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At least 343 records · Page 19Linked to original sources

PubMed1997

Basic science aspects of prostate cancer.

Prostate cancer carries significant morbidity and mortality, but its outcome is difficult to predict in the individual. Androgen ablation delays progression in men, but hormone resistance soon develops and much basic science research has focused on how prostate cancer 'escapes' hormonal control. Stem cell models of prostate development and homeostasis have been proposed, but have not yet been fully characterized. Some androgen-regulated signalling pathways and abnormalities that affect them have been defined recently. It is apparent that locally produced growth factors, often regulated by androgens, exert an effect both physiologically and pathologically and these too will be discussed.

Androgens↗

PubMedDate not supplied

[Nuclear magnetic resonance tomography in the diagnosis of prostatic cancer].

Prostatic cancer rates second among cancers occurring in males over fifty and occupies the third place among malignancies causing death. Early detection of this disease remains problematic. The authors analyze diagnostic value of NMR tomography in prostatic tumors. On NMR-tomograms prostatic cancer appears as a hypointensive focus in the peripheral prostatic zone characterized by defective intensity of the signals > 10 mm located in the craniodorsal part of the prostate. Other image characteristics are also described. NMR tomography is able of detecting metastatic involvement in the regional lymph collectors, bone destruction in the lumbosacral spine, pelvic bones. Differential diagnosis with other prostatic conditions is detailed. The results are confirmed morphologically and at target biopsies. The authors recommend to use NMR tomography in clinical manifestations of the tumor and negative histological findings.

Biopsy, Needle↗

PubMed2003

The role of vitamin D in prostate cancer.

Prostate cancer (PCa) cells harbor receptors for vitamin D (VDR) as well as androgens (AR). 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] increases AR expression and enhances androgen actions linking the two receptor systems. 1,25(OH)2D3 exhibits antiproliferative activity in both AR-positive and AR-negative PCa cells. Less calcemic analogs of 1,25(OH)2D3, with more antiproliferative activity, are being developed and will be more useful clinically. The mechanisms underlying differential analog activity are being investigated. In target cells, 1,25(OH)2D3 induces 24-hydroxylase, the enzyme that catalyzes its self-inactivation. Co-treatment with 24-hydroxylase inhibitors enhances the antiproliferative activity of calcitriol. Primary cultures of normal or cancer-derived prostatic epithelial cells express 1alpha-hydroxylase, the enzyme that catalyzes the synthesis of 1,25(OH)2D3, the levels being much lower in the cancer-derived cells and in PCa cell lines. This finding raises the possibility of using 25-hydroxyvitamin D3 [25(OH)D3] as a chemopreventive agent in PCa. In LNCaP human PCa cells, 1,25(OH)2D3 and its analogs exert antiproliferative activity predominantly by cell cycle arrest, but also induce apoptosis, although to a much lesser degree. Growth arrest is mediated by induction of IGF binding protein-3 (IGFBP-3), which in turn increases the expression of the cell cycle inhibitor p21, leading to growth arrest. Other actions of 1,25(OH)2D3 in PCa cells include promotion of pro-differentiation effects and inhibition of tumor cell invasion, metastasis and angiogenesis. Combination therapy with retinoids, other anticancer agents or 24-hydroxylase inhibitors augments the inhibitory activity of 1,25(OH)2D3 in PCa and provides another effective approach in PCa treatment. Small clinical trials have shown that 1,25(OH)2D3 can slow the rate of prostate specific antigen (PSA) rise in PCa patients, demonstrating proof of concept that 1,25(OH)2D3 or its analogs will be clinically effective in PCa therapy. Current research involves further investigation of the role of 1,25(OH)2D3 and its analogs for the therapy or chemoprevention of PCa.

Animals↗

PubMed2002

Cell adhesion molecules and adhesion abnormalities in prostate cancer.

Prostate cancer, the leading male cancer in Western countries, has accelerated in its incidence in the past decade. Patients with prostate cancer frequently have a poor prognosis as a result of local or distant spread of cancer. This review summarises some of the recent progress made in understanding the biology of cancer metastasis with a special emphasis on the role of cell adhesion molecules and adhesion abnormalities. The molecular and cellular function of cell adhesion molecules, their role in cancer and cancer progression, the clinical impact of these molecules, and therapeutic considerations are also discussed.

