program consists of 3 ongoing, randomized, double-blind, placebo controlled clinical trials (trials 23, 24, and 25). Men with localized or locally advanced (T1-T4, Nx/N0, M0) prostate cancer were randomized to receive 150 mg. bicalutamide daily or placebo, in addition to standard care with radical prostatectomy, radiotherapy or watchful waiting. Primary end points are time to objective progression and overall survival. In this first analysis data from the trials were combined in a single overview analysis according to protocol. RESULTS: Data are available for 8,113 patients (4,052 randomized to bicalutamide, 4,061 to standard care alone) at a median followup of 3.0 years. Treatment with bicalutamide provided a highly significant reduction of 42% in the risk of objective progression compared with standard care alone (9.0% versus 13.8%, hazards ratio 0.58; 95% confidence interval 0.51, 0.66; p <<0.0001). The overall result was reflected in 2 of the 3 trials (trials 24 and 25) with trial 3 (trial 23) showing a nonsignificant difference at this time. Reductions in the risk of disease progression were seen across the entire patient population, irrespective of primary treatment or disease stage. Overall survival data are currently immature and longer followup will determine if there is also a survival benefit with bicalutamide. The most frequently reported side effects of bicalutamide were gynecomastia and breast pain. CONCLUSIONS: Immediate treatment with 150 mg. bicalutamide daily, either alone or as adjuvant to treatment of curative intent, significantly reduces the risk of disease progression in patients with localized or locally advanced prostate cancer. This benefit must be balanced with the morbidity associated with long-term hormonal therapy. Followup is ongoing to determine potential survival benefits of this treatment approach.

Adult↗

PubMed1996

[Etiology of prostate cancer and significance of screening for early prostate cancer].

The incidence and mortality rate of prostate cancer in Japan are lower than in Western countries. Though studies of migrating populations would suggest that dietary or environmental factors may influence the etiology of the disease. The Westernized lifestyle after the Second World War may have influenced the increasing incidence of this disease in Japan. The screening by prostate specific antigen (PSA) on an asymptomatic healthy population can detect early prostate cancer. It is expected that the mortality may be decreased through such a system. However, some scientists hesitate to perform an aggressive program of early detection because of the possibility of latent cancer detection, the difficulty of distinguishing between clinically important and unimportant cancer, a high false positive rate to detect early stage cancer, and the lack of well-executed randomized prospective studies. Current clinical studies of the prostate cancer have demonstrated that the unimportant cancer detection rate by PSA was less than 10%. When a 4.0 ng/ml PSA cut-off value is applied for early detection, the false positive rate is approximately 80%. It is important to make subjects examined by the screening program aware of its the meaning. However, there is not a complete and cost-effective diagnostic modality to detect early prostate cancer. Moreover, it is confirmed that radical prostatectomy improves survival, but it has not been confirmed to improve the mortality based on population. We propose that well-executed randomized studies by the end point of the survival, cancer death rate, cost effective, QOL and etc. are urgently needed.

Adult↗

PubMed2000

Paradoxical stimulation of prolactin secretion by L-dopa in metastatic prostate cancer and its possible role in prostate-cancer-related hyperprolactinemia.

OBJECTIVE: In addition to sex steroids, prolactin (PRL) may also stimulate prostate cancer growth. Abnormally high blood levels of PRL have been noted in metastatic prostate cancer patients. However, most studies have been limited to the evaluation of basal levels of PRL rather than to investigate its secretion in response to classical endocrine dynamic tests. This study was carried out to analyze PRL secretion in metastatic prostate cancer patients both at basal conditions and in response to L-Dopa and metoclopramide, which represents the most classical inhibitory and stimulatory tests for PRL secretion, respectively. METHODS: The study included 12 patients with metastatic prostate cancer. On separate occasions, PRL secretion was evaluated in response to L-Dopa (500 mg orally) and to metoclopramide (10 mg i.v. as a bolus). Serum levels of PRL were measured by RIA. RESULTS: Mean PRL concentrations significantly increased after metoclopramide administration, even though no PRL response occurred in 6 of 12 patients. L-Dopa was unable to reduce PRL levels, which, in contrast, paradoxically significantly increased in response to L-Dopa, with mean values comparable to those achieved after metoclopramide injection. CONCLUSION: By showing a paradoxical stimulatory effect of L-Dopa on PRL secretion and a lack of response to metoclopramide in some patients, this study would suggest the existence of evident alterations in the neuroendocrine regulation of PRL release in advanced prostate cancer.

Aged↗

PubMed2005

Selective growth regulatory and pro-apoptotic effects of DIM is mediated by AKT and NF-kappaB pathways in prostate cancer cells.

Prostate cancer is the second leading cause of cancer related deaths in men in the United States. I3C and its in vivo dimeric product, DIM, have been found to inhibit the growth of prostate cancer cells. However, the molecular mechanism(s) by which DIM elicits its effects on prostate cancer cells has not been fully elucidated. We have previously shown that I3C induces apoptosis and inhibits the activation of NF-kappaB pathway, which could be mediated via Akt signaling pathway. In this study, we investigated whether there is any cross-talk between Akt and NF-kappaB during DIM-induced apoptosis in PC-3 prostate cancer cells. We found that DIM inhibited cell growth and induced apoptosis in PC-3 prostate cancer cells but not in non-tumorigenic CRL2221 human prostate epithelial cells. DIM also inhibited EGFR expression, PI3K kinase activity, and Akt activation, and abrogated the EGF-induced activation of PI3K in prostate cancer cells. NF-kappaB DNA-binding analysis and transfection studies with Akt cDNA constructs revealed that Akt transfection resulted in the induction of NF-kappaB activity and this was inhibited by DIM treatment. DIM treatment also showed significant induction of apoptosis in non-transfected cells compared to Akt and Akt-Myr transfected prostate cancer cells. From these results, we conclude that the inhibition of Akt and NF-kappaB activity and their cross-talk is a novel mechanism by which DIM inhibits cell growth and induces apoptotic processes in prostate cancer cells but not in non-tumorigenic prostate epithelial cells.

