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PubMed2004

Signal transducer and activator of transcription 3 (STAT3) activation in prostate cancer: Direct STAT3 inhibition induces apoptosis in prostate cancer lines.

Signal transducers and activators of transcription (STAT) were originally discovered as components of cytokine signal transduction pathways. Persistent activation of one STAT, STAT3, is a common feature of prostate cancer. Activated STAT3 was found in pathology specimens obtained from prostatectomy in the cancerous areas but not in the normal margins. Because the activation of STAT3 is mediated by the action of an upstream Janus kinase (JAK) kinase, usually JAK1 or JAK2, the activation step for STAT3 might itself be a target for therapy in prostate cancer. However, the redundancy of upstream kinases may make this strategy unreliable for therapy. To develop molecular targets for prostate cancer treatment, JAK kinase and STAT3 inhibition of two prostate cancer lines were compared. DU145 and NRP-154 cells were treated with JAK kinase inhibitors, analyzed for onset of apoptosis, and measured by annexin V binding and propidium iodide uptake. Activation of caspases in the cells was determined by measuring cleaved caspase-3 following treatment. For determining the effect on mitochondrial membrane depolarization that accompanies apoptosis, the fluorescent dye JC-1 was used. STAT3 was specifically inhibited by transfecting either a dominant-negative (DN) STAT3 plasmid or antisense STAT3 oligonucleotides into the cells. To look for reduction in STAT3 levels within cells, fixed and permeabilized prostate cancer cells were stained with antibody to STAT3. We found that more than one JAK kinase is involved in STAT3 activation in prostate cancer lines. AG490 (JAK2 specific) induced apoptosis in DU145 but not in NRP-154 prostate cancer lines, whereas piceatannol (JAK1 specific) induced apoptosis in NRP-154 but not in DU145 cells. Next, we demonstrated efficacy of specific STAT3 inhibitors in prostate cancer lines. Both induction of apoptosis and reduction in intracellular STAT3 protein were observed following treatment with antisense STAT3 oligonucleotides, while transfection of a DN-STAT3 plasmid into both prostate cancer cell lines resulted in loss of viability and onset of apoptosis. We conclude that STAT3-specific inhibitors, rather than JAK kinase-specific inhibitors, should be more useful therapeutically in treating androgen-resistant prostate cancer and that STAT3 is an appropriate target in the treatment of prostate cancer.

Animals↗

PubMed2000

Bacterial dna sequences in prostate tissue from patients with prostate cancer and chronic prostatitis.

PURPOSE: Although bacterial genetic material has been detected in prostate tissue from patients with various disorders, the prevalence of these organisms is unknown. We tested the hypothesis that bacterial detection rates differ between patients with prostate cancer and those with the chronic prostatitis/pelvic pain syndrome. MATERIALS AND METHODS: Sterile prostate biopsies were obtained during radical retropubic prostatectomy from 107 patients with prostate cancer and using a perineal approach from 170 with the chronic prostatitis/pelvic pain syndrome. Numerous controls were also evaluated. Bacterial ribosomal encoding DNA (165 rDNA) sequences were detected using a polymerase chain reaction assay. Selected positives were cloned, sequenced and compared with DNA databases. RESULTS: Bacterial DNA sequences were detected in 21 (19. 6%) of 107 patients with prostate cancer compared to 79 (46.4%) of 170 with chronic prostatitis (p <0.0001). These bacteria included urogenital pathogens, other described microorganisms and bacteria not reported previously. CONCLUSIONS: Bacterial DNA sequences may be identified in prostate tissue from many patients. Bacterial detection rates in prostate tissue appear to differ among populations, with higher rates among patients with the chronic prostatitis/pelvic pain syndrome than among those with prostate cancer. Future studies of the role of various bacteria in the prostate may provide insight into the pathophysiology of prostate disease.

Adolescent↗

PubMed2004

Differentiation of benign prostatic hyperplasia from prostate cancer using prostate specific antigen dynamic profile after transrectal prostate biopsy.

