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PubMed2002

Does amount or type of alcohol influence the risk of prostate cancer?

BACKGROUND: Prostate cancer is one of the most common cancers among men, and it is unknown whether alcohol is associated with the development of prostate cancer. METHODS: The relationship between amount or type of alcohol and prostate cancer was studied in a pooled prospective setting conducted from 1976 to 1994 in Copenhagen, Denmark. The study population consisted of 12,989 subjects drawn from three different cohorts. During a mean follow-up of 12.3 yr, 233 subjects developed prostate cancer. RESULTS: None of the estimates for consumed amount of total alcohol diverged significantly from unity. Furthermore, drinkers of more than 13 beers, 13 glasses of wine, and 13 drinks of spirits had a risk of 1.03 (CI: 0.67, 1.60), 0.92 (CI: 0.42, 1.99), and 1.01 (CI: 0.52, 1.98), respectively, compared with abstainers of the given beverage of alcohol. CONCLUSION: These results suggest that neither amount nor type of alcohol is associated with the risk of prostate cancer.

Adult↗

PubMed2004

Effective antigen cross-presentation by prostate cancer patients' dendritic cells: implications for prostate cancer immunotherapy.

Despite the potency with which dendritic cells (DCs) are able to utilize the exogenous MHC I antigen cross-presentation pathway to cross-present antigen for the activation of killer T cells in model systems, concern about defects in immune function in cancer patients has led to uncertainty regarding whether immune cells derived from patients can effectively be used to generate tumor vaccines. We have undertaken a careful analysis of the potency of using DCs obtained from prostate cancer patients to cross-present antigen derived from human prostate tumor cells for the activation of antigen-specific T cells. Such DCs can be matured ex vivo into functionally active cells and are capable of cross-presenting influenza antigen derived from internalized apoptotic prostate tumor cells. Importantly, we demonstrate effective stimulation of both CD4+ and CD8+ T cells, as evident by production of IFN-gamma, and the ability of CD8+ T cells to differentiate into effector CTLs. These results, defining conditions in which prostate cancer patient DCs can efficiently utilize the cross-presentation pathway and in which apoptotic tumor can serve as a source of antigen for DCs to activate T cells, demonstrate that this system warrants clinical study as a potential immunotherapy.

Antigens, Neoplasm↗

PubMed2003

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

There have been improvements in the outcome of patients with clinically localized prostate cancer treated by radical prostatectomy. However, some patients treated with radical prostatectomy will have clinical or biochemical progression. These men are at increased risk of dying of their disease. Identification of patients with adverse features at the time of radical prostatectomy may permit the use of additional multimodality therapies to improve outcomes. Whether this additional multimodality therapy should be administered in the neoadjuvant or adjuvant setting remains controversial. Further, whether a patient at increased risk for progression after radical prostatectomy requires additional therapy before the development of documented progression remains controversial. This article reviews the potential multimodality approaches to prevent or delay recurrence of prostate cancer in patients undergoing surgical treatment for prostate cancer.

Adenocarcinoma↗

PubMedDate not supplied

Usefulness of PSA density and PSA excess in the differential diagnosis between prostate cancer and benign prostatic hypertrophy.

The usefulness of PSA density (PSAD) was evaluated in relation to the volume of the transitional zone (PSAT) and PSA excess. With this purpose we conducted a study including 27 patients diagnosed as having prostatic cancer (PC) and 46 patients with benign prostatic hypertrophy (BPH). In all of them, the PSA concentration in the serum was determined as well as the total prostatic volume and the transitional zone volume; digital rectal examination (DRE) was also performed. The major diagnostic efficacy was obtained with the excess of PSA (73%, cutoff = -13 ng/ml), followed by DRE (68%), PSAT (64%, cutoff = 0.5), PSAD (64%, cutoff = 0.2), and lastly PSA and ultrasonography (60%). Multivariate analysis (logistic regression) demonstrated PSA excess and DRE to be the best predictors. The model obtained by regression shows the best positive predictive value, and PSA excess the best negative predictive value. Consequently, PSA excess could be relevant in prostate cancer diagnosis.