Apoptosis↗

PubMed2002

Contemporary trends in imaging test utilization for prostate cancer staging: data from the cancer of the prostate strategic urologic research endeavor.

PURPOSE: Previous investigators have reported widespread overuse of imaging tests for staging clinically localized prostate cancer. In this study imaging test utilization rates were analyzed in a contemporary group of patients, and clinical and demographic predictors of testing were identified. MATERIALS AND METHODS: Data were abstracted from the Cancer of the Prostate Strategic Urologic Research Endeavor (CaPSURE), a longitudinal registry of men with various stages of prostate cancer. A total of 4,966 men met study inclusion criteria of available treatment and staging data. The rates of computerized tomography, magnetic resonance imaging and bone scans performed between the dates of diagnosis and primary treatment were analyzed in patients at 3 levels of clinical risk based on serum prostate specific antigen, Gleason sum and T stage. Time trends in test utilization were analyzed by linear regression. Contemporary rates were compared with those identified in a previous analysis of an earlier CaPSURE cohort. Demographic and clinical predictors of utilization were identified using generalized linear model analysis. RESULTS: Since June 1997, the overall use of staging tests has decreased 63%, 25.9% and 11.4% in patients at low, intermediate and high risk, respectively. The most precipitous decrease was noted for bone scan but the use of cross-sectional imaging also decreased in all groups. Utilization rates were lower in 2001 than in any other year studied in CaPSURE. CONCLUSIONS: The rates of testing decreased significantly in all risk groups. However, in the absence of established clinical practice guidelines many patients at low and intermediate risk continue to undergo unnecessary testing, while a growing number of those at high risk are proceeding to treatment without previous imaging.

Aged↗

PubMed1998

[Prostate cancer screening using prostate specific antigen (PSA) in Tokatsu Hospital--examination of lost-to-followup cases].

We studied the usefulness of prostate cancer screening using prostate specific antigen (PSA) and PSA density (PSAD). In the first year of this screening (1995), we detected prostate cancer in 11 out of 550 (1.7%) subjects. Only 33 of the 47 (70%) subjects whose PSA values were greater than the cut-off value could be followed the following year. The remaining 14 subjects could not be followed mainly because of absence of urination difficulty at that time. The international prostate symptom score (I-PSS) sum and the quality of life (QOL) score at the screening in the unfollowed group were significantly lower than those in the followed group. The subjects who must be followed and whose QOL score and I-PSS sum are low at the time of screening need more careful and persuasive explanation from the urologist on the importance of long-term follow-up.

Age Factors↗

PubMed2006

DU145 human prostate cancer cells express functional receptor activator of NFkappaB: new insights in the prostate cancer bone metastasis process.

Prostate cancer metastases to bone are observed in around 80% of prostate cancer patients and represent the most critical complication of advanced prostate cancer, frequently resulting in significant morbidity and mortality. As the underlying mechanisms are not fully characterized, understanding the biological mechanisms that govern prostate cancer metastases to bone at the molecular level should lead to the determination of new potential therapeutic targets. Receptor activator of NFkappaB ligand (RANKL)/RANK/Osteoprotegerin (OPG) are the key regulators of bone metabolism both in normal and pathological condition, including prostate cancer bone metastases. In the present study, we demonstrated that human prostate cancer cell lines, DU145 and PC3 express biologically functional RANK. Indeed, soluble human RANKL (shRANKL, 100 ng/ml) treatment induced ERK 1/2, p38 and IkappaB phosphorylations in these cells. shRANKL administration also promoted DU145 and PC3 prostate cancer cell invasion in vitro. Whereas human OPG (hOPG) administration alone (100 ng/ml) had no marked effect, combined association of both agents abolished the RANKL-induced DU145 cell invasion. As RANKL had no direct effect on DU145 cell proliferation, the observed effects were indeed related to RANKL-induced cell migration. DU145 human prostate cancer cells promoted osteoclastogenesis of osteoclast precursors generated from mouse bone marrow. Moreover, DU145 cells produced soluble factor(s) that up-regulate the proliferation of MC3T3-E1 pre-osteoblasts through the activation of the ERK 1/2 and STAT3 signal transduction pathways. This stimulation of pre-osteoblast proliferation resulted in an increased local RANKL expression that can activate both osteoclasts/osteoclast precursors and prostate cancer cells, thus facilitating prostate cancer metastasis development in bone. We confirm that RANKL is a factor that facilitates metastasis to bone by acting as an activator of both osteoclasts and RANK-positive prostate cancer cells in our model. Furthermore, the present study provides the evidence that blocking RANKL-RANK interaction offer new therapeutic approach not only at the level of bone resorbing cells, but also by interfering with RANK-positive prostate cancer cells in the prostate cancer bone metastasis development.

3T3 Cells↗