PURPOSE: Serum prostate specific antigen (PSA) level is increased after needle biopsy (Bx) of the prostate. This study tested the hypothesis that the prostate harboring malignant lesions demonstrates less leakage of PSA after prostate biopsy and this phenomenon can be helpful in discriminating benign from cancer diagnosis. MATERIALS AND METHODS: This prospective study was divided into 3 separate phases. Sextant prostate biopsy was done with transrectal ultrasound guidance, and the change and PSA values after biopsy were evaluated. Phases 1 and 2 had 20 and 41 patients, respectively. PSA dynamic profiles were plotted. We defined the most appropriate timing for blood sampling and the cutoff value of the PSA ratio (post-Bx total PSA-to-pre-Bx total PSA) to be applied for further assessment. Phase 3 recruited 97 cases, of which 66 satisfied the end point criteria in which a diagnosis such as malignancy, or 3 successive benign biopsies or benign transurethral resection of prostate was obtained. RESULTS: From phases 1 and 2 the cutoff value for the PSA ratio was 2.0, and the timing of blood sampling was 60 minutes after the biopsy. In phase 3 of those whose PSA ratio was less than 2.0, 92.6% (25) had cancer. For those whose PSA ratio was greater than 2.0, 82.1% (32) were benign. Of the 4 cases with a PSA ratio less than 2.0 and an initial benign biopsy, 3 (75%) were proven to have cancer later. CONCLUSIONS: Evaluating the 1-hour PSA ratio might be helpful for clinicians to select the high risk patients who might have cancer in the prostate. Repeat biopsy should be suggested for cases with a smaller PSA ratio in spite of initial benign results.

Aged↗

PubMed1984

Glycosaminoglycans of human prostatic cancer.

The glycosaminoglycans of normal, benign hyperplastic and cancerous prostate were studied. In both prostatic hyperplasia and cancer the chondroitin sulfate:dermatan sulfate ratio was increased. In prostatic cancer this increase correlated with both the differentiation and extent of cancer in the prostate. The percentages heparan sulfate and heparan sulfate sulfation were decreased in prostatic cancer. Hyaluronic acid increased with dedifferentiation of the cancer. Histochemically, sulfated glycosaminoglycans were concentrated in the prostatic stroma at the stromal-epithelial interface. The increased chondroitin sulfate:dermatan sulfate ratio may be a nonspecific response or requirement for epithelial growth.

Adult↗

PubMed1999

The combination of human glandular kallikrein and free prostate-specific antigen (PSA) enhances discrimination between prostate cancer and benign prostatic hyperplasia in patients with moderately increased total PSA.

BACKGROUND: Prostate-specific antigen (PSA) is the most reliable tumor marker available and is widely used for the diagnosis and management of prostate cancer. Unfortunately, PSA cannot distinguish efficiently between benign and malignant disease of the prostate, especially within the range of 4-10 microg/L. Among the refinements developed to enhance PSA specificity is the free/total PSA ratio, which is useful in discriminating between the two diseases within the diagnostic "gray zone". Recent data indicate that human glandular kallikrein (hK2), a protein with high homology to PSA, may be an additional serum marker for the diagnosis and monitoring of prostate cancer. METHODS: We analyzed 206 serum samples (all before treatment was initiated) from men with histologically confirmed benign prostatic hyperplasia (n = 100) or prostatic carcinoma (n = 106) with total PSA in the range of 2.5-10 microg/L. Total and free PSA and hK2 were measured with noncompetitive immunological procedures. Statistical analysis was performed to investigate the potential utility of the various markers or their combinations in discriminating between benign prostatic hyperplasia and prostatic carcinoma. RESULTS: hK2 concentrations were not statistically different between the two groups of patients. There was a strong positive correlation between hK2 and free PSA in the whole patient population. hK2/free PSA ratio (area under the curve = 0.69) was stronger predictor of prostate cancer than the free/total PSA ratio (area under the curve = 0.64). At 95% specificity, the hK2/free PSA ratio identified 30% of patients with total PSA between 2.5-10 microg/L who had cancer. At 95% specificity, the hK2/free PSA ratio identified 25% of patients with total PSA between 2.5 and 4.5 microg/L who had cancer. CONCLUSIONS: Our data suggest that hK2 in combination with free and total PSA can enhance the biochemical detection of prostate cancer in patients with moderately increased total PSA concentrations. More specifically, the hK2/free PSA ratio appears to be valuable in identifying a subset of patients with total PSA between 2.5 and 4.5 microg/L who have high probability of cancer and who should be considered for biopsy.