Confidence Intervals↗

PubMed2005

Expectant management: an option for localized prostate cancer.

Localized prostate cancer demonstrates tremendous heterogeneity in the natural history of the disease. To this end, although prostate cancer may be present histologically in nearly 30% of all men above the age of 50 y, the lifetime risk of developing clinically significant disease is 18% (one in six). Furthermore, the lifetime risk of dying from prostate cancer is less than 4%. Therefore, in order to avoid unnecessarily treating potentially insignificant prostate cancer, the concept of expectant management has been considered for this disease. In this brief review, we discuss the evolution of expectant management for men with localized prostate cancer.

Humans↗

PubMed2000

Increased risk of prostate cancer and benign prostatic hyperplasia associated with a CYP17 gene polymorphism with a gene dosage effect.

The CYP17 gene (CYP17) codes for the cytochrome P450c17alpha enzyme, which mediates two key steps in the sex steroid synthesis. There is a polymorphism (a T-to-C substitution) in the 5'-untranslated region, which may influence the transcription level of CYP17 mRNA. There is a continuing controversy as to whether the variant allele is associated with a subset of breast cancer or polycystic ovary syndrome. In prostate cancer research, there are contradictory data concerning the CYP17 risk allele. We explored the association between CYP17 polymorphism and a risk of prostate cancer or benign prostatic hyperplasia (BPH) in a Japanese population. This study included 252 prostate cancer patients, 202 BPH patients, and 131 male controls. A 451-bp fragment encompassing the polymorphic site was amplified by PCR, treated with restriction enzyme MspA1, and electrophoresed on an agarose gel. The MspA1-undigested allele with the published sequence and the MspA1-digested variant allele were designated as A1 and A2, respectively. There was a significant difference (P < 0.05) in the genotypes between prostate cancer patients and male controls, and between BPH patients and male controls. Men with the A1/A1 CYP17 genotype had an increased risk of prostate cancer [odds ratio (OR), 2.57; 95% confidence interval (CI) = 1.39-4.78] and BPH (OR, 2.44; 95% CI = 1.26-4.72) compared with those with the A2/A2 genotype. Men with the A1/A2 genotype had an intermediate increased risk of prostate cancer (OR, 1.45; 95% CI = 0.84-2.54) and BPH (OR, 1.60; 95% CI = 0.89-2.87) compared with those with the A2/A2 genotype. The trend of an increasing risk of prostate cancer and BPH with an increasing number of the A1 allele was statistically significant (prostate cancer versus male control, P = 0.003; OR, 1.57; 95% CI = 1.16-2.12; BPH versus male control, P = 0.008; OR, 1.55; 95% CI = 1.12-2.13). There was no significant association between the CYP17 genotype and the tumor status (grade and stage) of prostate cancer. Our results suggest that the A1 allele of the CYP17 polymorphism is associated with an increased risk of prostate cancer and BPH, with a gene dosage effect. However, the CYP17 genotype does not seem to influence the disease status in prostate cancer.

Aged↗

PubMed2005

Sex steroid hormones and the androgen receptor gene CAG repeat and subsequent risk of prostate cancer in the prostate-specific antigen era.

