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PubMed2005

Differences in gene expression in prostate cancer, normal appearing prostate tissue adjacent to cancer and prostate tissue from cancer free organ donors.

BACKGROUND: Typical high throughput microarrays experiments compare gene expression across two specimen classes - an experimental class and baseline (or comparison) class. The choice of specimen classes is a major factor in the differential gene expression patterns revealed by these experiments. In most studies of prostate cancer, histologically malignant tissue is chosen as the experimental class while normal appearing prostate tissue adjacent to the tumor (adjacent normal) is chosen as the baseline against which comparison is made. However, normal appearing prostate tissue from tumor free organ donors represents an alterative source of baseline tissue for differential expression studies. METHODS: To examine the effect of using donor normal tissue as opposed to adjacent normal tissue as a baseline for prostate cancer expression studies, we compared, using oligonucleotide microarrays, the expression profiles of primary prostate cancer (tumor), adjacent normal tissue and normal tissue from tumor free donors. RESULTS: Statistical analysis using Significance Analysis of Microarrays (SAM) demonstrates the presence of unique gene expression profiles for each of these specimen classes. The tumor v donor expression profile was more extensive that the tumor v adjacent normal profile. The differentially expressed gene lists from tumor v donor, tumor v adjacent normal and adjacent normal v donor comparisons were examined to identify regulated genes. When donors were used as the baseline, similar genes are highly regulated in both tumor and adjacent normal tissue. Significantly, both tumor and adjacent normal tissue exhibit significant up regulation of proliferation related genes including transcription factors, signal transducers and growth regulators compared to donor tissue. These genes were not picked up in a direct comparison of tumor and adjacent normal tissues. CONCLUSIONS: The up-regulation of these gene types in both tissue types is an unexpected finding and suggests that normal appearing prostate tissue can undergo genetic changes in response to or in expectation of morphologic cancer. A possible field effect surrounding prostate cancers and the implications of these findings for characterizing gene expression changes in prostate tumors are discussed.

Adult↗

PubMed1975

The possible role of transurethral resection in the dissemination of prostatic cancer.

Prostatic carcinoma often reveals two different forms of tumour growth: (1) vigorous, almost therapy-resistant local growth, with absent or very slow metastasis (group 1), and (2) slight local growth responsive to therapy, combined however with swiftly forming distant metastasis (group 2). Two groups of such patients were examined in relation to primary findings and clinical course. Two factors were found in which they markedly differ. (1) The histological findings: in group 1 significantly more mature cancer forms appeared. (2) TREATMENT: a strikingly higher number of transurethral resections were performed upon in group 2 patient. The difference in the clinical development of prostatic cancer seems to be due to variations in the biology (as yet unknown) but may be partly to operative interference.

Adenocarcinoma↗

PubMed2005

Can we prevent prostate cancer? Rationale and current status of prostate cancer chemoprevention.

Prostate cancer has been one of the most frequent cancers among men in Western countries for the past decade. Investigation of prostate cancer prevention is very attractive, because prostate cancer has a high incidence, long-term natural history, regional difference in incidence, and is effected by sex steroids. Chemoprevention is defined as the use of specific agents to suppress or reverse carcinogenesis and to prevent the development of cancer. The development of chemoprevention strategies against prostate cancer would be of medical and economic importance. Basic and clinical research of chemoprevention of prostate cancer are under active investigation. This article aims to summarize and review the basic evidence and clinical trials on prostate cancer chemoprevention. Recent research has demonstrated that many agents, such as agents altering sex steroid signaling, drugs inducing antiproliferation/differentiation, retinoids, anti-inflammatory drugs, and antioxidants, could be potential preventatives for prostate cancer. Large-scale clinical trials have suggested that 5alpha-reductase inhibitor finasteride, selenium, and vitamin E can function as a chemopreventive agent. Although no definitely effective strategies of prostate cancer prevention have been identified yet, increasing evidence will provide effective and safe strategies that bring clinical benefits.

Anticarcinogenic Agents↗

PubMed1993

The prognostic value of the HNK-1 (Leu-7) antigen in prostatic cancer--an immunohistochemical study.

