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PubMed1996

Epidemiology, prevention and screening for prostate cancer.

Prostate cancer is a growing social problem. The economical impact is high and is likely to become greater in future years, not only because the number of patients diagnosed with prostatic neoplasias is increasing steadily, but also because of the promotion of screening programmes and the rise in the number of surgical procedures available. It can be concluded that, at the present stage, widespread implementation of screening cannot be recommended. The answer to the question of screening can only be provided by large randomised trials, comparing either screening versus no screening, or early versus delayed treatment in patients in whom early cancer is detected by screening.

Cost-Benefit Analysis↗
PubMed1996

A heterogeneous pattern of progression in endocrine-treated patients with prostate cancer.

Prostatic carcinoma often shows different behavior in the primary site than in the metastases after endocrine treatment. The pattern of disease progression was evaluated in prostate cancer patients. Two hundred and sixty consecutive patients were observed following the initiation of endocrine treatment (11 patients with stage T1 disease, 42 with stage T2 70 with stage T3, 11 with N + M0 and 126 with stage M1 disease). Of the 117 patients whose disease progressed, 100 could be evaluated in terms of the pattern of disease progression. Twenty-two (64.7%) of the 34 patients with stage T1-3N0M0 showed a pattern of local progression. On the other hand, 56 (84.8%) of the 66 patients with stage N + or M1 experienced a pattern of distant progression. Patients with only distant progression numbered 36 cases and patients with local progression and distant progression numbered 20 cases. Most of the distant progressions appeared in bone site. Local progression was observed in only 30 (45.5%) patients with stage N + or M1 disease. In patients with localized disease (T1-3N0M0), both the interval to disease progression and the time to cancer death from the start of disease progression were significantly longer than those of patients with stage N + or M1. However, once bone metastasis occurred, the disease tended to progress rapidly. There was no significant difference between the interval to cancer death after the appearance of bone metastasis in patients with initially localized stages (T1-3N0M0) and the time to cancer death after disease progression in patients with metastatic disease (N + or M1). The study shows a heterogenous behavior of the prostatic tumor after endocrine treatment. This suggests that metastases and primary tumor have different clonal compositions. The study also supports the idea that there is a preferential environment for the growth of prostatic carcinoma cells in bone sites.

Aged↗
PubMed2002

Catechol estrogen metabolites and conjugates in different regions of the prostate of Noble rats treated with 4-hydroxyestradiol: implications for estrogen-induced initiation of prostate cancer.

Prostate carcinomas arise in 100% of Noble rats treated with estradiol and testosterone. We hypothesize that estrogens initiate prostate cancer mainly by formation of 4-catechol estrogens (CE), followed by their oxidation to catechol estrogen-3,4-quinones (CE-3,4-Q), which can react with DNA. To avoid cancer initiation, CE can be detoxified by catechol-O-methyltransferase (COMT), and CE-3,4-Q by conjugation with glutathione (GSH) or by reduction to CE, catalyzed by quinone reductase and/or cytochrome P450 reductase. To investigate the prostatic metabolism of estrogens, Noble rats were treated with the CE 4-hydroxyestradiol (4-OHE2) or estradiol-3,4-quinone (E2-3,4-Q), and CE metabolites and conjugates were analyzed in the four regions of the prostate, which differ in susceptibility to carcinoma formation. Following treatment of rats with 4-OHE2 (6 micromol/100 g body weight in 200 microl of trioctanoin/dimethylsulfoxide (4:1) by intraperitoneal injection) for 90 min, the non-susceptible ventral (VP) and anterior (AP) prostate had higher levels of 4-methoxyCE and GSH conjugates than the susceptible dorsolateral prostate (DLP) and periurethral prostate (PUP). After treatment with the same molar amount of E2-3,4-Q, the VP and AP contained more GSH conjugates, 4-CE and 4-methoxyCE than the susceptible DLP and PUP. These results suggest that prostate areas susceptible to carcinoma induction have less protection by COMT, GSH, and quinone reductase and/or cytochrome P450 reductase, favoring reaction of CE-3,4-Q with DNA, presumably to initiate cancer.

Animals↗
PubMed1987

Prostatic intra-epithelial neoplasia and early invasion in prostate cancer.

