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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

On the basis of the analysis of 156 hospitalized patients, the most important traits differentiating metastasis of various organs to the bones have been presented. It has been found that the bones are most frequently invaded by kidney cancer, somewhat less frequently by breast cancer and the bronchus cancer and markedly more rarely by cancer of other organs. The types of metastasis expansion in the bones were determined radiologically: the most frequent--osteolytic, less frequent--mixed, and the osteoplastic type (prostate cancer, gall-bladder cancer, and pancreas cancer). Metastasis is situated most often in the spine and the femur. The authors have also presented the tactics of diagnosis of metastasis by using data from anamnesis, clinical and radiological examination and directed specialist examinations, for instance arteriography of the kidneys at suspicion of kidney cancer. In spite of complex diagnostics the source of metastasis was not found in over a dozen of patients.
Chir Narzadow Ruchu Ortop Pol 1990
PMID:[Characteristics and diagnosis of neoplastic metastasis to bones]. 136 53

A meeting of the American Association for Cancer Research was held in Toronto, Canada on March 18-22, 1995 to discuss advances in cancer research. Growing interest was shown in the molecular mechanisms of prostate cancer. Both breast cancer and colorectal cancer continued to be major scientific topics of interest. Research into the genetics of cancer was dominated by the issue of genomic instability due to failures in the mismatch DNA repair gene system of cells. Instability appeared to represent the key mechanism for the generation of mutations. Another common theme was the identification of putative tumor suppressor and metastasis loci using loss of heterozygosity and cell chromosome fusion approaches. A few novel sequences with a potential suppressive function were reported. Also, relationships between growth factor receptors, tumor suppressor genes, oncogenes, and proteins controlling cell cycle were analyzed. Progress in gene therapy and chemoprevention of malignant tumors was frequently discussed.
Pol J Pathol 1995
PMID:Advances in cancer research: report from the eighty-sixth annual meeting of the American Association for Cancer Research. 871 93

In the paper, pathophysiological and clinical foundations of modern conservative therapy of mild proliferation of prostatic cancer are discussed in a short outline. The problems of treatment with hormonal and non-hormonal preparations are presented against the background of the mechanism of action of pharmacological preparations. The drugs, their dosage, effectiveness and also side effects are discussed. The importance is stressed of the drugs blocking the alpha-1 adrenergic receptors in the treatment of mild proliferation of prostatic cancer with additional beneficial mechanisms of action for the organism.
Pol Tyg Lek 1996 Feb
PMID:[Pharmacologic treatment of mild proliferation of prostatic cancer]. 875 33

Nineteen men with BPH (benign prostatic hyperplasia) were studied who had up to 6 months prior to complete urine retention PSA levels measured (PSA I). Subsequent PSA levels were obtained at 2 weeks post catheterization upon catheter removal (PSA II) and at 4 (PSA III) and 6 weeks post catheterization (PSA IV). Analysed were 18 mean PSA values [ng/ml] (as one patient was found to have prostatic cancer and his data were discarded): PSA I - 6.46, PSA II - 14.26, PSA III - 9.83 and PSA IV - 7.47. Initial data suggest that the irritation of the adenoma by the catheter may cause PSA levels to rise.
Mater Med Pol
PMID:Bladder catheterization and a plasma prostate-specific antigen in patients with benign prostatic hyperplasia and complete urine retention. 893 94

Ki-67 and P53 expression were studied using immunohistochemistry on tissue samples obtained during transurethral electroresection or needle biopsy in 62 patients with prostatic lesions: group 1 (n = 15)--benign prostatic hyperplasia (BPH), group 2 (n = 10)--high-grade prostatic intraepithelial neoplasia (PIN 3), group 3 (n = 10)--low-grade prostatic carcinoma (PC, Gleason score 2-4), group 4 (n = 12) intermediate-grade prostatic carcinoma (PC, Gleason score 5-7) and group 5 (n = 15) high-grade prostatic carcinoma (PC, Gleason score 8-10). Moreover, in the groups examined the associations between expression of Ki-67 and P53 were analysed. Paraffin-embedded tissue samples were immunostained with monoclonal antibody anti-P53 and polyclonal antibody anti-Ki-67 using avidinbiotin-peroxidase method. Our study revealed lack of Ki-67 and P53 immunoreactivity in BPH. Only 3 out of 10 high-grade PIN exhibited Ki-67 positivity, but there was no immunopositivity of P53 protein in this group. Although immunopositivity of Ki-67 increased with the histological grade of prostatic cancer, the differences in Ki-67 expression between intermediate and high-grade cancer did not reach statistical significance. A similar level of Ki-67 reactivity in intermediately-differentiated and poorly-differentiated prostate cancer suggests a similar biology of these cancers. P53 protein positivity was noted in 62.2% cases of prostate cancer. Moreover, the highest level of P53 accumulation in intermediate-grade carcinomas may predict the aggressive progression and risk of metastases in these cases. No significant differences in P53 immunopositivity between low-grade and high-grade PC were noted. Interestingly, only in low-grade PC there was a significant positive correlation between expression of Ki-67 and P53 protein.
Pol J Pathol 2000
PMID:Ki-67 antigen and P53 protein expression in benign and malignant prostatic lesions. Immunohistochemical quantitative study. 1083 1