Aged↗

PubMed2005

Spiculated periosteal response induced by intraosseous injection of 22Rv1 prostate cancer cells resembles subset of bone metastases in prostate cancer patients.

BACKGROUND: Prostate cancer bone metastasis is distinguished by the predominance of osteoblastic lesions. This phenotype has been difficult to reproduce in animal models. Here, we describe a model utilizing the 22Rv1 human prostate cancer cell line that generates osteolytic lesions and a prominent spiculated periosteal osteoblastic response following intraosseous injection in scid mice. METHODS: We injected 22Rv1-luciferase prostate cancer cells directly into the tibiae of C.B-17 scid mice. We analyzed tumor growth and pathology every 2 weeks using radiographic and histologic techniques. RESULTS: X-ray analysis revealed that 22Rv1 tumors elicit a mixed-type lesion including some osteolysis and a robust induction of periosteal bone formation, in contrast to PC3M-luciferase intraosseous tumors which induce only extensive osteolysis. Micro-computerized tomographic imaging shows that 22Rv1 tumors exhibit both osteolytic and osteoblastic features which become apparent between 4 and 6 weeks post injection. There is initial disruption of the cortex and corresponding invasion of the periosteum which is associated with a vigorous osteoblastic response. Histological analysis of late stage tumors shows that the tumor has grown outside of the medullary cavity and surrounds the tibia underneath the periosteum and intermixed with spicules of woven bone which is detected in the radiographic analysis. CONCLUSIONS: The overall pattern of this model is suggestive of clinical cases of prostate cancer metastasis in which periosteal responses are noted, often in association with rapidly progressive disease. We expect that intraosseous injection of 22Rv1 cells will provide a new experimental model for the study of osteoblastic prostate cancer metastasis.

Animals↗

PubMed1998

Transforming growth factor-beta1 serum concentration in patients with prostatic cancer and benign prostatic hyperplasia.

OBJECTIVE: To assess serum levels of transforming growth factor-beta1 (TGF-beta1), normally markedly elevated in prostate cancer tissue, in patients with cancer of the prostate, and to correlate these levels with tumour stage and serum prostate specific antigen (PSA) levels. PATIENTS AND METHODS: Serum TFG-beta1 and PSA levels were determined in 32 patients with untreated prostate cancer. Patients were divided into: group 1, 14 patients with pT1-3pN0M0; group 2, four with T1-3pN+M0); and group 3, 14 with T1-4NxM+. Ten patients with histologically confirmed benign prostatic hyperplasia (BPH) served as controls. RESULTS: The median TGF-beta1 levels were no different between patients with cancer or BPH (30.7 ng/mL and 26.9 ng/mL, respectively; P > 0.05). Furthermore, there was no increase in TGF-beta1 concentrations with advancing tumour stage (group 1, 34.1 ng/mL; group 2, 33.0 ng/mL; group 3, 28.3 ng/mL; P > 0.05). There was no correlation with PSA levels (group 1, r= -0.42: group 2, r= -0.43; group 3, r= -0.23; BPH, r=0.38). CONCLUSION: TGF-beta1 levels did not discriminate between patients with BPH and prostate cancer, and there was no increase in TGF-beta1 levels with advancing tumour stage.

Aged↗

PubMed1994

Chemo-endocrine therapy for prostate cancer with bone metastasis. Nagasaki Prostate Cancer Research Group.

