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At least 865 records · Page 48Linked to original sources

PubMed2005

Ghrelin and a novel preproghrelin isoform are highly expressed in prostate cancer and ghrelin activates mitogen-activated protein kinase in prostate cancer.

PURPOSE: There is evidence that the hormone ghrelin stimulates proliferation in the PC3 prostate cancer cell line although the underlying mechanism(s) remain to be determined. A novel, exon 3-deleted preproghrelin isoform has previously been detected in breast and prostate cancer cells; however, its characterization, expression, and potential function in prostate cancer tissues are unknown. EXPERIMENTAL DESIGN: Expression of ghrelin and exon 3-deleted preproghrelin was investigated in prostate cancer cell lines and tissues by reverse transcription-PCR and immunohistochemistry. Proliferation and apoptosis assays were done in the LNCaP prostate cancer cell line to determine if ghrelin stimulates proliferation and/or cell survival. Stimulation of mitogen-activated protein kinase (MAPK) pathway activation by ghrelin was determined in PC3 and LNCaP cells by immunoblotting with antibodies specific for phosphorylated MAPKs. RESULTS: Prostate cancer tissues display greater immunoreactivity for ghrelin and exon 3-deleted preproghrelin than normal prostate tissues, and prostate cancer cell lines secrete mature ghrelin into conditioned medium. Treatment with ghrelin (10 nmol/L), but not the unique COOH-terminal peptide derived from exon 3-deleted preproghrelin, stimulates proliferation in the LNCaP cells (45.0 +/- 1.7% above control, P < 0.01) and rapidly activates the extracellular signal-regulated kinase-1/2 MAPK pathway in both PC3 and LNCaP cell lines. Ghrelin, however, does not protect prostate cancer cells from apoptosis induced by actinomycin D (1 microg/mL). The MAPK inhibitors PD98059 and U0126 blocked ghrelin-induced MAPK activation, as well as proliferation, in both cell lines. CONCLUSIONS: These data suggest that these components of the ghrelin axis may have potential as novel biomarkers and/or adjunctive therapeutic targets for prostate cancer.

Apoptosis↗

PubMed2003

Psychosocial and educational aspects in prostate cancer patients.

Prostate cancer was a neglected area in psycho-oncology. There is now a growing number of studies on the psychosocial aspects of having prostate cancer and the possibilities to reduce these problems in educational and group interventions. In this issue of Patient Education and Counseling, studies are presented on several psychosocial and educational aspects in prostate cancer patients: screening events and outcomes, assessing the unmet information, support and care delivery needs, reacting to the diagnosis of prostate cancer, informational needs of men on hormonal therapy, changes in health-related quality of life three months after the diagnosis, information-seeking behaviors and information needs of partners, quality of leaflets, video information in decision making, and patient perceptions and priorities in a rehabilitation program. Conclusions are presented on neglected research areas in psychosocial and educational aspects of living with prostate cancer.

Hormone Replacement Therapy↗

PubMed2006

Obesity, adipokines, and prostate cancer (review).

Prostate cancer, the third most common cancer in men worldwide, varies substantially according to geographic region and race/ethnicity. Obesity and associated endocrine variation are foremost among the risk factors that may underlie these regional and ethnic differences. The association between obesity and prostate cancer incidence is complex and has yielded inconsistent results. Studies that have linked obesity with prostate cancer mortality, advanced stage disease, and higher grade Gleason score, however, have produced more consistent findings, indicating that obesity may not necessarily increase the risk of prostate cancer, but may promote it once established. Additionally, metabolic syndrome, which includes disturbed glucose metabolism and insulin bioactivity, may also be associated with prostate carcinogenesis. Adipokines, defined as biologically active polypeptides produced by adipose tissue, have been linked with a number of carcinogenic mechanisms, including angiogenesis, cell proliferation, metastasis, and alterations in sex-steroid hormone levels. A number of emerging studies have implicated the role of adipokines in prostate carcinogenesis. This review explores the specific roles of several adipokines as putative mediating factors between obesity and prostate cancer with particular attention to leptin, interleukin-6 (IL-6), heparin-binding epidermal growth factor-like growth factor (HB-EGF), vascular endothelial growth factor (VEGF) and adiponectin.