The anti-HNK-1 (Leu-7) monoclonal antibody (MAb) was revealed to be reactive with noncancerous and cancerous prostatic epithelial cells, although this antibody was originally found to be reactive against natural killer cells. However, the prognostic significance of HNK-1 antigen in prostatic cancer patients remains unknown. The expression of HNK-1 antigen on prostatic cancer was investigated immunohistochemically using the avidin-biotin-peroxidase complex (ABC) method with the anti-HNK-1 monoclonal antibody. Of the 52 patients with prostatic cancer, 49 patients (94%) showed reactivity to anti-HNK-1 MAb and the immunoreaction was associated with the histological differentiation of prostatic cancer. Well differentiated cancer showed the highest percentage of positively stained cancer cells and poorly differentiated cancer showed the lowest percentage. No statistically significant differences existed between groups classified by stage, although the more advanced cancers tended to have weaker reactions. The five-year survival rate and interval free of progression were then studied using the Kaplan-Meier method on 33 patients with stage D2 disease who had received endocrine therapy. The findings indicated that a high survival rate and a longer interval free of progression were associated with a higher fraction of positively stained cancer cells. In conclusion, the expression of HNK-1 antigen on prostatic cancer may be a useful prognostic factor in patients with prostatic cancer.

Adult↗

PubMed1994

Characteristics of prostate cancer detected in the American Cancer Society-National Prostate Cancer Detection Project.

The American Cancer Society-National Prostate Cancer Detection Project is a prospective, comparative study of a cohort of 2,999 men 55 to 70 years old not suspected on entry of having prostate cancer. A total of 164 prostate cancers is available from this project for analysis. A small proportion of tumors detected were advanced in terms of the clinical stage at diagnosis. Cancer detected by digital rectal examination tended to be more advanced than that found on the basis of only transrectal ultrasound or prostate specific antigen (PSA). A large proportion of patients received curative therapy involving radical prostatectomy in 67.1% and radiotherapy in 18.3%. Of 103 men presumed to have organ confined disease and treated by prostatectomy 64 (37.9%) actually had locally extensive cancer pathologically. PSA level and PSA density were associated with the detection of organ confined cancer but several advanced tumors had PSA levels in the normal range. Age referenced PSA, compared to conventional standards, demonstrated lower sensitivity to cancer with little improvement in specificity. The disease resulting from this multimodality detection effort represented a spectrum of pathological conditions. Further followup and evaluation are needed to determine whether these benefits are reflected in long-term mortality and survival experience.

Aged↗

PubMed2006

Assessing prostate cancer risk: results from the Prostate Cancer Prevention Trial.

BACKGROUND: Prostate-specific antigen (PSA) testing is the primary method used to diagnose prostate cancer in the United States. Methods to integrate other risk factors associated with prostate cancer into individualized risk prediction are needed. We used prostate biopsy data from men who participated in the Prostate Cancer Prevention Trial (PCPT) to develop a predictive model of prostate cancer. METHODS: We included 5519 men from the placebo group of the PCPT who underwent prostate biopsy, had at least one PSA measurement and a digital rectal examination (DRE) performed during the year before the biopsy, and had at least two PSA measurements performed during the 3 years before the prostate biopsy. Logistic regression was used to model the risk of prostate cancer and high-grade disease associated with age at biopsy, race, family history of prostate cancer, PSA level, PSA velocity, DRE result, and previous prostate biopsy. Risk equations were created from the estimated logistic regression models. All statistical tests were two-sided. RESULTS: A total of 1211 (21.9%) men were diagnosed with prostate cancer by prostate biopsy. Variables that predicted prostate cancer included higher PSA level, positive family history of prostate cancer, and abnormal DRE result, whereas a previous negative prostate biopsy was associated with reduced risk. Neither age at biopsy nor PSA velocity contributed independent prognostic information. Higher PSA level, abnormal DRE result, older age at biopsy, and African American race were predictive for high-grade disease (Gleason score > or =7) whereas a previous negative prostate biopsy reduced this risk. CONCLUSIONS: This predictive model allows an individualized assessment of prostate cancer risk and risk of high-grade disease for men who undergo a prostate biopsy.

Black or African American↗

PubMed2026

Subclonal Complete Loss of CDKN1B as a Common Genomic Alteration in Prostate Cancer: Associations With Race and Prostate Cancer Outcomes.