Prostatic intra-epithelial neoplasia (PIN, or intraductal dysplasia) is considered a precursor of invasive carcinoma, characterized by proliferation and anaplasia of cells lining prostatic ducts and acini. The highest grade of PIN, Grade 3, is thought to represent carcinoma in situ. To quantitate the degree of disruption of the basal cell layer in human prostatic ducts and acini as a potential marker of early invasion in PIN, a monoclonal antibody to keratin proteins of 49, 51, 57, and 66 kd which selectively labels the prostatic basal cell layer was used. A total of 1093 acini with PIN were identified in 14 cases with invasive carcinoma. Tumor cells consistently failed to be decorated with this antibody. The frequency of disruption of the basal cell layer increased with increasing grades of PIN, with disruption present in 0.7% of cases of PIN 1, 15% of cases of PIN 2, and 56% of cases of PIN 3. The amount of disruption of the basal cell layer also increased with increasing grades of PIN, with loss of more than one third of the basal layer in 52% of foci of PIN 3 compared with less than 2% in lower grades of PIN. Disruption of the basal layer was more common in acini adjacent to invasive carcinoma than in distant acini. These findings suggest that early invasion in prostate cancer is characterized by disruption of the basal layer, and that invasion occurs commonly in association with foci of high-grade prostatic intra-epithelial neoplasia.

Antibodies, Monoclonal↗
PubMed1991

Pathologic changes associated with androgen deprivation therapy for prostate cancer.

Prostate glands exposed to androgen deprivation with leuprolide +/- flutamide were evaluated for pathologic changes which might be related to therapy. Comparing pretreatment and posttreatment tissue by visual discrimination using light microscopic study revealed treatment-related alterations in the size and distribution of neoplastic glands in 60% of cases. Quantitative measurements documented glandular changes in an even greater percentage of cases. Although distinctive, the histologic pattern was not specific for leuprolide/flutamide. The absence of appreciable degeneration and necrosis in tumor cells suggests that this type of androgen deprivation may act through suppression rather than ablation of prostatic cancers. The relationship between treatment-related histologic effects and initial tumor grade and clinical stage as well as expression of prostate-specific antigen was studied. Accurate histologic assessment of leuprolide/flutamide-treated prostate glands should not be a problem so long as specimens are thoroughly examined and drug-related variations in tumor morphologic features are appreciated.

Aged↗
PubMedDate not supplied

Brachytherapy for clinically localized prostate cancer.

Prostate brachytherapy is an effective treatment option for clinically organ-confined prostate carcinoma. Observed 5- and 10-year follow-up have documented prostate-specific antigen (PSA) levels that were comparable to published radical prostatectomy series and were better than several published external-beam radiation series. Between January 1987 and June 1988, a total of 152 consecutive patients with Stage T1 to T3 low to high Gleason grade prostate cancer were studied at Northwest Hospital in Seattle, Washington. Patients' median age was 70 years (range, 53 to 92 years). All patients received Iodine-125 prostate brachytherapy with or without a 45 Gy dose of external-beam radiation. The average preoperative PSA, clinical stage, and prostate needle biopsy Gleason sum were 11 ng/ml, T2, and (5), respectively, and were known in all but five patients. PSA follow-up, clinical examination, and biopsy results judged disease-free survival at 5 and 10 postoperative years. Elevation of PSA above 0.5 ng/ml or a positive biopsy or a positive bone scan was considered treatment failure. The authors provide an historical review of prostate brachytherapy in conjunction with up-to-date implant techniques and long-term outcome results.

Aged↗
PubMed2005

Bone microenvironment modulates expression and activity of cathepsin B in prostate cancer.

Prostate cancers metastasize to bone leading to osteolysis. Here we assessed proteolysis of DQ-collagen I (a bone matrix protein) and, for comparison, DQ-collagen IV, by living human prostate carcinoma cells in vitro. Both collagens were degraded, and this degradation was reduced by inhibitors of matrix metallo, serine, and cysteine proteases. Because secretion of the cysteine protease cathepsin B is increased in human breast fibroblasts grown on collagen I gels, we analyzed cathepsin B levels and secretion in prostate cells grown on collagen I gels. Levels and secretion were increased only in DU145 cells--cells that expressed the highest baseline levels of cathepsin B. Secretion of cathepsin B was also elevated in DU145 cells grown in vitro on human bone fragments. We further investigated the effect of the bone microenvironment on cathepsin B expression and activity in vivo in a SCID-human model of prostate bone metastasis. High levels of cathepsin B protein and activity were found in DU145, PC3, and LNCaP bone tumors, although the PC3 and LNCaP cells had exhibited low cathepsin B expression in vitro. Our results suggest that tumor-stromal interactions in the context of the bone microenvironment can modulate the expression of the cysteine protease cathepsin B.

Animals↗
PubMed2004

Gene expression profiling identifies clinically relevant subtypes of prostate cancer.