OBJECTIVE: Sex steroid hormones are thought to contribute to the growth, differentiation, and progression of prostate cancer. We investigated plasma levels of sex steroid hormones and length of the androgen receptor gene CAG repeat in relation to incident prostate cancer diagnosed in the prostate-specific antigen (PSA) era. METHODS: Using a nested case-control design, we included 460 prostate cancer cases diagnosed after providing a blood specimen in 1993 but before February 1998 among men in the Health Professionals Follow-up Study. Controls were 460 age-matched men without prostate cancer who had a screening PSA test after the date of providing a blood specimen. We measured plasma concentrations of total testosterone, free testosterone, dihydrotestosterone, androstanediol glucuronide, estradiol, and sex hormone binding globulin (SHBG) and determined the length of the androgen receptor gene CAG repeat. Conditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI) of prostate cancer. RESULTS: Mean concentrations of the sex steroids adjusted for SHBG, and mean CAG repeat length did not differ significantly between the prostate cancer cases and controls. No significant associations with total prostate cancer were detected for plasma total testosterone concentration (comparing highest versus lowest quartiles: OR, 0.78; 95% CI, 0.48-1.28; P(trend) = 0.73) or the other sex hormones after adjusting for SHBG. However, plasma total testosterone concentration was positively associated with low-grade disease (Gleason sum < 7: OR, 1.91; 95% CI, 0.89-4.07; P(trend) = 0.02) and inversely associated with high-grade disease (Gleason sum > or = 7: OR, 0.26; 95% CI, 0.10-0.66; P(trend) = 0.01). Similar patterns for grade were observed for free testosterone. Short CAG repeat length was not associated with total prostate cancer (< or = 19 versus > or = 24: OR, 0.84; 95% CI, 0.57-1.23; P(trend) = 0.22) or grade of disease. No clear associations with regionally invasive or metastatic (> or = T3b, N1, or M1) were found for any of the hormones or the CAG repeat, although the number of these cases was small. CONCLUSIONS: The overall lack of association of prostate cancer diagnosed in the PSA era with sex steroid hormones and the androgen receptor gene CAG repeat length is consistent with the hypothesis that these factors do not substantially contribute to the development of early prostate cancer in the PSA era. The influence of plasma total and free testosterone concentrations on prostate cancer grade merits further evaluation.

Age Factors↗

PubMedDate not supplied

Use of a SCID mouse model to select for a more aggressive strain of prostate cancer.

BACKGROUND: Prostate cancer is the most common non-cutaneous malignancy to affect men and has a propensity for metastasizing to bone. To better mimic the biology of metastatic prostate cancer, we have developed a model that utilizes both human prostate cancer and human bone in the SCID mouse. MATERIALS AND METHODS: Injection of a xenograft of human prostate cancer, LAPC-4, near a human bone core that was previously implanted within the hindlimb of a SCID mouse allowed for the selection of a more aggressive subset of cells, known as LAPC-4(2) (read as "LAPC-4 squared"). RESULTS: As compared to LAPC-4 cells, these "bone-selected" LAPC-4(2) cells form tumors more rapidly, develop PSA-positive serum at an earlier time-point as well as with higher levels, develop androgen independence, and metastasize to human bone after orthotopic injection. CONCLUSION: The selection of a more aggressive subset of prostate cancer cells that have developed androgen independence and the propensity to metastasize is of paramount importance as these are the cellular characteristics that are clinically linked to morbidity. Analysis of these "bone-selected" cells may lead to a better understanding of the molecular basis behind the conversion of low-grade prostate carcinoma to its more deadly, metastatic form.

Adult↗

PubMed1984

Review: prostate cancer epidemiology.

Prostate cancer is common among men in the United States. Factors of possible importance in the etiology of prostate cancer include diet, primarily implicated by ecologic studies of national, regional, and ethnic variation in rates; endocrine function, implicated by the importance of endocrine function in normal prostatic growth and in the treatment of prostate cancer; genetic susceptibility, supported by familial aggregation; some aspect of sexual behavior, suggested by case-control differences in sexual behavior; and occupational exposure, particularly cadmium exposure. Despite the public health importance of prostate cancer, it has received only moderate epidemiologic study; thus the etiologic importance of these and other possible determinants of prostate cancer risk is uncertain [55].

Aged↗

PubMed2000

Antibody immunity to prostate cancer associated antigens can be detected in the serum of patients with prostate cancer.

