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)

Preliminary data are reported from a study of 269 cadmium-nickel battery factory workers and 94 cadmium-copper alloy factory workers. The target group comprises all workers with more than 5 years exposure to cadmium at any time since the factories started production. An internal reference group of 328 alloy factory workers without cadmium exposure was also studied. The expected number of deaths and cancers was calculated with the "life-table" method by using national average incidence rates for men in different age groups and at different calendar years. It was found that among the workers in the battery factory who started work before 1948 there was an increased general mortality in the 1950's mainly due to respiratory disease. The same group had an increased renal disease mortality. There was no increase in general cancer mortality or in general cancer incidence. The risk ratio for nasopharyngeal cancer incidence was 10 (two cases), which was statistically significant. For some other sites like prostate, lung and colon-rectum the risk ratios were also greater than 1 but not statistically significant. In the alloy factory there was a tendency for an increased mortality in prostatic cancer (four cases). After correction for the "healthy worker effect" using the reference group, the risk ratio for prostatic cancer deaths was calculated as 2.4, but this was not statistically significant. The findings in this study support the earlier reports of an association between human cadmium exposure and increased risk for prostatic cancer.
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PMID:Mortality and cancer morbidity among cadmium-exposed workers. 48 34

Continuing observations on cadmium-exposed workers have failed to yield evidence of an increased mortality from prostatic cancer, as initially suspected. There is, however, evidence of an increased mortality from lung cancer and, in at least two of the studies, of a dose-response relationship, but interpretation of these studies with regard to the role of cadmium is complicated by concurrent exposure to other known or suspected carcinogens, including arsenic, nickel, beryllium, chromium and heated mineral oils. An update of a long-term cohort mortality study from 17 plants in England employing a wide range of cadmium processes, while confirming an increased lung cancer risk related to intensity of cadmium exposure, shows some evidence of this risk also being associated with exposure to arsenic. It is thus not possible at present to attribute the excess mortality from lung cancer to cadmium owing to the presence of multiple confounding factors in the populations studied. Their role in the 17-plant study is currently being further investigated.
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PMID:Is cadmium a human carcinogen? 130 71

The effect of hyperthermia was examined on the Dunning prostate tumor model in rats. Hyperthermia was created by heating self-regulating interstitial seeds with an external oscillating magnetic field. The seed alloy was comprised of 70% nickel and 30% copper. One treatment with 50C seeds for two hours did not provide significant delay in tumor growth compared to controls. However, regimens with two treatments separated by either 48 hours or one week did cause significant delay (p = 0.0013 and p = 0.0096, respectively). These results suggest that an interstitial hyperthermia seed may provide an efficacious outpatient therapy for prostate cancer. Further, interstitial hyperthermia may be readily combined with existing radiotherapy with interstitial gold coated seeds to provide additive or synergistic anti-tumor effects.
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PMID:The effect of interstitial hyperthermia on the Dunning prostate tumor model. 155 9

Several epidemiological studies of workers exposed to cadmium indicate an increased risk of lung and prostatic cancer. The increase is statistically significant in some of the studies but the SMR is greater than 100 in almost all. A cohort study of the mortality among 522 Swedish workers exposed to cadmium for at least one year in a nickel-cadmium battery plant support the earlier findings. The SMR for lung and prostatic cancer increased with increasing dose and latency but did not obtain statistical significance. A combination of all the available data from the most recent follow up of causes of death among cadmium workers in six different cohorts shows 28 cases of prostatic cancer (SMR = 162) and 195 cases of lung cancer (SMR = 121). This new analysis suggests that long term, high level exposure to cadmium is associated with an increased risk of cancer. The role of concomitant exposure to nickel needs further study.
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PMID:Cancer mortality of cadmium workers. 404 82

