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)

The natural history of clinically localized prostate cancer in individual patients is difficult to predict using currently available techniques. The majority of these patients will undergo treatment without knowledge of whether the tumor would have progressed during their lifetime. Because more patients are being diagnosed yearly with early stage prostate cancers it is becoming increasingly important to delineate factors that will clarify which patients have tumors with invasive potential. Using the Dunning R-3327 rat prostate animal tumor model we have previously shown that an increase in cell surface charge, as measured by individual cell electrophoresis, is associated with an increase in metastatic ability. This electrophoretic technique is limited by the small number of cells that can be analyzed during each assay. Therefore, we adapted a flow cytometric method for measurement of cell surface change, utilizing a large molecule (cationized ferritin) that binds quantitatively to the negative charges at the cell surface. With a fluorescent tag attached to the ferritin molecule, flow cytometric quantification of surface charge was possible, and this method was successful in identifying tumors with high metastatic ability in the Dunning prostate tumor model.
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PMID:Prediction of metastatic potential in an animal model of prostate cancer: flow cytometric quantification of cell surface charge. 281 May 30

The current investigation describes the purification and partial characterization of a new adenocarcinoma-associated antigen (ACAA). ACAA is a large molecular weight glycoprotein (Mr 790,000 by size chromatography on Sepharose CL-6B) that migrates in the alpha 1 region upon electrophoresis and is eluted from a DEAE-cellulose column at a 0.1 M NaCl concentration. ACAA is immunochemically and biochemically different from carcinoembryonic antigen, alpha-fetoprotein, pancreatic oncofetal antigen, human pancreatic tissue antigen, CA 19-9, ferritin, and acute-phase proteins. Assays for ACAA were carried out using a solid-phase sandwich enzyme immunoassay. The results indicate that ACAA is present in sera of all individuals. Patients with cancer have higher serum levels of ACAA than normal individuals. The greatest frequency of elevated serum values of ACAA was seen in patients with lung and pancreatic cancers followed by colorectal, breast, and prostate cancer. The measurement of ACAA levels may be valuable in the diagnosis and clinical management of patients with certain cancers.
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PMID:Purification, partial characterization, and clinical evaluation of an adenocarcinoma-associated antigen. 353 83

Recently, the study of the physiological role of the essential trace elements is being emphasized. Some environmental and disease factors has been demonstrated to perturb trace element homeostasis. A number of recent studies have described alterations in serum copper levels (SCLs) and serum zinc levels (SZLs) in human cancer patients and the relationship between the magnitude of their perturbation and disease activity. This report describes SCLs, SZLs and SCL/SZL ratios in patients with malignant neoplasms of the urogenital tract at various clinical stages and the relationship of the levels of these trace elements to disease activity. According to SCLs before treatment, patients with renal cell carcinoma appeared to be separated into two groups, normal SCL group and higher SCL group. In the higher SCL group, patients generally displayed increased erythrocyte sedimentation rate, CRP, alpha 2 globulin, beta 2 microglobulin, ferritin and CEA. In this group, SCL was a useful index of disease activity. In the normal SCL group, SCLs remained within normal limit even in patients with advanced disease. In renal cell carcinoma, SZLs did not reflect disease activity. In transitional cell carcinoma of the upper urinary tract, patients with metastasis had significantly elevated SCLs and significantly decreased SZLs, compared with normal controls or patients without metastasis. In transitional cell carcinoma of the bladder, no distinct relationships were observed between these trace elements and extent of malignancy. But there was a trend toward increasing SCLs and decreasing SZLs with progressing stage and SCL/SZL ratios fairly reflect stage of disease. Patients with prostatic cancer had nearly normal SCLs and SZLs, although there were a few exceptions. Testicular cancer patients with distant metastasis had significantly elevated SCLs and initially high SCLs decreased in patients responding to therapy and increased again in relapse. SZLs and, hence, SCL/SZL ratios had no relationship to activity of testicular cancer. Currently there is no satisfactory way of following the progress of malignancies of the urogenital tract except prostatic cancer with elevated acid phosphatase and non-seminomatous testicular tumors until the secondary tumor can be detected radiographically. Our study suggests that these trace element might be a useful indicator of disease activity of some of the urogenital malignancies.
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PMID:[Serum copper and zinc levels in patients with malignant neoplasm of the urogenital tract]. 408 94