We analyzed the clinical effects of initial chemoendocrine therapy on 31 prostate cancer patients with bone metastasis. These patients had been newly diagnosed between 1983 and 1991 and had received no previous therapy. As endocrine therapy, the patients received 1 mg ethynylestradiol daily with or without orchiectomy. In addition, they received three courses of chemotherapy consisting of 20 mg/m2 cisplatin given on days 1, 3, and 5 and 20 mg/m2 Adriamycin or 40 mg/m2 epirubicin given on day 5. Subsequently, for maintenance therapy, the patients received 1 mg ethynylestradiol and 150 mg 5-fluorouracil [or 300 mg tegafur plus uracil (UFT)] daily. Patients given our regimen of chemoendocrine therapy had a significantly better prognosis than did the controls treated with endocrine therapy alone (P = 0.05), although treatment was not randomized. The cause-specific survival rates at 5 years for the chemoendocrine-therapy patients and the control group were 65.4% and 37.4%, respectively. A multivariate analysis of possible prognostic factors, i.e., age, histological grade, prostatic acid phosphatase, tumor-related pain, the extent of disease (EOD) on bone scan, and the type of initial treatment, confirmed that the initial treatment (P = 0.03) and the EOD grade (P = 0.05) had a significant effect on survival. On the basis of these results, it is necessary to carry out a randomized trial to compare our chemoendocrine regimen with endocrine therapy alone in untreated patients with advanced prostate cancer.

Aged↗

PubMed2005

Obesity and the risk of prostate cancer.

BACKGROUND: Prostate cancer and obesity are common diseases among men in the United States. A link between obesity and prostate cancer risk has potential implications in understanding prostate cancer genesis and screening strategies. METHODS: We conducted a population-based case-control study examining the relationship between body mass index (BMI) and prostate cancer risk. Incident cases of prostate cancer were identified in King County, Washington, using the Surveillance, Epidemiology, and End Results (SEER) cancer registry. Interviews were completed with 753 men ages 40-64 that were diagnosed with prostate cancer between 1993 and 1996. Interviews were also completed with 703 age-matched controls identified from the same population through random digit dialing. Logistic regression was performed to generate odds ratios and 95% confidence intervals while controlling for age, race, education, smoking, family history, prostate cancer screening, dietary fat, and caloric intake. RESULTS: BMI was inversely related to prostate cancer risk (P for trend=0.04). Men with a BMI > 29 kg/m2 had the lowest risk of prostate cancer (odds ratio=0.77; 95% confidence interval=0.56, 1.06). Weight was also inversely associated with prostate cancer risk (P for trend=0.03), however, height was not. CONCLUSIONS: The results of this study support the hypothesis that obesity is inversely associated with prostate cancer risk in middle-aged men.

Adult↗

PubMed2003

Quality of life after a diagnosis of prostate cancer among men of lower socioeconomic status: results from the Veterans Affairs Cancer of the Prostate Outcomes Study.

OBJECTIVES: To evaluate prospectively the health-related and disease-specific quality of life (QOL) at diagnosis and during the first year thereafter for patients with newly diagnosed prostate cancer who received care at Veterans Affairs Medical Centers. METHODS: Interviewers administered the European Organization for Research and Treatment of Cancer-QOL Questionnaire, a valid and reliable measure of health status, to 140 patients with prostate cancer at baseline (at diagnosis, before the initiation of treatment) and at 3 and 12 months thereafter at five Veterans Affairs Medical Centers. The mean changes from baseline values were analyzed statistically for patients with localized disease stratified by treatment group and separately for patients with metastatic disease. RESULTS: Among the 98 men with localized prostate cancer, significant disease-specific QOL changes noted at 3 and 12 months included worsening of urinary and sexual function among men treated with radical prostatectomy or radiotherapy and worsening of urinary function among those who opted for watchful waiting (each P <0.05). Among the 42 men with metastatic prostate cancer, significant decrements in role and social and sexual function were noted at 3 months, but had resolved on average by 12 months of follow-up. CONCLUSIONS: At 12 months, disease-specific QOL decrements persisted for patients with localized disease, but for patients with metastatic disease, disease-specific QOL appeared to return to near baseline (at diagnosis, before treatment initiation) function. Our study, among the first to assess the QOL at baseline before treatment, provides meaningful information on general treatment effects, which are directly relevant to clinicians when discussing treatment options with patients.

Aged↗

PubMed2003

[Management of bladder cancer associated with prostate cancer].

The treatment decision in patients with simultaneous development of bladder cancer and prostate cancer is based on the prognostic factors of the two tumours, the life expectancy, and the complications of treatment influencing patient follow-up. This review of the literature tends to confirm a higher incidence of prostate cancer in patients with bladder cancer. The diagnostic and treatment options are proposed for each situation, but evidence-based recommendations cannot be proposed on the basis of the published data.

