Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigate the proliferative activity, prostatic specific antigen (PSA) secretion, morphology and androgen response of human prostate tumour epithelial cells co-cultured with stromal cells in a bicameral system. Stromal and epithelial cells were isolated from prostate adenocarcinoma by enzyme digestion and cultured in defined media. Immunocytochemistry for prostate carcinoma tumour antigen (PCTA-1) was performed for culture purity evaluation. Also, the morphology of the epithelial cells in co-culture was evaluated by electron microscopy. PSA was determined by microparticle enzyme immunoassay (MEIA) automatized protocol and the proliferation was evaluated by a commercial spectrophotometric kit, based on formazan salt formation. Both cell cultures showed more than 90% of purity. The epithelial cell co-cultures showed marked membrane processes and cell interdigitations. The proliferative activity of the epithelial cells was increased in presence of stromal cells. Also, PSA secretion was significantly increased and maintained for at least 14 days, whereas the androgen response for PSA secretion was evidenced only in co-culture condition. Primary co-cultures of epithelial and stromal cells from human prostate carcinoma are able to maintain, for a prolonged time, proliferative and secretory properties as well hormone response, and represent a valuable tool for cellular and molecular studies on prostate cancer.
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PMID:Secretion of prostatic specific antigen, proliferative activity and androgen response in epithelial-stromal co-cultures from human prostate carcinoma. 1567 20

To screen different combinations of prostate-specific membrane antigen (PSMA) promoter/enhancer with the strongest transcriptional activity in prostate-specific cells, we used PSMA regulatory elements to control specific expression of the target gene in gene therapy of prostate adenocarcinoma. PSMA promoter and enhancer DNA sequences were amplified from the LNCaP human prostate cancer cell line by polymerase chain reaction, then recombinant plasmids of the enhanced green fluorescent protein (EGFP: pEGFP-PSMA(Pro), pEGFP-PSMA(E-P), pEGFP-PSMA(E(r)-P), pEGFP-PSMA(E(d)-P), and pEGFP-PSMA(E(t)-P)) were constructed with molecular clonal techniques. At the same time, all experimental cell lines were analyzed for the expression of PSMA with the use of PSMA monoclonal antibody and the ABC immunohistochemical assay kit. After plasmids were transfected via liposome, we observed the expression of the reporter gene (EGFP) under a fluorescent microscope and compared the different levels of EGFP expression with reverse transcriptase polymerase chain reaction and flow cytometry so that we could choose the one with the highest transcriptional activity. Only the LNCaP cell line expressed PSMA positively with immunohistochemical stain. The PSMA promoter/enhancer had transcriptional activity in PSMA(+) cell lines and no activity in PSMA(-) cell lines. PSMA(E-P) achieved the strongest activity in different PSMA promoter/enhancer combinations. We confirmed the specific expression of PSMA in prostate cells again. Similarly, transcriptional activity of the PSMA promoter/enhancer was prostate specific. PSMA(E-P) achieved the strongest transcriptional activity among PSMA promoter/enhancer combinations, which could be used in advanced research for tissue-specific treatment.
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PMID:Construction of prostate-specific expressed recombinant plasmids with high transcriptional activity of prostate-specific membrane antigen (PSMA) promoter/enhancer. 1571 27