Ferritin, carcinoembryonic antigen (CEA), beta 2-microglobulin (beta 2-MG) and prostatic acid phosphatase (PAP) levels in serum from 77 patients with cancer (6 with renal adenocarcinoma, 9 with renal pelvic and ureteral cancer, 29 with bladder cancer and 33 with prostatic cancer) at various stages were clinically evaluated for their significance as a parameter of urinary tract malignancies. Although, ferritin, CEA and beta 2-MG levels in the poorly-differentiated and advanced stage groups of renal adenocarcinoma, renal pelvic and ureteral cancer, and bladder cancer were higher than those in the well-differentiated and early stage groups, those in most cases were within normal ranges. These proteins were not considered suitable for the screening test. Ferritin and beta 2-MG levels increased with advancement of the performance status (P.S.) proposed by Koyama and Saito; however, the latter was affected greatly by renal impairment. In prostatic cancer, PAP and ferritin levels were remarkably high in the poorly-differentiated group (PAP mean +/- S.E.: 57.6 +/- 22.5 ng/ml, ferritin 883 +/- 319 ng/ml) and the advanced stage group (27.2 +/- 10.5 ng/ml, 398 +/- 152 ng/ml) compared to the well-differentiated group (7.87 +/- 3.61 ng/ml, 88.5 +/- 25.8 ng/ml) and the early stage group (2.24 +/- 0.54 ng/ml, 186 +/- 91.7 ng/ml). PAP and ferritin levels of the untreated cases were positive in 10 out of 18 cases (55.6%) and 7 out of 18 cases (38.9%), respectively, and those of the relapsing cases were positive in 4 out of 7 cases (57.1%) and 6 out of 7 cases (85.7%), respectively. However, CEA and beta 2-MG levels were negative in most cases. Furthermore, increments of PAP and ferritin levels, especially that of the ferritin level, were significantly related to advancement of P.S., and high ferritin levels were obtained in all cases of P.S. 3 and 4. Therefore, determination of PAP and ferritin seems to be useful in monitoring prostatic cancer, and the latter to be useful in early detection of relapsing cases.
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PMID:[Assessment of serum ferritin, CEA, beta 2-MG and PAP determinations in patients with urinary tract malignancies]. 637 13

By means of the RIA-Gnost Ferritin and Spac Ferritin kits, the serum ferritin levels of patients with some urological malignant diseases were quantitated; and, the clinical significance of these values as a tumor marker was discussed. The normal (reference) level in serum obtained by the RIA-Gnost kit was 142.5 +/- 67.5 ng/ml (n = 58) for healthy males and 49.6 +/- 28.8 ng/ml (n = 76) for healthy females. The assay values for 22 cases of bladder cancer by both kits were somewhat lower than the normal range, and the positive rates presented were around 30%, being in rough agreement with each other. The positive rate for 22 patients with prostatic cancer was 45.5% by either method. The assay values obtained by the RIA-Gnost kit was higher and differed significantly (p less than 0.1%) from those obtained on healthy males. Furthermore, the same tendency was found in 6 cases of renal cancer. The assay values of RIA-Gnost were significantly higher (p less than 0.1%) than normal; and, the positive rate was 100% for RIA-Gnost and 67% for Spac . In conclusion, serum ferritin determination especially that by the RIA-Gnost kit proved to be a useful and significant tumor marker for the detection of renal cancer.
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PMID:[Clinical evaluation of serum ferritin levels in urologic cancer (II)]. 667 86