PURPOSE: Several immune based therapies targeting prostate cancer associated proteins are currently undergoing clinical investigation. In general, however, little is known about the immunogenicity of prostate cancer or which prostate cancer associated proteins elicit immune responses. We determine whether patients with prostate cancer have antibody immunity to known prostate cancer associated proteins, what the prevalence of this immunity is and whether immunity to individual proteins is associated with the stage of disease. MATERIALS AND METHODS: We evaluated the inherent humoral immune response against prostate specific antigen (PSA), prostatic acid phosphatase, p53 and HER-2/neu, all known prostate cancer associated proteins, in 200 patients with various stages of disease and male controls. RESULTS: Antibody immunity to PSA was significantly different between the patient (11%, 22 of 200) and control populations (1.5%, 3 of 100, p = 0.02), and titers 1:100 or greater were particularly prevalent in the subgroup of patients with androgen independent disease (11%, 6 of 56). Antibody immunity to prostatic acid phosphatase and p53 was detected (5.5%, 11 of 200 and 6%, 12 of 200), and was not different from the control population (4%, 4 of 100, p = 0.57 and 7%, 7 of 100, p = 0.74). Antibody immunity to HER-2/neu was significantly higher in patients with prostate cancer (15.5%, 31 of 200) compared to controls (2%, 2 of 100, p = 0.0004), and titers 1:100 or greater were most prevalent in the subgroup of patients with androgen independent disease (16%, 9 of 56). CONCLUSIONS: These findings suggest that prostate cancer is an immunogenic tumor. Moreover, for PSA and HER-2/neu the prevalence of antibody immunity was higher in patients with androgen independent disease, indicating that even patients with advanced stage prostate cancer can have an immune response to their tumor.

Acid Phosphatase↗

PubMed2005

Surrogate end point for prostate cancer specific mortality in patients with nonmetastatic hormone refractory prostate cancer.

PURPOSE: We determined whether prostate specific antigen (PSA) velocity can serve as surrogate end point for prostate cancer specific mortality (PCSM) in patients with nonmetastatic, hormone refractory prostate cancer. MATERIALS AND METHODS: The study cohort comprised 919 men treated from 1988 to 2002 at 1 of 44 institutions with surgery (560) or radiation therapy (359) for clinical stages T1c-4NxMo prostate cancer, followed by salvage hormonal therapy for PSA failure. All patients experienced PSA defined recurrence while on hormonal therapy. Prentice criteria require that the surrogate should be a prognostic factor and the treatment used did not alter time to PCSM following achievement of the surrogate end point. These criteria were tested using Cox regression. All statistical tests were 2-sided. RESULTS: PSA velocity greater than 1.5 ng/ml yearly was statistically significantly associated with time to PCSM and all cause mortality following PSA defined recurrence while undergoing hormonal therapy (Cox p <0.0001). While initial treatment was statistically associated with time to PCSM and all cause mortality (Cox p = 0.001 and 0.01), this association became insignificant when PSA velocity and potential confounding variables were included in the Cox model (p = 0.22 and 0.93, respectively). The adjusted HR for PCSM in patients who experienced a greater than 1.5 ng/ml increase in PSA within 1 year while on hormonal therapy was 239 (95% CI 10 to 5,549). CONCLUSIONS: These data provide evidence to support PSA velocity greater than 1.5 ng/ml yearly as a surrogate end point for PCSM in patients with nonmetastatic, hormone refractory prostate cancer. Enrolling these men onto clinical trials evaluating the impact of chemotherapy on time to bone metastases and PCSM is warranted.

Aged↗

PubMed2005

Blood and tissue selenium concentrations and glutathione peroxidase activities in patients with prostate cancer and benign prostate hyperplasia.