Adipose Tissue↗

PubMed2006

Identifying men diagnosed with clinically localized prostate cancer who are at high risk for death from prostate cancer.

PURPOSE: We identified factors at diagnosis that are significantly associated with time to prostate cancer specific mortality following radical prostatectomy or external beam radiation therapy. MATERIALS AND METHODS: The study cohort included 1,453 men treated with radical prostatectomy (1,095) or external beam radiation therapy (358) for localized prostate cancer between 1989 and 2002. Cox regression multivariate analysis was used to evaluate whether prostate specific antigen, prostate specific antigen velocity, biopsy Gleason score and clinical tumor category at diagnosis were significantly associated with time to prostate cancer specific mortality following radical prostatectomy or external beam radiation therapy. RESULTS: In addition to increasing prostate specific antigen (p < or =0.04) and biopsy Gleason score 8 to 10 disease (p < or =0.02), prostate specific antigen velocity more than 2 ng/ml yearly was significantly associated with shorter time to prostate cancer specific mortality in patients treated with radical prostatectomy (adjusted HR 12, 95% CI 3 to 54) and external beam radiation therapy (adjusted HR 12, 95% CI 3 to 54) compared with that in men with prostate specific antigen velocity 2 ng/ml yearly or less (p < or =0.001). Despite low risk disease 7-year estimates of prostate cancer specific mortality were 5% to 19% in patients in whom prostate specific antigen increased by more than 2 ng/ml during the year before diagnosis compared with less than 1% in those with a prostate specific antigen increase of 2 ng/ml or less. CONCLUSIONS: Despite prostate specific antigen level less than 10 ng/ml and Gleason score 6 cancer a prostate specific antigen increase of more than 2 ng/ml during the year before diagnosis places a man at high risk for prostate cancer death following radical prostatectomy or external beam radiation therapy.

Aged↗

PubMed2004

Inverse association between nonsteroidal anti-inflammatory drugs and prostate cancer.

BACKGROUND: Prostate cancer is considered a major health problem in western countries. Promising results from observational studies on cancer at other sites fuelled the publication of several studies assessing the association between nonsteroidal anti-inflammatory drug (NSAID) use and prostate cancer. However, these studies show conflicting results. METHODS: We conducted a cohort study with a nested case-control analysis to further study the association between NSAIDs and prostate cancer. We used data from the General Practice Research Database in United Kingdom. RESULTS: Aspirin use was associated with a reduced risk of prostate cancer [odds ratio (OR) = 0.70, 95% confidence interval (95% CI) = 0.61-0.79]. We also found that paracetamol use with a treatment duration longer than 1 year was associated with a decreased risk (OR = 0.65, 95% CI = 0.54-0.78). Non-aspirin-NSAID (NA-NSAID) and paracetamol short-term use was associated with a small increased risk whereas long-term users of NA-NSAIDs presented an OR of 0.89 (95% CI = 0.73-1.08). DISCUSSION: Our findings support a protective effect of aspirin and paracetamol against prostate cancer. The transient elevated risk observed among newly started users of NA-NSAIDs and paracetamol is most likely explained by prothopathic bias. We found some suggestion of a reduced risk with long-term use of NA-NSAID.

Acetaminophen↗

PubMed1996

Hormonal and Chemotherapeutic Systemic Therapy for Metastatic Prostate Cancer.

BACKGROUND: Prostate cancer is the most frequently diagnosed cancer and the second leading cause of cancer death in men in the United States. It is estimated that over 300,000 men will have been diagnosed with prostate cancer in 1996, and more than 40,000 will have died of this disease. METHODS: The authors combined their experience with a review of the literature on management of this disease to examine the effectiveness of treatments for both localized and metastatic prostate cancer. RESULTS: Surgery and radiation therapy are potentially curative modalities for cancer still limited to the gland. Androgen ablation therapy results in stabilization or regression of metastatic disease in most instances but is not curative. Some new approaches are described for patients with hormone-refractory prostate cancer. CONCLUSIONS: Newer tumor-biology-based combinations are promising in the treatment of hormone-refractory prostate cancer, but their effect on patient survival needs to be evaluated in larger clinical trials.