Homozygous biallelic inactivation of CDKN1B is thought to be rare in cancer, including prostate cancer. In the present study, we report that the prevalence of subclonal genomic loss of CDKN1B, especially among self-reported African-American or Black (AA) individuals, has likely been underestimated in primary prostate cancer. Using immunohistochemistry (IHC) for p27 protein and a large cohort of whole tissue sections from radical prostatectomy (N = 412) from AA and European American (EA) individuals, we discovered an unexpectedly high frequency of regions of intratumoral complete p27 protein loss (IPPL) within larger tumor nodules that otherwise showed intact p27 staining that was more prevalent among prostate cancer in AA individuals (18.1%) than EA individuals (12.2%). Regions of IPPL were tightly associated with loss of CDKN1B messenger RNA by in situ hybridization. Furthermore, these focal regions of IPPL were closely linked to CDKN1B genomic loss as detected by next-generation sequencing panel sequencing of laser-captured regions. The detection of IPPL by IHC was associated with ≥pT3 pathologic stage (extraprostatic extension and seminal vesicle involvement) and pN1 (local lymph node involvement) disease; however, when stratified by race, these associations were only significant among AA participants. IPPL was further associated in both univariate and multivariate analyses with the development of biochemical recurrence and metastasis after primary treatment, specifically in AA individuals. The prevalence of p27 genomic alterations in metastatic disease is higher than that of primary prostate cancer in publicly available data sets as well as in our analysis of autopsy specimens via IHC. Overall, subclonal biallelic loss of CDKN1B resulting in complete p27 protein loss is one of the most commonly occurring biallelic tumor suppressor genomic alterations in primary prostate cancer and could contribute to worse prostate cancer outcomes, specifically in AA individuals. Our findings warrant further exploration into the clinical utility of using IHC for p27 loss as a prognostic biomarker.

CDKN1B cancer disparities↗

PubMedDate not supplied

The benefit and cost of prostate cancer early detection. The Investigators of the American Cancer Society-National Prostate Cancer Detection Project.

Cost-effectiveness calculations of prostate cancer early detection have not been possible due to the lack of any data demonstrating reduction in mortality from any test or procedure. Prior analyses focused only on cost assessments without consideration of any possible benefits. We used current data from three consecutive years of the American Cancer Society-National Prostate Cancer Detection Project to assess different economic perspectives of test performance, marginal costs, and benefit-cost analysis. The marginal cost, or cost per cancer, of digital rectal examination (DRE) markedly increased by the third year relative to several proposed prostate-specific antigen (PSA) scenarios. Sensitivity analysis for average cost showed that at 4 ng/ml, pricing PSA below $30 would be the most potent factor in potentially lowering costs. Analysis of receiver operator characteristic curves suggested that optimal performance for PSA may be at 3 ng/ml when combined with DRE or between 2 to 3 ng/ml when used alone. Benefit-cost calculations demonstrated that DRE when performed by highly skilled examiners had the lowest cost. However, DRE became one of the most costly detection scenarios when a minor decrease in performance was assumed. Sensitivity analysis demonstrated that the three most determinant parameters of net benefit, in decreasing order, are: specificity, benefits from earlier therapy, and prevalence. If a slightly more specific PSA assay is developed, the higher prevalence of clinically detectable prostate cancer could also make screening less costly than breast cancer screening. Under the assumptions of these analyses, the combination of PSA and DRE appears to represent an ethical and economical detection choice for individual patients in consultation with their physicians. Additional research is needed to quantify the significance of differences between different screening strategies.

American Cancer Society↗

PubMed1996

Prostate specific antigen in the diagnosis and staging of prostate cancer.

Prostate Specific Antigen (PSA) has revolutionized our approach to managing patients with an established diagnosis of cancer of the prostate (CaP). Moreover, its use in early detection and screening has resulted in the most sensitive method of detecting CaP. Furthermore it is regarded as the most important tumour marker in tumour biology. This article will discuss some important advances in the application of PSA.

Aged↗

PubMed2002

Methylation and inactivation of estrogen, progesterone, and androgen receptors in prostate cancer.