Prostate cancer (PC) is the most common cancer in men and a leading cause of cancer death. Prostatic gland accumulates reasonably high amount of selenium (Se), the element that prevents the development of PC. It is hypothesized that some selenoproteins inhibit the transformation of normal prostate epithelium into neoplasm. We studied Se levels in whole blood, plasma and prostate of 32 PC and 40 benign prostate hyperplasia (BPH) patients and in the control group composed of 39 healthy subjects. The selenoenzyme glutathione peroxidase (GSH-Px) was also measured in the patients' red cells, plasma and prostate tissue. Se concentration in whole blood and plasma in both groups of patients was lower as compared with controls, while in prostate gland it was significantly higher in PC than in BPH patients and controls. Red cell GSH-Px activity was the same in PC patients and controls but significantly lower in BPH patients. Plasma GSH-Px activity was significantly lower in PC patients than in the control group, and prostate GSH-Px activity was significantly lower in PC patients as compared with BPH patients. Since Se has anticancer properties, it is very likely that its low level in blood may facilitate the development of cancer. A higher level of Se in prostate of PC patients has no influence on GSH-Px activity in the gland.

Aged↗

PubMed2001

BRCA2 mutation in a family with hereditary prostate cancer.

Hereditary prostate cancer is a genetically heterogeneous disease, and so far four different susceptibility loci have been identified. Reports of associated cancers are few, and it is generally considered a site-specific disease. However, some reports have shown an elevated risk for prostate cancer among BRCA2 mutation carriers. In this report, we present a family in which the father and four of his sons were diagnosed with prostate cancer at exceptionally early ages (51, 52, 56, 58, and 63 years, respectively). In addition, three daughters were diagnosed with breast cancer between the ages of 47 and 61. In this family, a truncating mutation in exon 11, 6051delA of the BRCA2 gene, leading to an early termination of the protein (codon 1962), was identified. Although BRCA2 is probably responsible only for a very small fraction of hereditary prostate cancers, this finding supports previous reports of an increased risk of prostate cancer in BRCA2 mutation carriers.

Aged↗

PubMed1998

The role of PSA and percent free PSA for staging and prognosis prediction in clinically localized prostate cancer.

Prostate-specific antigen (PSA) is the most important tumor marker for early detection, staging, and monitoring of men with prostatic cancer today. However, its sensitivity and specificity are not sufficient to use it as a single tool for screening for men with clinically localized prostate cancer. Recently, assays have become available that selectively detect several of the various molecular forms of PSA, especially the unbound or free PSA. Several studies have shown the clinical usefulness of percent free PSA (free PSA/total PSA) for the early detection of men with clinically localized prostate cancer. However, the use of percent free PSA for staging of prostate cancer remains controversial. Based on the case scenario presented, the value of total PSA and percent free PSA for the staging of men with clinically localized prostate cancer is reviewed.

Age Factors↗

PubMed1995

Prostate specific antigen in a community-based sample of men without prostate cancer: correlations with prostate volume, age, body mass index, and symptoms of prostatism.

The correlation between both prostate specific antigen levels (PSA) and prostate specific antigen density (PSAD) and age, prostate volume parameters, body mass index, and the International Prostate Symptom Score (IPSS) were studied in a community-based population. A sample of 502 men aged 55 through 74 years was evaluated, excluding those with a serum PSA above 10 ng/ml, those with biopsy proven prostate cancer, and those who had previously undergone a prostate operation. PSA and PSAD did not correlate with the body mass index. Weak correlations were found between PSA and age (r = 0.25; P < 0.001), PSAD and age (r = 0.17; P < 0.001) and between PSA and the total prostate volume (r = 0.58; P < 0.001). PSA did not correlate independently with age after adjustment for volume (P = 0.22). The finding that PSAD correlates with age (r = 0.17; P < 0.001) is partly explained by the incomplete volume adjustment of PSAD which is proved by the positive correlation between PSAD and prostate volume (r = 0.26; P < 0.001). In the main target age-range for prostate cancer screening there is a poor basis for the use of age-specific reference values or volume adjustment for PSA levels in order to increase the clinical usefulness of this serum marker. Comparison of the results of the present study and studies conducted in others regions shows that there may be significant differences in PSA values per age stratum. Further studies are needed to clarify the reasons for these differences.