Animals↗

PubMed2004

Bicalutamide (Casodex) in the treatment of prostate cancer.

Prostate cancer is an important healthcare issue in men worldwide. With the advent of prostate-specific antigen screening and improved diagnostic techniques, prostate cancer is now being diagnosed in younger men and at earlier disease stages. As a result, patients often live with their disease for many years after diagnosis. This shift in the patient profile has focused attention to the impact of treatment on quality of life. Medical/surgical castration has traditionally been the mainstay of hormonal therapy but is associated with side effects including loss of libido and impotence. Nonsteroidal antiandrogens such as bicalutamide (Casodex) offer an effective alternative to castration with potential quality-of-life benefits. This paper reviews the evidence concerning the use of bicalutamide at all stages of the disease.

Androgen Antagonists↗

PubMed2004

Alterations in the expression of androgen receptor, wild type-epidermal growth factor receptor and a mutant epidermal growth factor receptor in human prostate cancer.

Prostatic carcinogenesis has been associated with alterations in the expression of the androgen receptor (AR) and the epidermal growth factor receptor (WT-EGFR), and over-expression of the constitutively active variant epidermal growth factor receptor (EGFRvIII). Changes in the expression of AR, WT-EGFR and EGFRvIII were evaluated in serial sections from 26 normal and 26 benign hyperplastic and 50 prostate cancer tissues using specific immunostaining techniques. The loss of AR expression in peri-epithelial stroma as prostatic tissues de-differentiated correlated strongly with the depletion of WT-EGFR and with increasing expression of the EGFRvIII in the adjacent epithelium. In contrast, changes in epithelial AR immunopositivity in these tissues correlated weakly with the changes in normal and variant EGFR levels. This is the first report correlating the changes in the expression of these three proteins in archival material from the different human prostatic tissue histotypes. The loss of expression of proteins that contribute to the regulation of prostatic homeostasis (AR and WT-EGFR) correlates strongly with the expression of a constitutively active variant EGF receptor (EGFRvIII) in human prostate cancer. These changes occur at an early stage of neoplastic transformation and may contribute to the progression of the disease to hormone independence.

Endothelium, Vascular↗

PubMed2003

Active surveillance with selective delayed intervention: a biologically nuanced approach to favorable-risk prostate cancer.

Prostate cancer is an indolent, slow-growing disease in many patients and may not pose a threat during a patient's lifetime. The challenge is to identify those patients who are not likely to experience significant progression while offering radical therapy to those who are at risk. To date, molecular markers have failed to provide sufficiently reliable predictive information to influence decision-making. The approach to favorable-risk prostate cancer described in this article uses estimation of prostate-specific antigen doubling time (PSA DT) to stratify patients according to the risk of progression. Patients who select this approach initially undergo management with active surveillance; those who have a PSA DT 10 years and 20% had a PSA DT > 100 years. The majority of patients in this study continue to undergo surveillance. The approach of active surveillance with selective delayed intervention based on PSA DT represents a practical compromise between radical therapy for all (which results in overtreatment of patients with indolent disease) and watchful waiting with palliative therapy only (which results in undertreatment of patients with aggressive disease).

Disease Progression↗

PubMed2004

Genetic alterations in prostate cancer.

Prostate cancer is the number one malignancy among men. The search for causative factors has proven to be difficult and, accordingly, treatment options for advanced prostate cancer remain limited. However, technologic breakthroughs in the fields of genetics and molecular biology have advanced our understanding of the mechanisms involved in prostate carcinogenesis. The aim of this article is to review the most recent evidence for the role of various genetic insults at specific steps in tumor formation and to suggest potential therapeutic targets.

Humans↗

PubMedDate not supplied

The management of prostate cancer.

Prostate cancer is one of the most common malignancies in westernised countries. An alarming fact is that the incidence of prostate cancer is showing an upward trend. The author discusses the anatomy and physiology, epidemiology, aetiology and management of this disease.

Aged↗

PubMed1995

Heterogeneity in intratumor distribution of p53 mutations in human prostate cancer.