Prostate cancer, a leading cause of cancer death, displays a broad range of clinical behavior from relatively indolent to aggressive metastatic disease. To explore potential molecular variation underlying this clinical heterogeneity, we profiled gene expression in 62 primary prostate tumors, as well as 41 normal prostate specimens and nine lymph node metastases, using cDNA microarrays containing approximately 26,000 genes. Unsupervised hierarchical clustering readily distinguished tumors from normal samples, and further identified three subclasses of prostate tumors based on distinct patterns of gene expression. High-grade and advanced stage tumors, as well as tumors associated with recurrence, were disproportionately represented among two of the three subtypes, one of which also included most lymph node metastases. To further characterize the clinical relevance of tumor subtypes, we evaluated as surrogate markers two genes differentially expressed among tumor subgroups by using immunohistochemistry on tissue microarrays representing an independent set of 225 prostate tumors. Positive staining for MUC1, a gene highly expressed in the subgroups with "aggressive" clinicopathological features, was associated with an elevated risk of recurrence (P = 0.003), whereas strong staining for AZGP1, a gene highly expressed in the other subgroup, was associated with a decreased risk of recurrence (P = 0.0008). In multivariate analysis, MUC1 and AZGP1 staining were strong predictors of tumor recurrence independent of tumor grade, stage, and preoperative prostate-specific antigen levels. Our results suggest that prostate tumors can be usefully classified according to their gene expression patterns, and these tumor subtypes may provide a basis for improved prognostication and treatment stratification.

Biomarkers, Tumor↗
PubMed1992

Tumor markers in prostate cancer.

Prostatic specific antigen (PSA) is a tissue specific marker that is now the most widely used biochemical test for the assessment and follow-up of prostate cancer. The levels of PSA rise with tumor stage, but there is considerable overlap of their distribution between stages. PSA measurement now forms a part of the workup of a suspected carcinoma of the prostate, with a level of more than 4 ng/ml being an indication for further investigation. The sensitivity of PSA makes it an essential test for the postoperative assessment of radical prostatectomy and curative radiation therapy. The rates of change of PSA levels in locally advanced and metastatic disease treated by hormone manipulation can provide prognostic information. Low levels of PSA (less than 10 ng/ml) 6 months after treatment are a sign that the response will be prolonged. However, the sensitivity of PSA often results in a rising level preceding clinical evidence of progression by several months and is not necessarily an indication to change treatment. Alkaline phosphatase and prostatic acid phosphatase provide a less sensitive test for the bone response to skeletal metastases and tumor activity in advanced disease, respectively.

Acid Phosphatase↗
PubMed1994

[Early diagnosis of prostatic cancer].

Prostate cancer is the most common neoplasia in males and, since it is curable only when detected in the early stages, it was estimated that screening would detect tumours in curable stages which would enhance the results in the fight against the disease. This, however, has not been elucidated since the condition's natural history in many cases unknown and it may be that unnecessary and iatrogenic overtreatment is being induced. The paper analyzes the various tests and diagnostic procedures available, primarily digital rectal examination, PSA determination, and transrectal ultrasound all used individually and in combination. Several unknown aspects await to be answered and many long-term studies continue to be necessary to explain whether early diagnosis of asymptomatic disease and subsequent treatment can improve life expectancy and quality of life as compared to plain treatment of symptomatic cases. We hope the answer will be available shortly and that we are "able to diagnose cancer in time but treat it only when we know it is required.

Costs and Cost Analysis↗
PubMed2006

PTEN and GSK3beta: key regulators of progression to androgen-independent prostate cancer.

Prostate cancer (PrCa) is characterized by progression from an androgen-dependent phenotype to one that is inevitably androgen independent (AI) and lethal. Recent evidence strongly suggests that the phosphatidylinositol-3-kinase/Akt (PI3K/Akt) and androgen receptor (AR) signalling pathways provide prostatic epithelium with the necessary signalling events to escape the apoptotic response associated with androgen withdrawal therapy. Silencing of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) and glycogen synthase kinase beta (GSK3beta) are frequently associated with advanced PrCa systems and likely serve critical roles in promoting AR and PI3K/Akt gain-of-function. That PTEN negatively regulates AR and is sufficient to promote metastatic PrCa in murine models strongly implies its role as a gatekeeper of progressive PrCa. In human PrCa, PTEN loss is correlated with substantial increases in Akt(Ser473) and integrin-linked kinase expression, both of which promote Ser(9) phospho-inhibition of GSK3beta and inactivation of apoptotic factors. Sufficient evidence also suggests that GSK3beta is not only a critical regulator of proproliferative signalling but also a promiscuous one as PI3K/Akt pools of GSK3beta are, at least in part, functionally interchangeable with those of the Wnt/beta-catenin pathway. Thus, GSK3beta may serve not only as a mediator of PI3K/Akt activation but may also regulate the potent transactivation and proproliferative effects that Wnt3a and beta-catenin confer upon AR. These data suggest that prostate-specific activation of GSK3beta may serve as a viable pharmacological option. Thus, in this review, we emphasize that temporal changes in GSK3beta and PTEN expression during progression to AI PrCa are important factors when considering the potential for therapies targeting the oncogenic contributions of PI3K/Akt and AR signalling pathways.