Aged↗

PubMed1999

CAG repeat length in the androgen receptor gene is related to age at diagnosis of prostate cancer and response to endocrine therapy, but not to prostate cancer risk.

The length of the polymorphic CAG repeat in the N-terminal of the androgen receptor (AR) gene is inversely correlated with the transactivation function of the AR. Some studies have indicated that short CAG repeats are related to higher risk of prostate cancer. We performed a case-control study to investigate relations between CAG repeat length and prostate cancer risk, tumour grade, tumour stage, age at diagnosis and response to endocrine therapy. The study included 190 AR alleles from prostate cancer patients and 186 AR alleles from female control subjects. All were whites from southern Sweden. The frequency distribution of CAG repeat length was strikingly similar for cases and controls, and no significant correlation between CAG repeat length and prostate cancer risk was detected. However, for men with non-hereditary prostate cancer (n = 160), shorter CAG repeats correlated with younger age at diagnosis (P = 0.03). There were also trends toward associations between short CAG repeats and high grade (P = 0.07) and high stage (P = 0.07) disease. Furthermore, we found that patients with long CAG repeats responded better to endocrine therapy, even after adjusting for pretreatment level of prostate-specific antigen and tumour grade and stage (P = 0.05). We conclude that short CAG repeats in the AR gene correlate with young age at diagnosis of prostate cancer, but not with higher risk of the disease. Selection of patients with early onset prostate cancer in case-control studies could therefore lead to an over-estimation of the risk of prostate cancer for men with short CAG repeats. An association between long CAG repeats and good response to endocrine therapy was also found, but the mechanism and clinical relevance are unclear.

Adult↗

PubMed2003

Value of endocrine therapy for early and locally advanced prostate cancer.

Prostate-specific antigen-based screening and increased public awareness of prostate cancer have led to earlier detection of localised and potentially curable tumour stages. Nevertheless, disease recurrence after radical treatment of prostate cancer remains a problem for a considerable number of patients. Endocrine therapy plays a role in the treatment of almost all stages of prostate cancer, either as definitive or as temporary therapy. Neoadjuvant hormonal treatment has its place mainly in the external beam radiotherapy setting, where it reduces target volume and adverse effects. When used prior to and during external beam radiotherapy, endocrine therapy has shown a survival advantage in the subset of patients with locally advanced prostate cancer (cT2-4, N0-1, M0) with Gleason scores 2-6. Several studies have shown that adjuvant endocrine treatment is able to delay disease progression in any stage. There is, however, an ongoing controversy regarding the possible survival benefit of such treatment that has to be balanced against its considerable adverse effects and costs. Survival improvements associated with adjuvant hormonal treatments have mainly been seen in patients with lymph node metastases or those with a high probability of micrometastatic disease. Several large studies are under way to investigate the role of adjuvant treatment in the field of early prostate cancer.

Androgen Antagonists↗

PubMed2002

Relevant patient and tumor considerations for early prostate cancer treatment.

Prostate cancer remains the most commonly diagnosed noncutaneous malignancy in American men. Currently, there are 3 standard treatment options available to men with early prostate cancer: expectant management, radiation therapy, and radical prostatectomy. Although a number of studies have evaluated survival after treatment for early prostate cancer, the optimal choice of therapy for any given patient remains a difficult decision and requires the consideration of a variety of patient and tumor factors. The final selection of therapy for early prostate cancer should be based on an informed discussion between the physician and patient. To accomplish this goal, patients must be made familiar with the pertinent factors that affect survival. We review the factors most relevant for patients to understand as they consider their treatment options for early prostate cancer and summarize the data for physicians who counsel them.

Age Factors↗