Humans↗

PubMed2000

Use of artificial neural networks in the clinical staging of prostate cancer: implications for prostate brachytherapy.

PURPOSE: This review describes two studies to evaluate artificial neural networks (ANNs) in prostate cancer staging. In the first study, an ANN was trained to identify prostate cancer patients at low risk of lymph node spread (LNS). The second study evaluated an ANN to predict capsular penetration (CP) in men with clinically localized prostate cancer. An accurate assessment of lymph node status will help identify those brachytherapy patients in whom lymphadenectomy can be avoided. The accurate prediction of CP can help determine the appropriateness of brachytherapy as a treatment option. MATERIALS AND METHODS: An ANN to predict LNS was trained and tested using a database from one institution (n = 4,133) and validated using two databases (n = 330 and n = 227) from different institutions. The clinical variables used were clinical stage (cTNM), Gleason sum, and prostate-specific antigen concentration (PSA). The ANN to predict CP was trained and validated with data from a single institution (n = 409). The variables used were age, race, PSA, PSA velocity, Gleason sum, and cTNM. RESULTS: The LNS ANN was able classify 76%, 75%, and 30% of the patients in each database as being at low risk of LNS with 98% accuracy. The CP ANN correctly identified CP in 25 (84%) of patients and produced 5 (16%) false-negative predictions. CONCLUSIONS: These preliminary results suggest that ANNs can be useful in staging prostate cancer. If sufficiently accurate ANNs can be developed and tested, they have the potential to increase the accuracy of clinical staging and thus improve treatment decisions.

Biopsy↗

PubMed1997

Target to apoptosis: a hopeful weapon for prostate cancer.

BACKGROUND: Prostate cancer is the most commonly diagnosed neoplasm and the second leading cause of male death in this country. Multiple genetic and epigenetic factors have been implicated in the oncogenesis and progression of prostate cancer. However, the molecular mechanisms underlying the disease remain largely unknown. The major difficulty in the clinical management of prostate cancer stems from the reality that reliable and accurate diagnostic/prognostic biomarkers are not available and that effective treatment regimens for hormone-resistant prostate cancers are yet to be developed. METHODS: The present review, through extensive literature research, summarizes the most recently accumulated experimental and clinical data on the relationship between apoptosis and prostate cancer. We analyze the possibility of inducing prostate cancer cell apoptosis by: 1) androgen ablation by castration or biochemical antagonists: 2) chemotherapeutic drugs or natural/synthetic chemicals; 3) manipulation of apoptosis-related oncoproteins; and 4) modulation of intracellular signal transducers. RESULTS: 1) Prostate cancer, like most other solid tumors, represents a very heterogeneous entity. Most prostate cancers, at the time of clinical diagnosis, present themselves as mixtures of androgen-dependent and androgen-independent cells. 2) Most prostate cancers respond initially to androgen ablation since the population of androgen-dependent cells undergoes rapid apoptosis upon androgen withdrawal. However, androgen ablation rarely cures patients, most of whom will experience recurrence due to takeover of the tumor mass by androgen-independent tumor cells as well as the emergence of apoptosis-resistant clones as a result of further genetic alterations such as bcl-2 amplification. 3) On the other hand, although androgen-independent prostate cancer cells do not undergo apoptosis upon androgen blocking, they do maintain the appropriate molecular machinery of apoptosis. Therefore, certain conventional chemotherapy drugs can eliminate androgen-independent cancer cells by inducing apoptosis. 4) However, most drugs used in chemotherapy induce apoptosis or mediate cytotoxicity only in proliferating cancer cells. Human prostate cancer cells demonstrate very slow growth kinetics. Thus, novel chemical/natural products need be identified to eradicate those nonproliferating cancer cells. In this regard, the angiogenesis inhibitor, linomide, and a plant extract, beta-lapachone, demonstrate very promising apoptosis-inducing effects on prostate cancer cells in a proliferation-independent manner. 5) An alternative way to modulate the apoptotic response is by interfering with the expression levels of essential regulatory molecule of apoptosis. Bcl-2 and p53 represent two prime targets for such manipulations. 6) Finally, modulation of signal transduction pathways (e.g., intracellular Ca2+ levels, PKC activity) involved in apoptosis may also induce and/or enhance the apoptotic response of prostate cancer cells. CONCLUSIONS: Modulation of apoptotic response represents a novel mechanism-based approach which may help identify novel drugs and/or develop new therapeutic regimens for the treatment of prostate cancers.