The paper presents a retrospective evaluation of 47 patients with bone metastases treated surgically during the last 10 years at our ward. The mean age of the patients was 62.5 years. There were 31 females (mean age: 62.8 years) and 16 males (mean age: 62.3 years). In 37 cases (78.8%) it as possible to establish the primary localization of the tumour: breast carcinoma--16 cases, ovary cancer 5 cases, lung cancer--5 cases, prostate cancer--5 cases, kidney cancer--2 cases, stomach cancer--1 case, vagina cancer--1 case, hepatocarcinoma--1 cases and plasmocytoma--1 cases. In 10 cases (21.1%) we were unable to establish the primary focus of the tumour. The localization of the metastases was as follows: femur--32 cases, humerus--6 cases, tibia--3 cases, lumbar spine--1 case. Patients treated very briefly after qualification for surgery, in some cases during emergency service. In 2 cases of metastases to the tibia amputations at the femur were performed. The remaining patients were treated by local excisions of the metastatic tumours, followed by: in 33 cases internal osteosynthesis and bone cement application; in 7 cases osteosynthesis, in 4 cases hip arthroplasties and posterior spine instrumentation in 1 case. In 6.4% we had poor results because of the death of 3 patients. The mean follow-up was three months. In 93.6% we had good and very good results--no pain, good function and independence during daily activities. Mean survival time was 13.5 month (range 5-28 months).
Chir Narzadow Ruchu Ortop Pol 2000
PMID:[Efficacy of operative treatment for pathological fractures in bone metastases in relation to length and comfort of survival]. 1138 15

Retroperitoneal fibrosis (Ormond's disease) is rare chronic inflammatory process, that can occur at any age. It is characterised by development of periaortic fibrous mass leading to progressive obstruction of vessels around the abdominal aorta and ureters. In the one third of cases we can find the causes of disease. There are ergotamine abuse, radiation, retroperitoneal surgery or hemorrhage, urine extravasation and response to different cancers. The other cases are idiopathic disease. We report a case of prostate cancer with unique course. The first manifestations of disease were diffuse peritoneal fibrosis and ureteral obstruction leading to bilateral hydronephrosis. Clinical course and histopathology showed idiopathic Ormond's fibrosis. Patient received oral immunosuppressive treatment (prednisolone 1 mg/kg/day + azathioprine 1 mg/kg/day), followed by intravenous methylprednisolone puls (2 g). Treatment also consisted of DJ-stent placement on the left side. On the right side we were unable to overcome the obstruction of ureter. Because of persistent renal failure, thrombocytopenia, DIC and progressive lower back pain we did control MR and CT scan. The CT scans showed multiple osteolytic bone metastases in vertebral column (the sizes of them were between a few millimetres and 1.5 centimetre). Patient died due to renal failure and haemorrhagic diathesis in the course of disseminated cancer of unknown origin. The postmortem examination revealed diffuse peritoneal infiltration surrounding the ureters, intramural ventricular metastases, pulmonary metastases and vertebral metastases. The prostate was only slightly enlarged. Histological and immunohistochemical examinations of prostate showed primary low-differentiated prostate carcinoma (CK/+/, PAP/+/, PSA/+/). Peritoneal, ventricular and bone infiltrations also were metastases from low-differentiated carcinoma of prostate origin (CK/+/, PAP/+/, PSA/-/).
Pol Arch Med Wewn 2001 Jul
PMID:[Ormond's fibrosis, bone osteolysis and stomach intramural metastases in the course f low-differentiated prostatic cancer]. 1192 71

Relatively new targets in drug design projects in cancer pharmacology include cytostatic agents, immune system modulators, and angiogenesis inhibitors. Preventive oncology applies pharmacological agents to reverse, retard, or halt progression of neoplastic cells to invasive malignancy. Prevention of cancer, however, can be accomplished through many strategies, including changes in diet and lifestyle. For example, the vast majority of lung cancers (80-90%) can be attributed to cigarette smoking and therefore, the most effective primary preventive strategy for lung cancer is to quit smoking. Chemoprevention through interruption of multistage careinogenesis include different molecular targets. Selective estrogen receptor modulators (SERMs) act as estrogen receptor (ER) agonists. Ligands for the peroxisome proliferator-activated receptor gamma (PPAR-gamma) suppress breast carcinogenesis in experimental models and induce differentiation of human liposarcoma cells. Selective PPAR modulators (SPARMs), by analogy to the SERM concept, are designed to have desired effects on specific genes relevant to carcinogenesis. Enzymatic approach in endocrine-related tumors involve inhibition of aromatase to prevent breast cancer and inhibition of 5-alpha-reductase to prevent prostate cancer. Down-regulation of inflammatory prostaglandin synthesis by inhibition of cyclooxygenase-2 (COX-2). inhibition of the inducible nitric oxide synthase (iNOS), and stimulation of phase II detoxication system, are currently examined in experimental models and clinical trials. Overall, potential targets in preventive strategies to reduce the risk of cancer involve agonists of endocrine receptors, factors down-regulating inflammation, factors inducing programmed cell death (PCD)/apoptosis, enzymatic inhibitors and gene therapy.
Acta Pol Pharm
PMID:Current strategies for anticancer chemoprevention and chemoprotection. 1266 76