Journal Article↗

PubMedDate not supplied

The effect of hydrazine sulfate on prostate cancer growth.

Prostate cancer remains the most commonly diagnosed cancer in American males and is the second leading cause of cancer death in this group. Hydrazine sulfate, an inhibitor of gluconeogenesis, has been proposed as a means to improve nutritional status and improve survival in patients with solid tumors. We investigated the effects of hydrazine sulfate on both in vitro and in vivo models of prostate cancer. We examined the cytotoxicity of hydrazine sulfate in both human (LNCaP and PC-3) and animal (MAT-LyLu) prostate cancer cell lines. No growth inhibition was observed. In vivo, hydrazine sulfate did not suppress the growth of implanted Dunning rat prostate MAT-LyLu cells. Hydrazine sulfate does not have activity in these models of prostate cancer and may not be an appropriate therapy for patients with prostate cancer.

Animals↗

PubMed2007

Genomic scan of 12 hereditary prostate cancer families having an occurrence of pancreas cancer.

BACKGROUND: Prostate cancer is a genetically heterogeneous disease. Using the occurrence of other cancers in hereditary prostate cancer (HPC) families is a promising strategy for developing genetically homogeneous data sets that can enhance the ability to identify susceptibility loci using linkage analysis. METHODS: Twelve HPC families with the co-occurrence of adenocarcinoma of the pancreas were selected from the Prostate Cancer Genetic Research Study (PROGRESS). Non-parametric linkage analysis for a prostate/pancreas cancer susceptibility phenotype was performed using 441 genome-wide microsatellite markers. RESULTS: No statistically significant linkage signal was detected in this analysis. The strongest linkage signals, as measured by Kong and Cox LOD score (KC LOD), were observed on chromosomes 2q37.2-q37.3 (KC LOD = 1.01; P = 0.02) and 16q23.2 (KC LOC = 1.05; P = 0.01). CONCLUSIONS: Despite the lack of statistically significant findings, four chromosomal regions, three of which (2q, 16q, 17q) were previously noted as harboring potential susceptibility loci, showed suggestive linkage results in this scan.

Aged↗

PubMed2006

Detection rates of high-grade prostate cancer during subsequent screening visits. Results of the European Randomized Screening Study for Prostate Cancer.

Screening for prostate cancer using prostate-specific antigen (PSA) tests has led to a stage and grade shift as compared to the pre-PSA era. Effectiveness of screening for prostate cancer should be manifested by a reduction in detection rate of aggressive cancers during subsequent screening. In 6 centers of the European Randomized Screening study for Prostate Cancer, a total of 58,710 men were tested for prostate cancer. Screening centers differed with regard to age-range, screening interval and biopsy indications. During the 2nd visit, the proportion of Gleason score 6 cancers increased from 62.5 to 75%, mainly at the expense of Gleason score 7 cancers. High-grade (Gleason score 8-10) cancer detection rates varied per screening center during the 1st visit from 5.1 to 41.1, and during the 2nd visit from 6.4 to 29.3/10,000 men. The overall detection rate of high-grade cancers showed a reduction during the 2nd visit from 26 to 12/10,000 men, an effect mainly attributable to the screening center with the highest cancer detection rate (i.e. 507/10,000 men). Variations in detection rates among screening centers related among others to biopsy compliance and age range.

Age Factors↗

PubMed1998

Perceived benefits: a predictor of participation in prostate cancer screening.