BACKGROUND: Prostate cancer development is initially steroid hormone dependent. Estrogen receptors (ERs), androgen receptors (ARs), and progesterone receptors (PRs) have been identified in normal and cancerous prostate tissues. We investigated whether the promoter regions of these steroid receptor genes are methylated and inactivated in prostate cancer cells and tissues. METHODS: The expression and promoter methylation status of three ERalpha isoforms (ERalpha-A, ERalpha-B, and ERalpha-C), ERbeta, two PR isoforms (PR-A and PR-B), and AR were investigated in five prostate cancer cell lines (ND1, DU145, PC3, LNCaP, and DUPro) and in pairs of normal and cancerous prostate tissues from 38 patients with prostate cancer. Methylation-specific polymerase chain reaction, reverse transcription--polymerase chain reaction, and 5' rapid amplification of complementary DNA ends were used. All statistical tests were two-sided. RESULTS: ERalpha-C was expressed in all cell lines, but ERalpha-A and ERalpha-B were not expressed in any cell line. ERalpha-A and ERalpha-B promoters were methylated, but ERalpha-C was unmethylated. Promoters for ERbeta, AR, PR-A, and PR-B were methylated and thus inactivated in some cell lines but not in others. Treating cells with the demethylating reagent 5-aza-2'-deoxycytidine restored expression of all steroid receptor genes with previously methylated promoters. All 38 pairs of cancer and normal tissues had unmethylated ERalpha-C promoters. Thirty-six (95%) of 38 cancers had methylated ERalpha-A, 35 (92%) of 38 cancers had methylated ERalpha-B, but all normal tissues had unmethylated ERalpha-A and ERalpha-B (both P<.001). ERbeta was methylated in 30 (79%) of 38 cancers but unmethylated in all normal tissues. AR was methylated in three (8%) of 38 cancers but unmethylated in all normal tissues. PR-A and PR-B were unmethylated in all tissues. CONCLUSION: Certain steroid receptor genes appear to be inactivated by CpG methylation in prostate cancer tissue and cell lines.

DNA Methylation↗

PubMed1995

Immunohistochemical study of HNK-1 (Leu-7) antigen in prostate cancer and its clinical significance.

Anti-HNK-1 monoclonal antibody (MAb) was reactive with non-cancerous and cancerous prostatic epithelia, as well as natural killer cells, myelinated nerves and cells from APUD systems. The expression of HNK-1 antigen on prostate cancer was investigated immunohistochemically by avidinbiotin-peroxidase complex (ABC) method with anti-HNK-1 MAb to clarify the relationship between anti-HNK-1 immunostaining of the cancerous tissue and the tumor differentiation, and that between the former and the survival rate of patients. Of 52 patients with prostate cancer, 49 were reactive with anti-HNK-1 MAb, the positive rate being 94%. The well differentiated cancer showed the highest percentage of positive cancer cells and the strongest staining, while the poorly differentiated cancer had the lowest percentage of positive cancer cells and the weakest staining. HNK-1 antigen was highly expressed on prostate cancer, and the better differentiated the cancer, the more HNK-1 antigen expressed. We also analyzed the total 5-year survival rate of the 52 patients, and the average 5-year survival rate and non-progression rate of 32 patients in stage D2 who had received only endocrinotherapy. Significantly higher survival rate and non-progression rate were observed in the group with more than two-thirds positive cancer cells as compared with the group with less than two-thirds positive cancer cells. The results suggest that the expression of HNK-1 antigen on prostate cancer may be a useful prognostic factor for patients with prostate cancer.

Adenocarcinoma↗

PubMed1999

Prostate cancer risk assessment program. A model for the early detection of prostate cancer.

Prostate cancer is the most common form of cancer (except skin cancer) in men. Several factors have been associated with an increased risk for prostate cancer, including age, ethnicity, family history, lifestyle, and environmental exposures. Recognition of the importance of the interaction of these factors in prostate cancer has led to an interest in their evaluation as a model both for studying genetic susceptibility patterns and for studying and providing educational tools and preventive interventions. One such model has been developed at Fox Chase Cancer Center. Critical to the implementation of the model has been the establishment of the Prostate Cancer Risk Registry (PCRR) and Prostate Cancer Risk Assessment Program (PRAP). Together, they serve as a unique resource for investigating the interaction between environmental factors and genetic susceptibility patterns; exploring the early, premalignant biological markers of prostate cancer; and prospectively assessing the quality of life (QOL) of men at risk. In addition, PRAP facilitates the evaluation of models for prostate cancer risk counseling and screening in the community. This paper describes this model for early detection and risk reduction, along with preliminary data from its first two study aims. The program is particularly relevant in view of the wealth of genetic information emerging from the Human Genome Project.