Elevated body iron stores (serum ferritin >300 microg/L, transferrin saturation TS >50%) are associated with increased risk of liver and lung cancers. To determine whether such association also exists for prostate cancer (PC), we measured serum ferritin, serum iron, total iron-binding capacity (TIBC), and TS in serum samples from 34 men with newly diagnosed, untreated PC and 84 healthy men, ranging in age from 49-78 years. In contrast with other malignancies, men with PC had significantly lower mean concentrations of serum ferritin (156 microg/L) and TS (24.35%) than those without PC (ferritin, 245 microg/L; TS, 31.98%) (p<0.05). The 95% confidence intervals for ferritin were 109-203 microg/L and 205-286 microg/L, and those for TS were 20.29-28.4% and 28.35-35.61% for men with and without PC, respectively. Significant differences were observed between both groups in the distribution of serum ferritin (<100, 101-300, >300 microg/L) and TS (<16, 16-50, >50%) (p<0.05). A lower percentage of cases than of controls had serum ferritin (17.6% versus 29.8%) and TS (5.9% versus 14.7%) above normal. These differences persisted when the analysis was limited to African-American men (31 cases and 52 controls). Data suggest that elevated body iron stores are less common in men with PC compared to those without PC.
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PMID:Serum ferritin levels and transferrin saturation in men with prostate cancer. 1516 Sep 79

The serum transferrin receptor (sTfR) is a sensitive indicator of iron-deficiency erythropoiesis that is not affected by inflammation. Concentrations of this molecule are inversely correlated with body-iron stores, and increased body-iron stores are associated with an increased risk of cancer of the liver and lungs. However, an association between iron status as assessed on the basis of sTfR and prostate cancer has not been previously investigated. We measured sTfR and serum ferritin by means of an enzyme immunoassay in 27 men with newly diagnosed, untreated prostate cancer and in 72 controls. Our study population ranged in age from 38 to 78 years. The mean serum ferritin concentration in men with prostate cancer was 44.8% lower than that in men without this tumor ( P < .05). In contrast, the mean values of sTfR and sTfR/log serum ferritin were 32% and 60% higher, respectively, in men with prostate cancer than in those without this tumor ( P < .05). Differences between groups persisted after we took into account inflammation (alpha 1-acid glycoprotein > 1 g/L, C-reactive protein > 10 mg/L; P < .05). Among the entire study population and among men without inflammation, a higher percentage of subjects (29%-31%) than of controls (14%-22%) had sTfR values greater than 8 mg/L, suggestive of iron-deficiency erythropoiesis ( P < .05). The odds ratios for men with prostate cancer to have sTfR values of less than 2.9 mg/L (suggestive of increased body-iron stores) was 0, compared with 1.745 to 3.65 for the same men to have sTfR values greater than 8 mg/L. sTfR was negatively correlated with log ferritin ( r = -.422, P < .05) but did not correlate with tissue inflammation, tumor stage, or acute-phase proteins. It appears that prostate cancer is not associated with increased body-iron stores.
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PMID:Increased levels of serum transferrin receptor and serum transferrin receptor/log ferritin ratios in men with prostate cancer and the implications for body-iron stores. 1553 86

To identify genes associated with insulin-like growth factor-I receptor (IGF-IR)-mediated cellular transformation, we isolated genes that are differentially expressed in R- cells (derived from the IGF-IR knockout mouse) and R+ cells (R- cells that overexpress the IGF-IR). From these, 45 genes of known function were expressed at higher levels in R+ cells and 22 were expressed at higher levels in R- cells. Differential expression was confirmed by Northern blot analysis of R+ and R- cells. Genes expressed more abundantly in R+ cells are associated with (1) tumour growth and metastasis including, betaigH3, mts1, igfbp5 protease, and mystique; (2) cell division, including cyclin A1 and cdk1; (3) signal transduction, including pkcdeltabp and lmw-ptp; and (4) metabolism including ATPase H+ transporter and ferritin. In MCF-7 cells IGF-I induced expression of two genes, lasp-1 and mystique, which could contribute to metastasis. Lasp-1 expression required activity of the PI3-kinase signalling pathway. Mystique was highly expressed in metastatic but not in androgen-dependent prostate cancer cell lines and Mystique overexpression in MCF-7 cells promoted cell migration and invasion. We conclude that genes identified in this screen may mediate IGF-IR function in cancer progression.
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PMID:Gene expression profiles in cells transformed by overexpression of the IGF-I receptor. 1594 Feb 54