Prostate cancer is the most frequently diagnosed major cancer and the second cause of cancer-related deaths among men. With early detection through screening and timely treatment, 9 out of 10 men will survive a minimum of 5 years. However, with late diagnoses, only 3 out of 10 men will have a 5-year minimum survival rate. Guided by a conceptual map, this correlational research examined perceived benefits as a predictor of participation in free prostate cancer screening. Perceived benefits are the personal belief and valuing of screening for early detection of prostate cancer. All subjects received one of four educational interventions: traditional, peer educator, client navigator, or combination. Participation in prostate cancer screening was measured by compliance with the American Cancer Society's Guidelines, which included a digital rectal exam (DRE) and/or a prostate-specific antigen (PSA) blood test. The purposive sample (n = 1,522) of men, ages 40 to 70 years, was recruited from randomly selected churches, barbershops, industries, housing projects, and car dealerships in a southeastern state. Seventy-two percent of the sample was African American. Predictors of participation in free prostate cancer screening were these: perceived benefits, being white, having at least a high school education, being married, and receiving the client navigator or combination educational intervention. The Benefits Scale was significant (p = 0.013, odds ratio (OR) = 1.059) as a predictor for participation in screening when all demographic variables and educational interventions were controlled. Practice implications for nursing are discussed and recommendations for future research are presented.

Adult↗

PubMed2006

Ras inhibition results in growth arrest and death of androgen-dependent and androgen-independent prostate cancer cells.

Prostate cancer is one of the most frequently diagnosed cancers in human males. Progression of these tumors is facilitated by autocrine/paracrine growth factors which activate critical signaling cascades that promote prostate cancer cell growth, survival and migration. Among these, Ras pathways have a major role. Here we examined the effect of the Ras inhibitor S-trans, trans-farnesylthiosalicylic acid (FTS), on growth and viability of androgen-dependent and androgen-independent prostate cancer cells. FTS downregulated Ras, inhibited signaling to Akt and reduced the levels of cell-cycle regulatory proteins including cyclin D1, p-RB, E2F-1 and cdc42 in LNCaP and PC3 cells. Consequently the anchorage-dependent and anchorage-independent growth of LNCaP and PC3 cells were inhibited. FTS also induced apoptotic cell death which was inhibited by the broad-spectrum caspases inhibitor, Boc-asp-FMK. Our study demonstrated that androgen-dependent and androgen-independent prostate cancer cells require active Ras for growth and survival. Ras inhibition by FTS results in growth arrest and cell death. FTS may be qualified as a potential agent for the treatment of prostate cancer.

Amino Acid Chloromethyl Ketones↗

PubMed1998

1997 American Urological Association Gallup survey: Changes in diagnosis and management of prostate cancer and benign prostatic hyperplasia, and other practice trends from 1994 to 1997.

PURPOSE: The American Urological Association first commissioned the Gallup Organization to conduct a study to assess urologist practice patterns in 1992. We present the results of the 1997 survey, the sixth consecutive Gallup survey performed for the Association. MATERIALS AND METHODS: A random sample of 502 American urologists who had completed urological residency and practiced at least 20 hours weekly in 1996 was interviewed by telephone in February and March 1997. RESULTS: Emerging trends showed significant changes since 1994 in how urologists diagnosed and treated prostate cancer. The survey revealed a significant change in the tests routinely ordered to stage newly diagnosed prostate cancer and for diagnostic evaluation of patients with benign prostatic hyperplasia. CONCLUSIONS: Urologists are becoming more cost conscious and effective in ordering pretreatment testing. Urologists are becoming more oriented toward medical treatment for the management of benign prostatic hyperplasia, and less laser surgery is being performed.

Adult↗

PubMedDate not supplied

Evaluating polymorphic status of glutathione-S-transferase genes in blood and tissue samples of prostate cancer patients.

Prostate cancer is the most common urologic malignancy, involving multiple factors. There is evidence that suggests that detoxification enzymes and growth factors may play a role in its development . The glutathione S-transferase (GST) enzymes detoxify several carcinogens and genetic polymorphisms in GSTM1, T1, and P1 (Ile105Val) have been reported to be associated with prostate cancer, mainly from blood samples. As expression studies suggest differential expression of different genes in tissues, we hypothesize that polymorphic status may be differently expressed for GSTM1, GSTT1 and GSTP1 gene in blood and tissues of prostate cancer patients and BPH controls, impacting on the development of prostate cancer. To study this, we extracted DNA from blood and tissue samples of patients undergoing biopsy procedures or transurethral resection of prostate tissue. Genotyping for GSTM1 and T1 was conducted by multiplex PCR and for GSTP1 by the PCR-RFLP method. Our results suggested no significant differences in frequency distribution of M1, T1 and P1 between blood and tissue samples of patients and controls, but in a few patients differences in polymorphic status were observed. However, they were not significant. Furthermore, we observed a significant risk of prostate cancer with null allele of GSTT1 and GSTM1 and Val allele of GSTP1, supporting our previous findings. A study with large sample size using radical prostectomy tissue now needs to be performed to attain a specific conclusion.

