Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with regular use of nonsteroidal antiinflammatory drugs (NSAIDs) appear to have a reduced mortality from colon cancer. As NSAID use is associated with gastrointestinal bleeding, endoscopic exploration of patients on NSAID may lead to more efficient screening and frequent detection of colon cancer. A case-control study was conducted among 12,304 veterans with a colon cancer diagnosed between 1988 and 1992. Four controls were matched by age, sex, and race to each case. The frequency distributions of previous discharge diagnoses in cases and controls were compared. Arterial embolism and thrombosis, spondylosis, peripheral vascular disease, angina, osteoarthrosis, and ischemic heart disease protected against future development of colon cancer. On the other hand, atrial fibrillation and flutter, as well as phlebitis and thrombophlebitis, were associated an increased occurrence of colon cancer after 5-10 years. The study contrasts diseases that are treated with aspirin with those that are treated with other anticoagulants. Both cause bleeding, but the reduced risk of colon cancer was seen only in conditions treated with aspirin. The difference between the two disease groups from the same VA patient population suggests that chronic use of NSAID truly protects against future development of colon cancer.
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PMID:Diseases preceding colon cancer. A case-control study among veterans. 795 19

Postmenopausal estrogen deficiency may result in a wide variety of physiologic disorders, including vasomotor symptoms, urogenital atrophy, an increase in the risk of coronary heart disease, osteoporotic fractures, and Alzheimer's disease. The growing body of evidence, including much that is newly published, demonstrating that hormone replacement therapy (HRT) can largely prevent or mitigate these sequelae, will be reviewed in this paper. The efficacy of HRT in alleviating vasomotor and urogenital discomfort, the most common symptoms of postmenopausal estrogen deficiency, is well established. Evidence from over 30 epidemiologic studies indicates that estrogen reduces the risk of coronary heart disease (CHD) by 50%. The risk of major CHD has been found to be markedly reduced in women who receive combined estrogen/progestogen therapy compared to nonusers (or estrogen-alone users). Estrogen is recommended as the modality of choice to prevent bone loss: data supporting a positive effect of estrogen on the risk of wrist and vertebral fracture are quite favorable. Similarly, outcomes of recent investigations have demonstrated a positive impact of HRT on both psychological function and the risk of osteoarthritis. In addition, HRT substantially reduces the risk of colon cancer. Moreover, the potential for HRT to delay the progression or reduce the risk for developing Alzheimer's disease is a new area of research that shows promise. Improvements in quality-of-life assessments have also been reported in conjunction with the relief of menopausal symptoms by HRT. Clinicians should be aware of the large amount of new evidence that strengthens the case for wider use of HRT. Based on these new data, physicians may conclude that HRT would benefit the majority of their postmenopausal patients and thus encourage HRT use in the absence of known risk factors.
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PMID:Benefits of hormone replacement therapy--overview and update. 939 82

This study was undertaken to update and revise the estimate of the economic impact of obesity in the United States. A prevalence-based approach to the cost of illness was used to estimate the economic costs in 1995 dollars attributable to obesity for type 2 diabetes mellitus, coronary heart disease (CHD), hypertension, gallbladder disease, breast, endometrial and colon cancer, and osteoarthritis. Additionally and independently, excess physician visits, work-lost days, restricted activity, and bed-days attributable to obesity were analyzed cross-sectionally using the 1988 and 1994 National Health Interview Survey (NHIS). Direct (personal health care, hospital care, physician services, allied health services, and medications) and indirect costs (lost output as a result of a reduction or cessation of productivity due to morbidity or mortality) are from published reports and inflated to 1995 dollars using the medical component of the consumer price index (CPI) for direct cost and the all-items CPI for indirect cost. Population-attributable risk percents (PAR%) are estimated from large prospective studies. Excess work-lost days, restricted activity, bed-days, and physician visits are estimated from 88,262 U.S. citizens who participated in the 1988 NHIS and 80,261 who participated in the 1994 NHIS. Sample weights have been incorporated into the NHIS analyses, making these data generalizable to the U.S. population. The total cost attributable to obesity amounted to $99.2 billion dollars in 1995. Approximately $51.64 billion of those dollars were direct medical costs. Using the 1994 NHIS data, cost of lost productivity attributed to obesity (BMI> or =30) was $3.9 billion and reflected 39.2 million days of lost work. In addition, 239 million restricted-activity days, 89.5 million bed-days, and 62.6 million physician visits were attributable to obesity in 1994. Compared with 1988 NHIS data, in 1994 the number of restricted-activity days (36%), bed-days (28%), and work-lost days (50%) increased substantially. The number of physician visits attributed to obesity increased 88% from 1988 to 1994. The economic and personal health costs of overweight and obesity are enormous and compromise the health of the United States. The direct costs associated with obesity represent 5.7% of our National Health Expenditure in the United States.
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PMID:Current estimates of the economic cost of obesity in the United States. 954 25

Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase (COX) activity, thereby suppressing the synthesis of proinflammatory prostaglandins. The identification and molecular-biological characterization of an inducible COX isoform (COX-2) in inflammatory cells led to the hypothesis that a selective inhibition of COX-2 would result in relief of inflammation and pain without causing the COX-1-dependent side effects (gastrointestinal ulceration, platelet dysfunction, kidney damage) of conventional NSAIDs. On the basis of data obtained in several laboratories by means of the "human whole blood assay" there is now convincing evidence that none of the currently available NSAIDs is a selective COX-2 inhibitor. Meanwhile, the specific COX-2 inhibitors celecoxib and rofecoxib are being tested worldwide in phase III clinical trials on patients with rheumatoid arthritis and osteoarthritis. However, the simple concept of COX-2 being an exclusively proinflammatory inducible enzyme cannot be upheld any longer. In addition, COX-2 is expressed constitutively in brain, spinal cord and kidney, as well as in numerous other organs. In the present review the perspectives and possible risks of specific COX-2 inhibitors are discussed, as well as additional indications for their implementation (e.g. colon cancer).
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PMID:[Specific COX-2 inhibitors: prospects of therapy with new analgesic and anti-inflammatory substances]. 1009 92

Animal and human data demonstrate that cyclooxygenase (COX)-2 upregulation in osteoarthritis and rheumatoid arthritis is associated with the pain and inflammation of the disease state. The COX-1 isoform, however, is a constitutive enzyme with homeostatic functions. Unlike conventional nonsteroidal anti-inflammatory drugs, which inhibit both forms of the COX enzyme, celecoxib inhibits COX-2 preferentially to COX-1 in vitro. Celecoxib reversed signs of arthritis and pain in an animal model as effectively as indomethacin. Data from murine studies as well as in vitro and epidemiologic data indicate that COX-2 plays a role in the development of colon cancer, and epidemiologic studies also suggest that COX inhibition can slow the progression of Alzheimer's disease.
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PMID:Role of cyclooxygenase-1 and -2 in health and disease. 1019 97

A nationwide, computer-based survey of all total joint arthroplasties performed in Finland has been carried out since January 1980. From these records, a cohort of 9,444 patients, with 51,756 person-years, after primary operation with a total polyethylene-on-metal knee arthroplasty (TKA) was followed up for cancer through the Finnish Cancer Register up to December 31, 1996. During the follow-up, 706 cancers were observed. The expected number, based on national rates, was 719; therefore, the standardized incidence ratio (SIR) for all cancers was 0.98. The SIRs for non-Hodgkin's lymphoma (1.40), Hodgkin's disease (1.24) and multiple myeloma (1.54) were increased, but only that of non-Hodgkin's lymphoma was statistically significant 3-10 years after the operation. The numbers of observed cases of prostate cancer exceeded that of expected, with a SIR value of 1.49. A low SIR of lung cancer was observed among men, especially during the first 3 years (0.61), but not in women. The SIR for colon cancer was below unity in women only (SIR 0.70). The SIR for cancer of the urinary organs was close to unity (0.97). SIR relating to soft tissue and bone cancer did not differ significantly from unity, and none of the 6 sarcomas was observed at the site of a prosthesis. The overall cancer risk after TKA done for primary osteoarthrosis seems not to be increased. The increases in lymphoma and prostate cancer risk, however, are observations that could be related to TKA and justify further follow-up of the cohort.
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PMID:Cancer incidence after total knee arthroplasty: a nationwide Finnish cohort from 1980 to 1996 involving 9,444 patients. 1066 28