Procollagen (I) carboxyterminal propeptide (PICP) is a metabolite of procollagen, a precursor molecule of collagen type I, which accounts for more than 90% of the organic matrix of the bones. Serum PICP levels indicate the rate of bone collagen synthesis and therefore the osteoblastic activity. In this study we evaluate the clinical usefulness of serum PICP as an indicator of bone metastases in patients with prostate cancer in relation to bone scan and to prostate specific antigen (PSA) measurements. We found no similar study in the literature relating these three tests. Seventy-eight patients (median age 63+/-4,3 years) with prostate adenocarcinoma were examined. The diagnosis was confirmed histologically. Bone metastases were diagnosed in 42 (54%) of them assessed by bone scans (Group A), while the remaining 36 patients (46%) had no bone metastases (negative bone scans and X-rays) (Group B). We also examined 21 patients with benign prostate hyperplasia as a control group (Group C). All patients had serum PICP measurements, bone scans with (99m)Tc-MDP and PSA measurements. None of them had a history of disease or of using drugs known to affect bone metabolism. Serum levels of PICP were assayed by a radioimmunoassay (RIA) kit (Orion Cooperation, Farmos Diagnostics, Finland). Serum PSA was also tested by a RIA kit (Tandem-R, Hybritech Inc, USA). PICP levels in Group A were 265+/-89 microg/l, in Group B 128+/-39 microg/l and in Group C patients 110+/-48 microg/l. High levels of PICP above 170 microg/l, were diagnostic of bone metastases with sensitivity 54%, specificity 93% and accuracy 84%. In comparison, PSA levels above 4 ng/ml were also diagnostic with a sensitivity of 68%, specificity of 91% and accuracy 88%. Patients with low levels of PICP, lower than 90 microg/l, n=31, had no bone metastases. The positive prognostic value of bone scan was 74% with a sensitivity of 76%, specificity of 58% and accuracy 71%. Positive bone scans combined with very high levels of PICP and PSA, had positive prognostic value 97%, with sensitivity of 78%, specificity of 96% and accuracy 97%, while bone scans with levels of PICP lower than 170 microg/l, had positive prognostic value of 32%. Levels of PICP and PSA were significantly higher in patients with prostate cancer and bone metastases in comparison to patients with benign prostate hyperplasia (P<0.0001) respectively. Also, levels of PICP and PSA were higher in patients with prostate cancer without metastases as compared to prostate hyperplasia (P<0.0005 and P<0.0001 respectively) (Wilcoxon-Mann-Whitney test). When metastases were more extensive, PICP levels were higher than PSA. It is concluded that PICP as a marker of osteoblastic activity is useful for diagnosing bone metastases of prostate adenocarcinoma but when co-evaluated with PSA and the bone scan, the diagnostic accuracy of these three diagnostic procedures is much higher.
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PMID:[Correlation of procollagen (I) with prostate specific antigen and bone scan for the diagnosis of bone metastases in patients with prostate carcinoma]. 1584 Dec 91

Recent studies have highlighted that Activin A, a member of the transforming growth factor-beta (TGF-beta) superfamily, may be involved in the regulation of osteoblastic activity and in osteoclast differentiation. Therefore, we have investigated the clinical significance of its circulating levels in patients with bone metastasis. Activin A serum concentrations were determined, by a commercially available enzyme-linked immunosorbent assay kit, in 72 patients with breast cancer (BC) or prostatic cancer (PC) with (BM+) or without (BM-) bone metastases, in 15 female patients with age-related osteoporosis (OP), in 20 patients with benign prostatic hypertrophy (BPH) and in 48 registered healthy blood donors (HS) of both sex (25 female and 23 male). Activin A serum concentrations were significantly increased in BC or PC patients as compared to OP (P < 0.0001) or BPH (P = 0.045), respectively, or to sex matched HS (P < 0.0001). Additionally, these levels resulted more elevated in PC patients as compared to BC patients (P = 0.032). Interestingly, Activin A was significantly higher in BM+ patients than in BM- patients (BC, P = 0.047; PC, P = 0.016). In BC patients, a significant correlation was observed only between Activin A and number of bone metastases (P = 0.0065) while, in PC patients, Activin A levels were strongly correlated with the Gleason score (P = 0.011) or PSA levels (P = 0.0001) and, to a lessen extent, with the number of bone metastases (P = 0.056). Receiver operating characteristic curve (ROC) analysis showed a fair diagnostic accuracy of Activin A to discriminate between BM+ and BM- patients (BC: AUC = 0.71 +/- 0.09, P = 0.03; PC: AUC = 0.73 +/- 0.081, P = 0.005). These findings indicate that Activin A may be implicated in the pathogenesis of bone metastasis. Therefore, this cytokine may be considered a novel potential target for a more selective therapeutic approach in the treatment of skeletal metastasis and may be also useful as additional biochemical marker of metastatic bone disease.
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PMID:Activin A circulating levels in patients with bone metastasis from breast or prostate cancer. 1684 Dec 34