We have shown previously that generation of reactive oxygen species (ROS) is a critical event in G(2)-M phase cell cycle arrest caused by diallyl trisulfide (DATS), which is a highly promising anticancer constituent of processed garlic. Using DU145 and PC-3 human prostate cancer cells as a model, we now report a novel mechanism involving c-Jun NH(2)-terminal kinase (JNK) signaling axis, which is known for its role in regulation of cell survival and apoptosis, in DATS-induced ROS production. The DATS-induced ROS generation, G(2)-M phase cell cycle arrest and degradation, and hyperphosphorylation of Cdc25C were significantly attenuated in the presence of EUK134, a combined mimetic of superoxide dismutase and catalase. Interestingly, the DATS-induced ROS generation and G(2)-M phase cell cycle arrest were also inhibited significantly in the presence of desferrioxamine, an iron chelator, but this protection was not observed with iron-saturated desferrioxamine. DATS treatment caused a marked increase in the level of labile iron that was accompanied by degradation of light chain of iron storage protein ferritin. Interestingly, DATS-mediated degradation of ferritin, increase in labile iron pool, ROS generation, and/or cell cycle arrest were significantly attenuated by ectopic expression of a catalytically inactive mutant of JNK kinase 2 and RNA interference of stress-activated protein kinase/extracellular signal-regulated kinase 1 (SEK1), upstream kinases in JNK signal transduction pathway. In conclusion, the present study provides experimental evidence to indicate existence of a novel pathway involving JNK signaling axis in regulation of DATS-induced ROS generation.
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PMID:c-Jun NH(2)-terminal kinase signaling axis regulates diallyl trisulfide-induced generation of reactive oxygen species and cell cycle arrest in human prostate cancer cells. 1670 65

Urokinase-type plasminogen activator (uPA) on prostate cancer cell surfaces mediates pericellular proteolysis and destruction of extracellular matrix barriers to tumor invasion and metastasis. Increased expression of tumor-associated uPA leads to enhanced tumor dissemination and poor cancer outcomes in men with prostate cancer. Expression of uPA is regulated in part by the oxidant-sensitive transcription factor, NF-kappa B (NF-kappaB), which is activated by intracellular reactive oxygen intermediates (ROI). This study examined the effect of iron on the production of ROI, activation of NF-kappaB and expression of uPA in the human prostate cancer cell line, PC-3. Treatment of PC-3 cells with iron in the form of ferric nitrilotriacetate (FeNTA) in the absence of added transferrin resulted in a dose-dependent increase in cellular ferritin content in both the presence and absence of neutralizing antibody to the transferrin receptor. Cellular uptake of iron resulted in stimulation of intracellular ROI production, and increases in uPA mRNA, antigen, and activity. Concurrent treatment with the iron chelator, desferrioxamine (DFO) abrogated these effects, and treatment with DFO alone inhibited constitutive uPA production. Finally, we observed nuclear translocation, and therefore activation of NF-kappaB in response to iron exposure. We conclude that iron enters PC-3 cells via a non-transferrin dependent pathway and increases uPA expression. Our data indicate that one mechanism by which iron may stimulate uPA production is through the generation of intracellular ROI and activation of NF-kappaB-mediated signaling pathways.
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PMID:Iron stimulates urokinase plasminogen activator expression and activates NF-kappa B in human prostate cancer cells. 1757 74


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