One hundred and one patients with histologically confirmed prostate cancer and 202 hospital controls individually matched by age (+/- 2 years), hospital admittance and place of residence, were interviewed during the period 1990-94 in two towns in central Serbia (Yugoslavia). In an analysis using multivariate logistic regression, the followng factors were significantly related to prostate cancer: (1) occupational physical activity during the year preceding the disease [odds ratio (OR)=3.87, 95% confidence interval (95% CI)=2.09-7.16]; (2) occupational exposure to asbestos, steel, dyes and lacquers, bitumen, pitch, iron, nickel, lead, fertilizer and certain other agents (OR=2.13, 95% CI=1.05-4.32); (3) nephrolithiasis (OR=4.52, 95% CI=1.34-15.30); (4) 'other' diseases in medical history such as chronic bronchitis, chronic rheumatic diseases, hypertension, cardiomyopathy, diabetes mellitus, renal diseases, eye diseases and tuberculosis (OR=3.14, 95% CI=1.56-6.33); (5) a greater number (> or = 3) of brothers (OR=2.08, 95% CI=1.35-3.22); and (6) greater numbers (> or = 8) of sexual partners (OR=2.24, 95% CI=1.13-4.44). Marital status, age at first marriage, educational level, age at first sexual intercourse, frequency of sexual intercourse, venereal diseases, tonsillectomy, appendectomy, hernia inguinale and hydrocele, anthropometric characteristics, smoking history, sport and recreational activities and family history of prostatic neoplasms were not found to be independently related to prostate cancer.
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PMID:Case-control study of risk factors for prostate cancer. 893 56

Temporary metallic intraprostatic stent is a new alternative treatment for patients with urinary obstructive syndrome caused by prostate cancer. Definitive radiotherapy is a treatment of choice for localized prostate cancer. This study evaluates in vitro the effect of a urethral intraprostatic metallic stent on the dose absorbed by the surrounding tissue. The study was designed to mimic the conditions under which the prostatic stent is placed in the body during pelvic irradiation. A urethral stent composed of a 50% nickel-50% titanium alloy (Uracoil-InStent) was imbedded in material mimicking normal tissue (bolus) at a simulated body depth of 10 cm. The distribution of the absorbed dose of irradiation was determined by film dosimetry using Kodak X-Omat V film. Irradiation was done in a single field at the isocenter of a 6 MV linear accelerator with a field size of 7 x 7 cm. The degree of film blackening was in direct proportion to the absorbed dose. The measurements showed an increase in dose of up to 20% immediately before the stent and a decrease of up to 18% immediately after the stent. These changes occurred within a range of 1-3 mm from both sides of the stent. In practice, irradiation in prostate cancer is given by two pairs of opposed co-axial fields; a total of four fields (Box Technique). The dose perturbations are partly cancelled in a pair of opposed beams resulting in a net variation of +/- 4%; therefore, the presence of the intraprostatic stent should not influence radiotherapy planning for prostate cancer.
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PMID:Dose perturbation due to the presence of a prostatic urethral stent in patients receiving pelvic radiotherapy: an in vitro study. 924 65

Hypotonicity-induced Ca2+ signals and volume regulation were studied in proliferating and quiescent subpopulations of multicellular prostate cancer spheroids. Enzymatic dissociation of multicellular spheroids 100+/-19 microm in diameter, which are entirely proliferative, yielded a population of cells with a mean cell diameter of 17.5+/-1.4 microm. After dissociation of spheroids in a size class of 200+/-30, 300+/-60, and 400+/-65 microm in diameter, two subpopulations of cells with mean cell diameters corresponding to 12.9+/-1.9 microm and 16.7+/-2 microm were discriminated. The subpopulation of large cells was shown to be proliferative by positive Ki-67 antibody staining; the subpopulation of small cells was Ki-67 negative, indicating cell quiescence. In a spheroid size class of 100+/-19 microm, a distinct subpopulation of quiescent cells was absent. Superfusion by hypotonic solutions revealed that only the proliferating cell fraction showed a regulatory volume decrease (RVD) and a [Ca2+]i transient. Both effects were absent in the quiescent cell population. The [Ca2+]i transient persisted in low (10 nM) Ca2+ solution and in the presence of 4 mM extracellular Ni2+ but was abolished in the presence of the endoplasmic reticulum Ca2+-ATPase blocker 2,5-di-tert-butyl-hydrochinone (t-BHQ). The t-BHQ likewise inhibited RVD, indicating that Ca2+ release from intracellular stores was necessary for RVD. Moreover, [Ca2+]i and RVD were dependent on an intact microfilament cytoskeleton because after 30 min of preincubation with cytochalasin B the [Ca2+]i transient was significantly reduced and RVD was abolished. The absence of RVD and [Ca2+]i transient in quiescent cells may be due to differences in the amount and the cytosolic arrangement of F-actin observed in quiescent cells.
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PMID:Hypotonic Ca2+ signaling and volume regulation in proliferating and quiescent cells from multicellular spheroids. 952 71