Humans↗

PubMed1999

[Intra-arterial chemotherapy in combination with radiotherapy for invasive bladder cancer and prostate cancer].

Forty-five patients with muscle-invasive bladder cancer treated with intra-arterial doxorubicin chemotherapy plus low-dose radiotherapy between September 1979 and March 1990 were retrospectively studied. Twenty-eight (62%) patients achieved a complete response (CR) and in all of them, a functional bladder could be preserved. The 10-year cause-specific survival rate of patients with CR was 95.5%, but that of patients not achieving a CR was 39%. These results demonstrate that in patients who achieve a CR with this treatment, we may be able to preserve a functional bladder. In a prospective study, we designed a new intra-arterial chemotherapy regimen in order to achieve a higher degree of effectiveness and to preserve a functional bladder. Twenty-three patients were treated with concurrent pirarubicin/cisplatin intra-arterial chemotherapy and radiotherapy after complete transurethral resection. Twenty-one (91%) patients achieved CR. One of these patients had relapse with lung metastases and was treated surgically. Two patients who did not achieve a CR died of cancer, and 21 patients are alive with preservation of functional bladder. For treatment of prostate cancer, we now administer only adjuvant intra-arterial chemotherapy plus irradiation for patients after radical prostatectomy.

Adult↗

PubMed2006

Does incidence of breast cancer and prostate cancer decrease with increasing degree of visual impairment.

OBJECTIVE: The issue of light at night and cancer continuously attracts discussion. The major hypotheses are that melatonin may decrease risk of hormone-related cancers, particularly breast cancer, or even act as a potent antioxidant and thus have a protective effect against cancer development in general. METHODS: We tested the hypothesis that blind persons are at lower risk of cancer in a follow-up study linking a cohort of 17,557 persons with visual impairment identified from the Finnish Register of Visual Impairment with cancer incidence data of the Finnish Cancer Registry for years 1983-2003. RESULTS: Breast cancer risk in females decreased by degree of visual impairment, and a similar but less consistent trend was observed for prostate cancer in males. The incidence for the remaining cancers among nearly to totally blind persons was significantly higher than in average Finnish population. CONCLUSIONS: Our findings add to the suggestive epidemiological evidence for a decreased risk of hormone-related cancers in people with visual impairment and, consequently, a relationship between visible light at night and breast cancer risk. The result is strongly against the hypothesis of a systemic protective effect related lack of visible light.

Blindness↗

PubMedDate not supplied

Immunotherapy for prostate cancer using prostatic acid phosphatase loaded antigen presenting cells.

Dendritic cells from patients with cancer are deficient in number and functional activity, leading to inadequate tumor immunosurveillance as a result of poor induction of T-cell antitumor responses. Loaded dendritic cell therapy is a vaccination strategy aimed at eliciting tumor antigen-specific, T-cell immune responses. Loaded dendritic cell therapy using prostatic acid phosphatase (APC8015; Provenge, Dendreon Corp., Seattle, WA) as an immunogen has shown a survival benefit in patients with metastatic hormone-refractory prostate cancer in a randomized phase III trial. This review will summarize the prostate cancer clinical trials using APC8015 and discuss the potential future role of APC8015 in prostate cancer treatment.

Acid Phosphatase↗

PubMed2000

Health outcomes after prostatectomy or radiotherapy for prostate cancer: results from the Prostate Cancer Outcomes Study.