Heterocyclic amines (HCAs) are formed when meat products such as beef, chicken, pork and fish are cooked at high temperatures. The most abundant HCA found in the human diet is 2-amino-1-methyl-6-phenylimidazo[4,5-b] pyridine (PhIP). PhIP causes mammary carcinomas in female rats and mice, and is associated with an increased risk of developing colon, breast, and prostate cancer in humans. PhIP is metabolized by cytochrome P-450s producing N-OH-PhIP. The N-OH-PhIP can be esterified by phase II enzymes forming an arylnitrenium ion that binds to DNA causing adducts. Furthermore, N-OH-PhIP may be reduced by cytochrome b5 reductase producing superoxide anions and hydroxyl radicals causing DNA strand breaks. Diallyl sulfide (DAS) has been shown to prevent cancer in several animal models, presumably by metabolic modulation. We hypothesize that PhIP produces reactive oxygen species causing DNA strand breaks and that DAS will inhibit the formation of PhIP induced DNA strand breaks. To test this hypothesis we treated normal breast epithelial (MCF-10A) cells with PhIP, DAS and a combination of PhIP and DAS. The detection of lipid peroxides was used as a surrogate for ROS. Lipid peroxides were detected using a PeroxiDetect kit (Sigma). PhIP increased the production of lipid peroxides and DAS decreased the PhIP-induced peroxidation by 47%. To determine if PhIP causes DNA strand breaks in MCF-10A cells, cells were treated for 3, 6, 9, and 24 h with PhIP (100 microM), DAS (100 microM) and a combination of PhIP (100 microM) and DAS (100 microM). DNA strand breaks were evaluated using the Comet assay. PhIP produced DNA strand breaks in a dose- and time-dependent fashion. We have shown that DAS inhibits PhIP-induced DNA strand breaks by inhibiting the production of reactive oxygen species. Therefore, we propose that DAS can prevent PhIP-induced breast cancer.
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PMID:Diallyl sulfide inhibits PhIP-induced DNA strand breaks in normal human breast epithelial cells. 1734 19

HIFU therapy is one of epoch-making, low-invasive treatments for prostate cancer. We investigated 71 patients who had undergone HIFU therapy from June 2004 through September 2005. We mainly gave a single spinal injection followed by epidural catheterization with a combined spinal-epidural anesthesia kit. Three patients received general anesthesia because of various problems such as allergy for local anesthetics, ankylosing spondylitis and severe spinal deformity causing difficulty in lumbar puncture. Spinal anesthesia was successfully achieved in most patients. Twelve patients with insufficient anesthetic levels required additional local anesthetics via epidural catheters. We found no serious perioperative complications.
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PMID:[Anesthetic management for high-intensity focused ultrasound (HIFU) therapy in prostate cancer patients]. 1744 57

It is shown that for verification of human sperm presence on the spots on material evidence it is feasible to apply solid phase enzyme immunoassay (EIA) with the kit "PSA-EIA-BEST T-8458" which is used in clinical practice for diagnosis of prostatic cancer and some other diseases. The method is specific and highly sensitive, convenient for objective registration and computer processing. It is also cost-effective and provides not only significant identification of sperm on the exhibits but also its human origin in complete absence of spermatozoa on the spot.
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PMID:[Identification of sperm on the spots located on material evidences using solid phase enzyme immunoassay with human prostate-specific antigen]. 1752 Aug 99

PCA3 gene has been discovered in 1999 because of its differential expression between prostate cancer and nonneoplastic tissue. Several studies evaluated its value for prostate cancer diagnosis. These papers are consistent with significant statistical accuracy of measure of the urinary number of PCA3 copies (PCA3 test). While sensitivity is slightly weaker than that of seric PSA, specificity as well as positive and negative predictive values are quite better. PCA3 test seems therefore to be a good indicator of prostate biopsy results. As a commercial kit is available, large studies will be conducted to confirm these results, precise when to perform the test and evaluate the benefit/cost ratio. One of the aims is better selection of those patients who will really benefit from prostate biopsies.
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PMID:[Value of urinary PCA3 test for prostate cancer diagnosis]. 1853 69