Aged↗

PubMed1994

The Prostate Cancer Intervention Versus Observation Trial: a randomized trial comparing radical prostatectomy versus expectant management for the treatment of clinically localized prostate cancer.

The Prostate Cancer Intervention Versus Observation Trial (PIVOT) is a randomized controlled trial sponsored by the Department of Veterans Affairs and the National Cancer Institute. PIVOT will enroll 2,000 participants from at least 80 Veterans Administration and National Cancer Institute medical centers. The purpose of PIVOT is to determine which of 2 strategies is superior for managing clinically localized prostate cancer (stage T1/T2NXM0) of all histological grades. Patients less than 75 years old will be randomized to either radical prostatectomy with early intervention for disease persistence/recurrence or expectant management with palliative therapy reserved for symptomatic or metastatic disease progression. Participants will be excluded if they have received prior therapy for prostate cancer (except transurethral resection of the prostate) or are judged not to be candidates for radical prostectomy. All patients with newly diagnosed prostate cancer will be recorded on the PIVOT screening log. Registry information will include patient age, race, prostate specific antigen level, clinical stage, histological tumor grade, initial therapy, and vital status. Patients meeting eligibility criteria will watch an information and randomization video tape developed for PIVOT. Participants will be randomized over a 3-year period and followed for a minimum of 12 years. Data collected at followup will include urological symptoms, disease and treatment related morbidity, and disease specific and overall quality of life. Evidence of symptomatic or asymptomatic disease persistence, recurrence or progression will be measured by questionnaire, physical examination, digital rectal examination, prostate specific antigen and annual bone scan. The primary study end point will be all cause mortality. Secondary outcomes will include prostate cancer and treatment specific morbidity and mortality rates, health status, predictors of disease specific outcomes and cost-effectiveness. PIVOT will provide a 90% power to detect a 15% relative decrease in all cause mortality and a 35% relative decrease in prostate cancer specific mortality rate by either treatment strategy.

Aged↗

PubMed1999

Distinct CXC chemokines mediate tumorigenicity of prostate cancer cells.

Prostate cancer is the second leading cause of malignancy-related mortality in males in the United States. As a solid tumor, clinically significant tumor growth and metastasis are dependent on nutrients and oxygen supplied by tumor-associated neovasculature. As such, there is a selective tumorigenic advantage for those neoplasms that can produce angiogenic mediators. We show here that human prostate cancer cell lines can constitutively produce angiogenic CXC chemokines. Tumorigenesis of PC-3 prostate cancer cells was shown to be attributable, in part, to the production of the angiogenic CXC chemokine, interleukin (IL)-8. Neutralizing antisera to IL-8 inhibits PC-3 tumor growth in a human prostate cancer/SCID mouse model. Furthermore, angiogenic activity in PC-3 tumor homogenates was attributable to IL-8. In contrast, the Du145 prostate cancer cell line uses a different angiogenic CXC chemokine, GRO-alpha, to mediate tumorigenicity. Neutralizing antisera to GRO-alpha but not IL-8 reduced tumor growth in vivo and reduced the angiogenic activity in tumor homogenates. Thus, prostate cancer cell lines can use distinct CXC chemokines to mediate their tumorigenicity.

Animals↗

PubMed2006

Amygdalin induces apoptosis through regulation of Bax and Bcl-2 expressions in human DU145 and LNCaP prostate cancer cells.