Androgens↗

PubMed2003

Second primary cancers in men with prostate cancer: an increased risk of male breast cancer.

PURPOSE: Evaluation of second primary cancers provides valuable insight about etiology and shared risk factors. Studies of second primary cancers following prostate cancer conclude that overall risk of second primary cancers decreases. However, risk of bladder cancer and kidney cancer increases. We examine the risk of common and rare second primary cancers following prostate cancer in a large population based cohort to identify possible common etiological factors. MATERIALS AND METHODS: All prostate cancer cases in the Swedish Cancer Registry (135, 713) from 1958 to the end of 1996 constituted the study base. Risk (standardized incidence ratio) of second primary cancers was calculated as the ratio between observed and expected number of cancers. We used 2-tailed 95% confidence intervals (CI) to test significance. RESULTS: An overall increased risk (standardized incidence ratio 1.17, 95% CI 1.15-1.19) of second primary cancers was found but was only seen in the first 6 months of followup (ratio 3.45, 3.32-3.57). The most interesting finding was an increased risk (ratio 2.01, 95% CI 1.44-2.74) of male breast cancer. Other tumor sites with increased risk were the small intestine (standardized incidence ratio 1.39, 95% CI 1.09-1.51), skin melanoma (ratio 1.33, 95% CI 1.16-1.51) and endocrine tumors (ratio 1.41, 95% CI 1.13-1.74). CONCLUSIONS: A small but increased risk of second primary cancers following prostate cancer was found, most likely due to increased surveillance during the first 6 months after diagnosis. However, following prostate cancer there is an increased risk of endocrine related second primary cancers such as male breast cancer and carcinoids in the small intestine. To our knowledge these associations have not been reported previously, and they warrant more study.

Adenocarcinoma↗

PubMed1995

Extent of disease based on initial bone scan: important prognostic predictor for patients with metastatic prostatic cancer. Experience from the Scandinavian Prostatic Cancer Group Study No. 2 (SPCG-2).

The skeleton is the most frequent site of metastases from prostate cancer. Quantitation of the amount of tumor burden has a great prognostic value and is of importance for clinical trials. The present study reviews 194 bone scans from the SPCG-2 study which consisted of 294 patients entered into a randomized prospective multicenter trial, comparing total androgen suppression with standard treatment in patients with metastatic prostatic cancer (orchiectomy plus cyproterone acetate vs. orchiectomy plus placebo). Evaluation of the initial bone scans based on the extension of the disease (EOD) as proposed by Soloway and associates gives a convenient stratification of the patients. With regard to time to progression and cancer-related as well as overall survival, this EOD grading system had a significant prognostic value (p < 0.001). There was no statistical difference between the two treatment arms in the different categories of the EOD grading system with regard to time to progression and time to death. By analyzing exclusively the subgroup of patients with minimal disease (EOD I) and good performance status (WHO score 0), there was a nonsignificant trend toward a better 2-year progression-free survival as well as a better 2-year cancer-related survival for those who were subjected to total androgen suppression as compared with the patients subjected to the standard treatment (orchiectomy).

Androgen Antagonists↗

PubMed2002

Prospective evaluation of prostate cancer detection by prostate specific antigen related parameters: comparison in serum and plasma samples.