Epigallocatechin-3-gallate (EGCG) is the major and most potent polyphenol compound of green tea that has been shown to have anticancer effects against various types of cancers. In this study, in addition to the EGCG compound, a synthetic derivative, the peracetate of EGCG (EGCG-P), was used to investigate the inhibitory effects on growth of androgen-independent prostate cancer in vivo. The advantage of EGCG-P is that it may act as a prodrug, leading to higher bioavailability than EGCG itself. The aim of our study was to compare the differences between EGCG and EGCG-P on their inhibitory effect on androgen-independent prostate cancer, CWR22R, xenograft model in nude mice. The mice were administrated daily with solvent dimethyl sulfoxide, EGCG, and EGCG-P separately through intraperitoneal injection for 20 days. Tumor volume and body weight of nude mice were recorded daily. Serum prostate-specific antigen (PSA) levels were also measured before and after the treatment. The effects of both EGCG and EGCG-P on tumor cell proliferation were assessed by immunohistochemical (IHC) method using antibodies against Ki-67 and proliferating cell nuclear antigen. The apoptotic effect was evaluated by IHC against B-cell non-Hodgkin lymphoma-2 and terminal deoxynucleotidyl transferase dUTP nick-end labeling assay by in situ apoptosis detection kit. Moreover, the potential suppression of angiogenesis by EGCG and EGCG-P on prostate cancer was examined by IHC against CD31. Our results revealed that treatment of EGCG and EGCG-P compounds suppressed the growth of CWR22R xenografts without causing any detectable side effects in nude mice. The suppression of growth of the tumor was correlated with the decrease of serum PSA level together with the reduction in tumor angiogenesis and an increase in apoptosis on prostate cancer cells. The results showed that treatment of EGCG and EGCG-P inhibited tumor growth and angiogenesis while promoting apoptosis of the prostate cancer cells in vivo. Our results suggest that EGCG-P may be a more stable and useful compound for increasing the therapeutic anticancer effects in androgen-independent prostate cancer.
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PMID:Effect of a prodrug of the green tea polyphenol (-)-epigallocatechin-3-gallate on the growth of androgen-independent prostate cancer in vivo. 1858 82

The present study examined the anti-proliferative effects of piplartine on the human prostate cancer cell line PC-3. This is the first report demonstrating the piplartine anti-cancer activity toward prostate cancer cell lines, although its precise mechanism of action is still not completely defined. In MTT assays, it preferentially inhibited growth of androgen-independent PC-3 cells in a dose-dependent (3-30 microM) and time-dependent (12-48 h) manner. In PC-3 cells, it showed an IC50 of 15 microM after 24 h of treatment. After a 24-30 microM treatment for 24 h, there were some reduction of cell volume, cell vacuolization, chromatin condensation and increased number of apoptotic cells visible by light and fluorescence microscopy. Agarose gel electrophoresis revealed that cells treated with piplartine exhibited DNA fragmentation. In addition, growth inhibition of PC-3 cells was associated with G2/M arrest and sub-G1 accumulation. Higher concentrations (24-30 microM) of piplartine modulated apoptosis-related protein expression by down-regulating cdc-2 expression and up-regulating PARP/procaspase-3 cleavage. Also, PC-3 cells treated with piplartine demonstrated caspase-3 activation, as observed with an in vitro caspase-3 colorimetric assay kit. Taken together, these results demonstrated that high concentrations of piplartine exhibited anti-proliferative and anti-cancer effects on PC-3 cells and that caspase-3-mediated PARP cleavage and cell cycle arrest at G2/M phase are involved in the underlying cellular mechanism of the apoptosis process.
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PMID:Piplartine induces caspase-mediated apoptosis in PC-3 human prostate cancer cells. 1881 19


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