Prostate cancer is one of the most common non-skin cancers in men. Amygdalin is one of the nitrilosides, natural cyanide-containing substances abundant in the seeds of plants of the prunasin family that have been used to treat cancers and relieve pain. In particular, D-amygdalin (D-mandelonitrile-beta-D-gentiobioside) is known to exhibit selective killing effect on cancer cells. Apoptosis, programmed cell death, is an important mechanism in cancer treatment. In the present study, we prepared the aqueous extract of the amygdalin from Armeniacae semen and investigated whether this extract induces apoptotic cell death in human DU145 and LNCaP prostate cancer cells. In the present results, DU145 and LNCaP cells treated with amygdalin exhibited several morphological characteristics of apoptosis. Treatment with amygdalin increased expression of Bax, a pro-apoptotic protein, decreased expression of Bcl-2, an anti-apoptotic protein, and increased caspase-3 enzyme activity in DU145 and LNCaP prostate cancer cells. Here, we have shown that amygdalin induces apoptotic cell death in human DU145 and LNCaP prostate cancer cells by caspase-3 activation through down-regulation of Bcl-2 and up-regulation of Bax. The present study reveals that amygdalin may offer a valuable option for the treatment of prostate cancers.

Amygdalin↗

PubMed2006

Comparison of genetic alterations detected in circulating microsatellite DNA in blood plasma samples of patients with prostate cancer and benign prostatic hyperplasia.

Prostate cancer is the most frequent malignant disease and the second most frequent cause of death due to cancer in men in the Western world. Since serum prostate-specific antigen (PSA) and its subforms show poor specificity in clinical practice, a molecular marker for the detection and discrimination of prostate cancer (PCa) could be of great interest. To investigate the potential significance of genetic aberrations, such as loss of heterozygosity (LOH), in PCa we identified and characterized allelic losses in circulating tumor-associated DNA in blood from patients with localized PCa. Genomic DNA extracted from cell-free plasma of blood samples drawn from 65 PCa patients was analyzed using a panel of 15 polymorphic microsatellite markers mapping to known tumor-suppressor genes. Comparative analyses were performed with a control group of 36 patients with benign prostatic hyperplasia (BPH). In the current study, we demonstrate that PCa patients had higher DNA concentrations in their blood circulation than BPH patients. In the marker panel studied, LOH was more frequently detected in PCa patients (34%) than in BPH patients (22%). The incidence of LOH in the plasma DNA of PCa patients was highest at chromosomal regions 3p24 (THRB, 22%) and 8p21 (D8S360, 22%) in comparison to the BPH control cohort, which frequently showed LOH at loci 8q21, 8p21, 9p21, and 11q22 (D8S286, D8S360, D9S1748, and D11S898, each 6%). These results indicate that microsatellite analysis using plasma DNA may be an interesting tool for molecular screening of PCa patients.

Biomarkers, Tumor↗

PubMed1995

Association of p53 mutations with metastatic prostate cancer.

In prostate cancer, mutation of the p53 tumor suppressor gene has been associated with locally advanced disease and hormone-resistant disease that is predominantly localized to bone. However, little is known regarding the status of the p53 gene in metastatic prostate cancer that has not been treated with hormonal manipulation. We evaluated formalin-fixed, paraffin-embedded malignant tissues from 86 patients with various stages of prostate cancer, including pathologically confined, locally advanced, and metastatic disease, to detect abnormal p53 nuclear protein accumulation using immunohistochemistry. No abnormal p53 immunostaining was detected in 18 patients with prostate cancer confined to the gland. Two tumors from 21 patients with locally advanced disease (extracapsular extension and/or seminal vesicle invasion) had abnormal nuclear p53 accumulation, and a mutation in exon 7 of the p53 gene was detected in tumor DNA from one patient using single-strand conformation polymorphism-direct sequencing analysis. Of the remaining 47 patients studied in whom tissues from the prostate gland and a metastatic site (44 lymph node, 2 bone, and 1 lung) were available, only 3 had received hormonal therapy prior to obtaining metastatic tissue. In four patients both primary and metastatic tumors demonstrated accumulation of p53 protein, whereas seven additional patients exhibited p53 accumulation only at the metastatic site. In three patients the metastatic tumors harbored missense single-base substitutions in exon 5, as detected using single-strand conformation polymorphism-direct sequencing. These results indicate that p53 abnormalities are associated with lymph node metastases derived from prostate cancer patients that had not undergone hormonal therapy.

Adenocarcinoma↗