Prostatic carcinoma from 65 patients have been examined for the occurrence of point mutations in the p53 tumor suppressor gene locus within the region of exons 5 to 8. Overall, only a small fraction of tumors (12.3%) was found to contain p53 mutations. No significant correlation was detected between the presence of the mutant gene and either tumor volume or histopathological grade. However, metastatic prostatic tumors are found to display a higher percentage (21.4%) of p53 mutations compared with primary adenocarcinomas (9.8%). Analysis of the topographical distribution of the p53 mutant genotype revealed two remarkable findings. First, multifocal tumors within a prostate appear to differ in harboring the mutant gene, and second, evidence is obtained for intratumor heterogeneity in the distribution of the mutant p53 allele. Together these findings appear to explain, at least in part, why there has been a wide discrepancy in the reported detection frequency of p53 mutations in prostate cancer specimens. It appears that the outcome of mutation analysis would depend not only on which tumors but also which regions of the tumors are included in the study. Furthermore, the observed heterogeneous topographical distribution of the mutation, if confirmed to be unique to prostate cancer, may have important implications in the understanding of the biology of prostate carcinogenesis.

Adenocarcinoma↗

PubMed1988

[Clinical application of MRI for urological malignancy. 3: A new trial of MRI for bladder cancer and prostatic cancer; surface coil and GD-DTPA].

We performed MRI in several recent cases of bladder cancer and prostatic cancer using a general coil or a 5-inch general purpose surface coil with or without Gd-DTPA. The surface coil improves the spacial resolution, density resolution and signal to noise ratio but reduces the field and the signal detection drops off as the depth from the surface increases. Moreover, additional time is required for patient positioning. In Gd-DTPA enhanced images of bladder cancer, the muscle layer became more distinct, and the images of tumor and bladder mucosa were enhanced, suggesting that facilitates evaluation of the extent of bladder wall invasion of the tumor. In Gd-DTPA enhanced images of prostatic cancer, the area conside to correspond to the tumor was enhanced. MRI using a surface coil and Gd-DTPA is considered to provide detailed information of bladder and prostatic cancer.

Contrast Media↗

PubMed2006

Endocrine complications of androgen-deprivation therapy in men with prostate cancer.

Prostate cancer is one of the most common cancers in men. Androgen-deprivation therapy (ADT) is often employed in the treatment of recurrent and metastatic prostate cancer. Although its use as an adjuvant therapy has resulted in improved survival in a subset of patients, ADT also results in a multitude of endocrine complications. These complications affect quality of life and sense of well-being in these men. Some of the endocrine complications of ADT such as osteoporosis, sexual dysfunction, hot flashes, gynecomastia, and adverse body composition are well-known. Recently, insulin resistance, hyperglycemia, and metabolic syndrome have emerged as metabolic complications of castration and may be responsible for increased cardiovascular mortality in this population. In this article, we provide a detailed review of the endocrine complications of ADT, touching upon management strategies where applicable.

Androgen Antagonists↗

PubMed1991

[Acid phosphatase as tumor marker of prostatic cancer].

Prostatic cancer was the first malignancy in which tumor markers could be used to follow the response to therapy or progression of the prostate cancer. The use of these tumor markers has been of significant clinical value in diagnosis and follow-up of patients. Over the years, significant technical improvements have been made on the sensitivity and specificity of the assays for prostatic acid phosphatase.

Acid Phosphatase↗

PubMed2000

Prospects for vaccination in prostate cancer.

Prostate cancer continues to be a major cause of morbidity and mortality. Surgical and medical management of the disease has improved but there is little effect upon overall survival. Novel therapies such as immunotherapy offer the potential of treating the disease by stimulating the immune system to mount a response to the cancer systemically. This review highlights the pitfalls and progress in the understanding of the role of the immune system in malignancy and also explains the theory behind prostate cancer vaccine trials.

Antigen Presentation↗

PubMed1988

[Therapy of advanced prostatic cancer].

Prostate cancer is a polyclonal tumor. There are about 70 bis 75% responders after hormone therapy among previously untreated patients in EORTC trials. Therefore 25 to 30% of the tumors are resistant to androgen. Surgical and hormonal castration show similar results. After progression under hormone therapy response can be reached with antiandrogenic therapy in 30 to 38%. All this leads to the conclusion that it is necessary to base treatment on tumor adaptation and selection. Cell clones insensitive to androgen therefore need cytostatic chemotherapy. It is not yet proofed whether polychemotherapy really shows better results than monotherapy does. Following the thesis of a polyclonal tumor, therapy of advanced prostate cancer must be based on hormone therapy and cytostatic chemotherapy. Prostate specific antigen is a marker for an early recognition of progression.