Androgens↗
PubMed2005

A novel component of the ubiquitin pathway, ubiquitin carboxyl extension protein 1 is overexpressed in prostate cancer.

Prostate cancer is among the most common tumors in industrialized nations. However, little is known about the molecular events underlying its development. In the present study we used suppressive subtraction hybridization (SSH) in combination with laser-assisted microdissection in order to compare gene expression between prostate carcinoma and the normal prostate proper. Both are mixed tissues which consist of an epithelial and a stromal compartment. We first compared mRNA (cDNA) expression by SSH and then used real-time quantitative RT-PCR analysis of microdissected tissue probes in order to verify differential expression of subtracted cDNA clones. We also used differentially expressed cDNAs for the synthesis of radiolabelled riboprobes in order to attribute differential expression to specific cell types in tissue sections by in situ hybridization. Using this approach we found an up-regulation of ubiquitin carboxyl extension protein 1 (UBCEP-1) mRNA in prostate carcinoma cells compared to the normal glandular epithelium of the prostate proper. UBCEP-1 mediated ubiquitin chain elongation may promote prostate carcinoma development by increasing via the proteasome pathway the degradation of proteins which are involved in growth inhibition or apoptosis.

Aged↗
PubMed1991

Multiple marker evaluation in prostatic cancer with prostatic acid phosphatase, gamma-seminoprotein and prostate-specific antigen.

Serum prostatic acid phosphatase (PAP), gamma-seminoprotein (gamma-Sm), and prostate-specific antigen (PA) levels were measured in 63 untreated patients with prostatic cancer. The sensitivities of PAP, gamma-Sm, and PA as markers of malignancy were 68%, 83%, and 77%, respectively. The latter two markers were more sensitive than PAP, especially in stage B disease. The specificities of PAP, gamma-Sm, and PA were 95%, 93%, and 93%, respectively. Patients with multiple positive markers were very likely to have prostatic cancer. In reactivation of the disease, positive rates for gamma-Sm and PA were higher than for PAP, indicating that the former two markers are more reliable for monitoring prostatic cancer.

Acid Phosphatase↗
PubMedDate not supplied

Role of dietary modification and vitamins in prostate cancer.

Prostate cancer incidence and nutrition are closely connected and show large food-related differences. Lowest cancer incidence in Asian countries is observed under low-calorie, soy-based food. Mediterranean nutrition has cancer protective components (fruit, vegetables, oil, seafood). The highest cancer incidence in the United States goes along with high-calorie food, red meat and fat ingestion. Changes in lifestyle and nutrition can influence the cancer risk. Dietary supplements and vitamins are in wide use and part of a complementary and alternative medicine.

Diet↗
PubMed1989

Multiple marker evaluation in prostatic cancer using prostatic specific antigen, gamma-seminoprotein and prostatic acid phosphatase.

Serum prostatic specific antigen (PA), gamma-seminoprotein (gamma-Sm) and prostatic acid phosphatase (PAP) were evaluated in 141 patients with prostatic cancer, 121 of whom were newly diagnosed. Of the 121 untreated patients, 77, 71 and 67% were detectable by the PA, gamma-Sm and PAP markers, respectively. PA was equally or more sensitive in all stages than the other two markers. Using the benign prostatic hypertrophy group (131 patients) as a negative control, the specificities of PA, gamma-Sm and PAP were 89, 76 and 83%, respectively. Combination of PA, gamma-Sm and PAP increased sensitivity to 86%, especially in localized disease (stages A, B and C) to 74%, but did not improve specificity (67%) or efficiency (76%). During the follow-up period of 1-53 months, 24 of 141 patients with prostatic cancer had disease progression. All serial levels of gamma-Sm, PA, and PAP were positive in 17, 12 and 10 of the 24 patients within 6 months prior to detectable disease progression. gamma-Sm appeared to be more sensitive than the other two markers for early detection of disease progression. These results suggest that PA and gamma-Sm are reliable markers for detection and monitoring of prostatic cancer.

Acid Phosphatase↗
PubMed2005

[Selection criteria for the expected management of localised prostate cancer].

Prostate cancer harbours the possibility of overtreatment more than any other malignant disease. Due to its slow growth, expected management is an established therapeutic option in newly diagnosed carcinomas. Improved diagnostic methods and the widespread use of PSA lead to earlier diagnosis of cancers that would not adversely affect the life expectancy of the patient, even when they were left untreated. Several statistical models have been published to identify such insignificant cancers; however, all such nomograms suffer from limited sensitivity and specificity. For the indication of expected management, comorbidity and life expectancy must be considered using risk scores and life tables. In general, expected management is a suitable option for elderly patients with low grade cancers. Young patients and those with intermediate or high-grade cancers are most likely to benefit from active local treatment.

Decision Support Systems, Clinical↗