PURPOSE: We compared the usefulness of serum and plasma samples for enhancing the specificity of prostate cancer detection. MATERIALS AND METHODS: We analyzed receiver operating characteristics curves to evaluate prospectively the cancer detection performance of prostate specific antigen (PSA) related parameters derived from serum and plasma samples in 248 and 249 consecutive patients, respectively. RESULTS: Receiver operating characteristics curve analysis showed that PSA density and transition zone PSA density were more powerful predictors of prostate cancer than total or free PSA in the group overall at intermediate serum PSA 2.1 to 10 ng./ml. and in the subgroup with total PSA 4.1 to 10 ng./ml. regardless of digital rectal examination findings. Percent free PSA performed significantly better than total PSA in patients with serum total PSA 4.1 to 10 ng./ml. PSA density, transition zone PSA density and percent free PSA did not differ substantially in patients with serum total PSA 4.1 to 10 ng./ml. However, none of these parameters distinguished patients with prostate cancer from those with benign histology when PSA was in the lower range of 2.1 to 4 ng./ml. The performance of these parameters was worse when plasma sample data were used for calculation. CONCLUSIONS: The performance of percent free PSA appears at least comparable to that of PSA density and transition zone PSA density in patients in this cohort with serum total PSA 4.1 to 10 ng./ml. without regard to digital rectal examination. The poor performance of these parameters in the lower PSA range underscores the need for other parameters to improve the specificity of cancer detection in elderly Japanese males. Continued use of serum samples is justified for measuring PSA related parameters by current assay techniques.

Biomarkers, Tumor↗

PubMed1997

Antiproliferative effects of c-myc antisense oligonucleotide in prostate cancer cells: a novel therapy in prostate cancer.

OBJECTIVES: To explore the possibility of using antisense oligonucleotide therapy for prostate cancer, we investigated the effect of c-myc-antisense-oligonucleotide (c-myc-As-ODN) in human prostate cancer cell lines such as LNCaP, PC3, and DU145. METHODS: LNCaP, PC3, and DU145 cells were incubated in the presence of c-myc-As-ODN. Dose (0 to 10 microM) and time dependent (1 to 6 days) effects on proliferation and viability were examined by [3H]thymidine incorporation and MTT assay, respectively. Flow cytometry analysis was carried out to analyze cell cycle status by determining the DNA content in LNCaP cells. Control cultures received either c-myc-sense-ODN or scrambled (nonsense) nucleotides. RESULTS: Time- and dose-dependent decreases in DNA synthesis and cell viability were noted for all three prostate cancer cell lines after c-myc-As-ODN treatment. Further studies using LNCaP cells indicated that these changes were accompanied by an increase in the percentage of cells with less than 2N DNA content after c-myc-As-ODN treatment. The results suggest that c-myc-As-ODN induces cell death. Comparison of a c-myc-As-ODN-treated group with a group subjected to isoleucine deprivation revealed that thymidine incorporation was almost the same in c-myc-As-ODN-treated LNCaP cells and in LNCaP cells at early S phase. CONCLUSIONS: These results suggest that c-myc-As-ODN inhibits prostate cancer cell growth and proliferation mainly by decreasing cell viability.

Analysis of Variance↗

PubMed2004

The contemporary management of prostate cancer in the United States: lessons from the cancer of the prostate strategic urologic research endeavor (CapSURE), a national disease registry.

PURPOSE: The epidemiology and treatment of prostate cancer have changed dramatically in the prostate specific antigen era. A large disease registry facilitates the longitudinal observation of trends in disease presentation, management and outcomes. MATERIALS AND METHODS: The Cancer of the Prostate Strategic Urologic Research Endeavor (CaPSURE) is a national disease registry of more than 10000 men with prostate cancer accrued at 31 primarily community based sites across the United States. Demographic, clinical, quality of life and resource use variables are collected on each patient. We reviewed key findings from the data base in the last 8 years in the areas of disease management trends, and oncological and quality of life outcomes. RESULTS: Prostate cancer is increasingly diagnosed with low risk clinical characteristics. With time patients have become less likely to receive pretreatment imaging tests, less likely to pursue watchful waiting and more likely to receive brachytherapy or hormonal therapy. Relatively few patients treated with radical prostatectomy in the database are under graded or under staged before surgery, whereas the surgical margin rate is comparable to that in academic series. CaPSURE data confirm the usefulness of percent positive biopsies in risk assessment and they have further been used to validate multiple preoperative nomograms. CaPSURE results strongly affirm the necessity of patient reported quality of life assessment. Multiple studies have compared the quality of life impact of various treatment options, particularly in terms of urinary and sexual function, and bother. CONCLUSIONS: The presentation and management of prostate cancer have changed substantially in the last decade. CaPSURE will continue to track these trends as well as oncological and quality of life outcomes, and will continue to be an invaluable resource for the study of prostate cancer at the national level.

Biomedical Research↗