Antineoplastic Agents↗

PubMed2001

Trends in incidence of testicular cancer and prostate cancer in Denmark.

This article presents a detailed analysis of the incidence trends of testicular cancer and prostate cancer, using information from the Danish Cancer Registry in the period 1943-1996. The rate of increase of testicular cancer was about 2.6% per year. The analyses indicated that incidence was more strongly dependent on the man's birth cohort than on the calendar period. The analysis confirmed the significantly reduced incidence of testicular cancer in the 1943 cohort and suggested a levelling off in the increase in testicular cancer incidence from cohorts born after around 1963. This may imply that the great part of the recent increase in incidence has been due to a rapid increase in incidence in successive birth cohorts born in the relatively short period from 1945 to 1960. The rate of increase of prostate cancer was about 1.6% per year. The analyses indicated a stronger dependency on period than on birth cohort. The cohort parameters had very low values in the three earliest cohorts (1858-1868) and the period parameters showed a low incidence in the most recent period. The epidemiological pattern of prostate cancer incidence seems dominated by changes in diagnosis and registration and does not permit inferences about changes in causal factors.

Adult↗

PubMed2003

Genetic markers useful for distinguishing between organ-confined and locally advanced prostate cancer.

Prostate cancer is one of the most commonly diagnosed cancers and the second leading cause of cancer deaths among men in the United States. In this study, we performed comparative genomic hybridization (CGH) on 45 primary prostate adenocarcinomas to determine genetic markers that could be useful for distinguishing between organ-confined and locally advanced prostate cancer. Of these tumors, 24 were pT2 stage, 21 were pT3b; 20 had low Gleason scores (GS), 25 had high GS. The most common chromosomal alterations in all 45 tumors included losses on 8p (57.8%), 10q21-->qter (40.0%), 16q (35.6%), 11q21-->qter (28.9%), 16p (22.2%), 6q22-->24 (22.2%), 10p (20.0%), 5q31-->qter (17.8%), 6p (17.8%), 15q22-->qter (15.6%), and 17p (15.6%) as well as gains on 7cen-->p14 (20.0%), 7cen-->q22 (20.0%), and Xcen-->q21 (17.8%). Contingency table analysis showed that losses of 8p, 10q25-->qter, 6p21, 6q24-->qter, and 15q22-->qter were significantly increased in frequency (P < 0.05) with increasing stage and/or GS. A model was created following multivariate logistic regression analysis that was predictive of tumor stage in approximately 90% of the tumors studied. This model suggests that loss of 8p is the most valuable predictor of stage. These findings suggest that chromosomal regions identified in this study may be useful for distinguishing between organ-confined and locally advanced prostate tumors.

Adenocarcinoma↗

PubMed2006

Bisphenol A facilitates bypass of androgen ablation therapy in prostate cancer.

Prostatic adenocarcinomas depend on androgen for growth and survival. First line treatment of disseminated disease exploits this dependence by specifically targeting androgen receptor function. Clinical evidence has shown that androgen receptor is reactivated in recurrent tumors despite the continuance of androgen deprivation therapy. Several factors have been shown to restore androgen receptor activity under these conditions, including somatic mutation of the androgen receptor ligand-binding domain. We have shown previously that select tumor-derived mutants of the androgen receptor are receptive to activation by bisphenol A (BPA), an endocrine-disrupting compound that is leached from polycarbonate plastics and epoxy resins into the human food supply. Moreover, we have shown that BPA can promote cell cycle progression in cultured prostate cancer cells under conditions of androgen deprivation. Here, we challenged the effect of BPA on the therapeutic response in a xenograft model system of prostate cancer containing the endogenous BPA-responsive AR-T877A mutant protein. We show that after androgen deprivation, BPA enhanced both cellular proliferation rates and tumor growth. These effects were mediated, at least in part, through androgen receptor activity, as prostate-specific antigen levels rose with accelerated kinetics in BPA-exposed animals. Thus, at levels relevant to human exposure, BPA can modulate tumor cell growth and advance biochemical recurrence in tumors expressing the AR-T877A mutation.

Adenocarcinoma↗