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

A previous retrospective mortality study of 292 U.S. cadmium production workers employed for a minimum of 2 years showed increased mortality from respiratory and prostate cancer and from nonmalignant lung disease. To examine further the mortality experience of these workers, investigators from the National Institute for Occupational Safety and Health extended the study to include 602 white males with at least 6 months of production work in the same plant between 1940 and 1969. Vital status was determined through 1978, which included the addition of 5 years to the original follow-up. Cause-specific mortality rates for seven causes of death potentially related to cadmium exposure were compared between the overall cohort and U.S. white males and between subgroups. Mortality from respiratory cancer and from nonmalignant gastrointestinal disease was significantly greater among the cadmium workers than would have been expected from U.S. rates. All deaths from lung cancer occurred among workers employed for 2 or more years. A statistically significant dose-response relationship was observed between lung cancer mortality and cumulative exposure to cadmium. A 50% increase in lung cancer mortality, which was not statistically significant, was observed even among workers whose cumulative exposure to cadmium was between 41 and 200 micrograms/m3 over 40 years. Since the previous investigation, no new deaths from prostate cancer and no excess of deaths from nonmalignant respiratory disease have been observed.
 ...
PMID:Mortality among a cohort of U.S. cadmium production workers--an update. 385 46

We studied risk of second malignancies and causes of death in 1829 cases of adenocarcinoma and 3055 cases of carcinoid tumours in the small bowel reported to the Swedish Cancer Registry from 1960 through to 2000. Data on causes of death were analysed as from 1966 whereas data on second tumours was available during the whole registry-period. Follow-up was available until 2001. Standard mortality ratio (SMR) and standard incidence ratio (SIR) were calculated. Female patients with adenocarcinoma had increased risk of acquiring cancer in the female genital organs (SIR 3.2; 95% confidence intervals (CI) 1.9-5.0) and breasts (SIR 2.7; 95% CI 1.1-5.4). Both sexes combined had increased risk of second tumours in the gastrointestinal tract (SIR 1.5; 95% CI 1.1-2.1) and skin (SIR 4.6; 95% CI 1.2-12). Men with carcinoid tumour had increased risk of prostate cancer (SIR 2.8; 95% CI 1.6-4.6). Increased risk was seen for both sexes with carcinoid for malignant melanoma (SIR 6.3; 95% CI 2.7-12), malignant skin tumours (SIR 3.6; 95% CI 1.7-6.7) and malignancies of endocrine organs (SIR 2.3 95% CI 1.3-3.8). Patients with adenocarcinoma had increased risk of dying from malignant diseases other than the primary cancer (SMR 9.5; 95% CI 8.6-10) and gastrointestinal disease (SMR 2.6 95% CI 1.6-4.2). The cohort with carcinoid had higher than expected risk of dying from malignant disease (SMR 4.3; 95% CI 4.0-4.6), gastrointestinal disease (SMR 2.8; 95% CI 2.1-3.6) and cardiovascular disease (SMR 1.1; 95% CI 1.0-1.3). The increased risk of second malignant tumours is an indication of common aetiology, or possibly, a general vulnerability to malignant disease for these patients. A detailed analysis of causes of death in a population-based cohort of small intestinal malignancies has not been presented before in the literature.
 ...
PMID:Risk of second primary malignancies and causes of death in patients with adenocarcinoma and carcinoid of the small intestine. 1820 33

Cyclooxygenase-2 (COX-2) plays a significant role in tumor development and progression. Nonsteroidal anti-inflammatory drugs (NSAID) exhibit potent anticancer effects in vitro and in vivo by COX-2-dependent and COX-2-independent mechanisms. In this study, we used microarray analysis to identify the change of expression profile regulated by a COX-2-specific NSAID NS-398 (0.01 and 0.1 mmol/L), a nonspecific NSAID ibuprofen (0.1 and 1.5 mmol/L) and RNA interference (RNAi)-mediated COX-2 inhibition in PC3 prostate cancer cells. A total of 3,362 differentially expressed genes with 2-fold change and P<0.05 were identified. Low concentrations of NSAIDs and COX-2 RNAi altered very few genes (1-3%) compared with the higher concentration of NS-398 (17%) and ibuprofen (80%). Ingenuity Pathway Analysis was used for distributing the differentially expressed genes into biological networks and for evaluation of functional significance. The top 3 networks for both NSAIDs included functional categories of DNA replication, recombination and repair, and gastrointestinal disease. Immunoresponse function was specific to NS-398, and cell cycle and cellular movement were among the top functions for ibuprofen. Ingenuity Pathway Analysis also identified renal and urologic disease as a function specific for ibuprofen. This comprehensive study identified several COX-2-independent targets of NSAIDs, which may help explain the antitumor and radiosensitizing effects of NSAIDs. However, none of these categories were reflected in the identified networks in PC3 cells treated with clinically relevant low concentrations of NS-398 and ibuprofen or with COX-2 RNAi, suggesting the benefit to fingerprinting preclinical drug concentrations to improve their relevance to the clinical setting.
 ...
PMID:NS-398, ibuprofen, and cyclooxygenase-2 RNA interference produce significantly different gene expression profiles in prostate cancer cells. 1913 36