BACKGROUND: Radical prostatectomy and external beam radiotherapy are the two major therapeutic options for treating clinically localized prostate cancer. Because survival is often favorable regardless of therapy, treatment decisions may depend on other therapy-specific health outcomes. In this study, we compared the effects of two treatments on urinary, bowel, and sexual functions and on general health-related quality-of-life outcomes over a 2-year period following initial treatment. METHODS: A diverse cohort of patients aged 55-74 years who were newly diagnosed with clinically localized prostate cancer and received either radical prostatectomy (n = 1156) or external beam radiotherapy (n = 435) were included in this study. A propensity score was used to balance the two treatment groups because they differed in some baseline characteristics. This score was used in multivariable cross-sectional and longitudinal regression analyses comparing the treatment groups. All statistical tests were two-sided. RESULTS: Almost 2 years after treatment, men receiving radical prostatectomy were more likely than men receiving radiotherapy to be incontinent (9.6% versus 3.5%; P:<.001) and to have higher rates of impotence (79.6% versus 61.5%; P:<.001), although large, statistically significant declines in sexual function were observed in both treatment groups. In contrast, men receiving radiotherapy reported greater declines in bowel function than did men receiving radical prostatectomy. All of these differences remained after adjustments for propensity score. The treatment groups were similar in terms of general health-related quality of life. CONCLUSIONS: There are important differences in urinary, bowel, and sexual functions over 2 years after different treatments for clinically localized prostate cancer. In contrast to previous reports, these outcome differences reflect treatment delivered to a heterogeneous group of patients in diverse health care settings. These results provide comprehensive and representative information about long-term treatment complications to help guide and inform patients and clinicians about prostate cancer treatment decisions.

Aged↗

PubMed1993

Characterization of human prostate cancer, benign prostatic hyperplasia and normal prostate by in vitro 1H and 31P magnetic resonance spectroscopy.

In vitro 1H and 31P magnetic resonance spectra were acquired from perchloric acid extracts of human prostate tissue obtained by transurethral resection. This included tissue of patients with benign prostatic hyperplasia and prostatic adenocarcinoma; one tissue sample was obtained from a patient without any sign of BPH or malignancy. Major resonances in the magnetic resonance spectra were assigned to prostate compounds and were quantified. The citrate/lactate, citrate/total choline, phosphocholine/total creatinine, choline/total creatine, alanine/total creatine, phosphoethanolamine/total phosphate, phosphocholine/total phosphate and glycerophosphoethanolamine/total phosphate ratios were statistically different for the prostate cancer samples as compared with the BPH specimens. These observations may contribute to the understanding of in vivo magnetic resonance spectra of the prostate and indicate that magnetic resonance spectroscopy can aid in the diagnosis of prostate malignancy.

Adenocarcinoma↗

PubMed1991

Characterization of prostate cancer, benign prostatic hyperplasia and normal prostates using transrectal 31phosphorus magnetic resonance spectroscopy: a preliminary report.

We assessed the ability of 31phosphorus (31P) transrectal magnetic resonance spectroscopy to characterize normal human prostates as well as prostates with benign and malignant neoplasms. With a transrectal probe that we devised for surface coil spectroscopy we studied 15 individuals with normal (5), benign hyperplastic (4) and malignant (6) prostates. Digital rectal examination, transrectal ultrasonography and magnetic resonance imaging were used to aid in accurate positioning of the transrectal probe against the region of interest within the prostate. The major findings of the in vivo studies were that normal prostates had phosphocreatine-to-adenosine triphosphate (ATP) ratios of 1.2 +/- 0.2, phosphomonoester-to-beta-ATP ratios of 1.1 +/- 0.1 and phosphomonoester-to-phosphocreatine ratios of 0.9 +/- 0.1. Malignant prostates had phosphocreatine-to-beta-ATP ratios that were lower (0.7 +/- 0.1) than those of normal prostates (p less than 0.02) or prostates with benign hyperplasia (1.1 +/- 0.2, p less than 0.01). Malignant prostates had phosphomonoester-to-beta-ATP ratios (1.8 +/- 0.2) that were higher than that of normal prostates (p less than 0.02). Using the phosphomonoester-to-phosphocreatine ratio, it was possible to differentiate metabolically malignant (2.7 +/- 0.3) from normal prostates (p less than 0.001), with no overlap of individual ratios. The mean phosphomonoester-to-phosphocreatine ratio (1.5 +/- 0.5) of prostates with benign hyperplasia was midway between the normal and malignant ratios, and there was overlap between individual phosphomonoester-to-phosphocreatine ratios of benign prostatic hyperplasia glands with that of normal and malignant glands. To verify the in vivo results, we performed high resolution magnetic resonance spectroscopy on perchloric acid extracts of benign prostatic hyperplasia tissue obtained at operation and on a human prostatic cancer cell line DU145. The extract results confirmed the differences in metabolite ratios observed in vivo. We conclude that transrectal 31P magnetic resonance spectroscopy can characterize metabolic differences between the normal and malignant prostate.

Adult↗