Studies from our laboratory and others have shown that indole-3-carbinol (I3C) and its in vivo dimeric product, 3,3'-diindolylmethane (DIM), inhibit the growth of PC3 prostate cancer cells and induce apoptosis by inhibiting nuclear factor (NF)-kappaB and Akt pathways. To obtain comprehensive gene expression profiles altered by I3C- and DIM-treated PC3 cells, we utilized cDNA microarray to interrogate the expression of 22,215 known genes using the Affymetrix Human Genome U133A Array. We found a total of 738 genes that showed a greater than twofold change after 24 h of DIM treatment. Among these genes, 677 genes were down-regulated and 61 were up-regulated. Similarly, 727 genes showed a greater than twofold change in expression, with down-regulation of 685 genes and up-regulation of 42 genes in I3C-treated cells. The altered expressions of genes were observed as early as 6 h and were more evident with longer treatment. Upon cluster analysis, we found that both I3C and DIM up-regulated the expression of genes that are related to the Phase I and Phase II enzymes, suggesting their increased capacity for detoxification of carcinogens or chemicals. We also found that I3C and DIM down-regulated the expression of genes that are critically involved in the regulation of cell growth, cell cycle, apoptosis, signal transduction, Pol II transcription factor and oncogenesis. Real-time reverse transcription-polymerase chain reaction analysis was conducted to confirm the cDNA microarray data, and the results were consistent. We conclude that I3C and DIM affected the expression of a large number of genes that are related to the control of carcinogenesis, cell survival and physiologic behaviors. This may help determine the molecular mechanism(s) by which I3C and DIM exert their pleiotropic effects on PC3 prostate cancer cells; in addition, this information could be further exploited for devising chemopreventive and/or therapeutic strategies for prostate cancer.
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PMID:Gene expression profiles of I3C- and DIM-treated PC3 human prostate cancer cells determined by cDNA microarray analysis. 1267 12

Recent reports suggest that the beta-catenin-T-cell factor (Tcf) (BCT) signaling pathway is important in the progression of prostate cancer. Evidence suggests that the androgen receptor (AR) can repress BCT-mediated transcription both in prostate cancer and colon cancer cells (Chesire and Isaacs, 2002). In this study, we validate such findings and show that repression of BCT signaling is facilitated by competition between the AR and Tcf. Measurements of the Tcf transcriptional reporter (TOPFLASH) indicated that AR+DHT-mediated repression can inhibit BCT transcription in the presence of WT and exogenous activating beta-catenin (Delta1-130 bp). Transient transfections in SW480 cells (APC(mut/mut)) showed that this mode of repression is functionally independent of APC-mediated beta-catenin ubiquitination. Using a recently developed red flourescent protein (HcRed), we demonstrate novel observations about the nuclear distribution of Tcf. Furthermore, with the use of red (HcRed-AR and HcRed-Tcf) and green fusion proteins (beta-catenin-EGFP), we provide morphological evidence of a reciprocal balance of nuclear beta-catenin-EGFP (BC-EGFP). By cotransfecting in LNCaP prostate tumor cells and using quantitative imaging software, we demonstrated a 62.0% colocalization of HcRed-AR and BC-EGFP in the presence of DHT and 63.3% colocalization of HcRed-Tcf/BC-EGFP in the absence of DHT. Costaining for activated RNA Pol II (phosphoserine 2) and HcRed-Tcf suggested that Tcf foci contain transcriptional 'hotspots' validating that these sites have the capacity for transcriptional activity. Given this apparent androgen-dependent competition for nuclear BC-EGFP, we chose to assess our hypothesis by in vivo and in vitro binding assays. SW480 cells transiently transfected with an AR expression construct, treated with DHT and immunoprecipitated for Tcf showed less associated beta-catenin when compared to Tcf precipitates from untreated cells. Furthermore, by treating cells with DHT+Casodex, we were able to abrogate the androgen-sensitive AR/beta-catenin interaction, in addition to relieving transcriptional repression of the TOPFLASH reporter. In vitro binding assays, with increasing amounts of AR(S35), resulted in decreased Tcf(S35) association with immunoprecipitated recombinant beta-catenin-HIS. These data suggest that in steady-state conditions, AR has the ability to compete out Tcf binding for beta-catenin. Finally, using SW480 cells, we show that AR-mediated repression of the BCT pathway has implications for cell cycle progression and in vitro growth. Using FACs analysis, we observed a 26.1% increase in accumulation of cells in the G1 phase of the cell cycle, while in vitro growth assays showed a 35% reduction in viable cells transfected with AR+DHT treatment. Together, our data strongly suggest that a reciprocal balance of nuclear beta-catenin facilitates AR-mediated repression of BCT-driven transcription and cell growth.
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PMID:Functional localization and competition between the androgen receptor and T-cell factor for nuclear beta-catenin: a means for inhibition of the Tcf signaling axis. 1294 8


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