Ferromagnetic Ni-Cu alloy wires were characterized in order to obtain well-defined thermoseeds for application in interstitial hyperthermia of prostate cancer. Thermoseeds have been produced which possess Curie points in the therapeutic hyperthermia range, approximately 40 to 50 degrees C. The effect of thermal treatment and composition on the heating characteristics of the thermoseeds were investigated. The preliminary study shows that the recrystallization is crucial for altering thermoseeds' heating characteristics. Obtaining thermoseeds which behave as desired depends on changes in annealing times and temperatures. One may increase the maximum heating temperature (similar to Curie temperature) by increasing the annealing time and cooling time. Decreasing the lower annealing plateau temperature also increases the maximum seed heating temperature. Higher nickel content compositions did not affect rise time but increased the maximum heating temperature.
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PMID:Effect of thermal treatment on heating characteristics of Ni-Cu alloy for hyperthermia: preliminary studies. 1014 46

1. In the present study, we investigated the mechanisms involved in the induction of apoptosis by the Ca2+-ATPase inhibitor thapsigargin (TG), in androgen-sensitive human prostate cancer LNCaP cells. 2. Exposure of fura-2-loaded LNCaP cells to TG in the presence of extracellular calcium produced an increase in intracellular Ca2+, the first phase of which was associated with depletion of intracellular stores and the second one with consecutive extracellular Ca2+ entry through plasma membrane, store-operated Ca2+ channels (SOCs). 3. For the first time we have identified and characterized the SOC-mediated membrane current (Istore) in prostate cells using whole-cell, cell-attached, and perforated patch-clamp techniques, combined with fura-2 microspectrofluorimetric and Ca2+-imaging measurements. 4. Istore in LNCaP cells lacked voltage-dependent gating and displayed an inwardly rectifying current-voltage relationship. The unitary conductance of SOCs with 80 mM Ca2+ as a charge carrier was estimated at 3.2 +/- 0.4 pS. The channel has a high selectivity for Ca2+ over monovalent cations and is inhibited by Ni2+ (0.5-3 mM) and La3+ (1 microM). 5. Treatment of LNCaP cells with TG (0.1 microM) induced apoptosis as judged from morphological changes. Decreasing extracellular free Ca2+ to 200 nM or adding 0.5 mM Ni2+ enhanced TG-induced apoptosis. 6. The ability of TG to induce apoptosis was not reduced by loading the cells with intracellular Ca2+ chelator (BAPTA-AM). 7. These results indicate that in androgen-sensitive prostate cancer cells the depletion of intracellular Ca2+ stores may trigger apoptosis but that there is no requirement for the activation of store-activated Ca2+ current and sustained Ca2+ entry in induction and development of programmed cell death.
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PMID:Store depletion and store-operated Ca2+ current in human prostate cancer LNCaP cells: involvement in apoptosis. 1094 71

The cell--cell adhesion molecule 1 (C-CAM1) plays an important role as a tumor suppressor for prostate cancer. Decreased expression of C-CAM1 was detected in prostate, breast, and colon carcinoma. Reexpression of C-CAM1 in prostate and breast cancer cell lines was able to suppress tumorigenicity in vivo. These observations suggest that C-CAM1 may be used as a marker for cancer detection or diagnosis. To generate monoclonal antibodies specific to C-CAM1, we have overexpressed full-length human C-CAM1 in Sf9 cells using a baculovirus expression system. The protein was purified 104-fold using nickel affinity chromatography. About 0.4 mg purified C-CAM1 was obtained from 200 mg of infected cells. When the purified protein was digested with peptidyl-N-glycosidase, the apparent mobility of the protein on SDS--PAGE changed from 90 to 58 kDa, which is close to the molecular weight predicted from the cloned cDNA sequence. This observation suggests that C-CAM1 was glycosylated on asparagine residues when expressed in Sf9 cells. Western blotting and internal protein sequencing analysis confirmed that the purified protein is human C-CAM1. Biochemical and functional assays indicate that this protein expressed in Sf9 cells displays characteristics similar to those of native protein, including adhesion function and glycosylation modification. Using this protocol, sufficient quantity of this protein can be produced with purity suitable for monoclonal antibody generation and biochemical study.
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PMID:Purification and characterization of human cell--cell adhesion molecule 1 (C-CAM1) expressed in insect cells. 1123 97


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