Evidence derived from several lines of investigation suggest that prostaglandins, metabolites of arachidonic acid, play an important role in colon cancer development. Elevated prostaglandin levels are found in colon cancers and their precursor lesions, adenomatous polyps. Agents such as aspirin and NSAIDs, which inhibit the generation of these arachidonic acid metabolites, are associated with a decreased risk of developing or dying from colon cancer. Both the amount of the agent used and the duration of exposure seem to be important variables. In animals, NSAIDs are among the most potent agents discovered for the reduction of tumors in both genetic and carcinogen-induced models. Data from human trials also suggests that NSAIDs such as sulindac can reduce the size and number of polyps in individuals with familial adenomatous polyposis (FAP). In parallel with the above findings, it is now understood that at least two forms of the enzyme responsible for the metabolism of arachidonic acid exist. One of these forms, COX-1, is generally considered a constitutive form that is responsible for maintaining normal physiologic function. Inhibition of COX-1 leads to many of the clinically undesirable side effects associated with NSAID use. The other known form of the enzyme, COX-2, is an inducible form that is found in increased levels in inflammatory states and in many cancers and their associated pre-malignant lesions. Levels of COX-2 are increased by exposure to mitogens and growth factors. Agents that specifically inhibit COX-2 are now in clinical development and appear to be well-tolerated and effective for the treatment of osteoarthritis and rheumatoid arthritis. The potential for use of COX-2 specific NSAIDs in the prevention of colon cancer is suggested from the distribution of COX-2 in adenomatous polyps and colon cancer and the effectiveness of these agents in genetic and carcinogen-induced animal models of colon cancer. The development of these agents for the prevention of colon cancer will be discussed.
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PMID:COX-2 and colon cancer: potential targets for chemoprevention. 1076 21

Prostaglandins are formed from arachidonic acid by the action of cyclooxygenase and subsequent downstream synthetases. Two closely related forms of the cyclooxygenase have been identified which are now known as COX-1 and COX-2. Both isoenzymes transform arachidonic acid to prostaglandins, but differ in their distribution and their physiological roles. Meanwhile, the responsible genes and their regulation have been clarified. COX-1, the pre-dominantly constitutive form of the enzyme, is expressed throughout the body and performs a number of homeostatic functions such as maintaining normal gastric mucosa and influencing renal blood flow and platelet aggregation. In contrast, the inducible form is expressed in response to inflammatory and other physiological stimuli and growth factors, and is involved in the production of the prostaglandins that mediate pain and support the inflammatory process. All the classic NSAIDs inhibit both COX-1 and COX-2 at standard anti-inflammatory doses. The beneficial anti-inflammatory and analgesic effects are based on the inhibition of COX-2, but the gastrointestinal toxicity and the mild bleeding diathesis are a result of the concurrent inhibition of COX-1. Agents that inhibit COX-2 while sparing COX-1 represent a new attractive therapeutic development and could represent a major advance in the treatment of rheumatoid arthritis and osteoarthritis. Apart from its involvement in inflammatory processes, COX-2 seems to play a role in angiogenesis, colon cancer and Alzheimer's disease, based on the fact that it is expressed during these diseases. The benefits of specific and selective COX-2 inhibitors are currently under discussion and offer a new perspective for a further use of COX-2 inhibitors.
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PMID:Cyclooxygenase inhibitors--current status and future prospects. 1131 43

Many genetic, environmental, behavioral, and cultural factors affect health. Diet is as vital as any of them for preventing disease and promoting well-being. We know that what we eat can lead to premature disability and mortality: to obesity, coronary heart disease, type 2 diabetes, degenerative arthritis, sleep apnea, and other illnesses. Now scientific evidence points to links between dietary patterns and illness. The study of these links is a new approach to understanding the role that diet plays in chronic disease. Initial studies include those on eating patterns and risk of colon cancer. More recently, researchers have investigated all-cause mortality and leading causes of chronic disease. Novel epidemiological approaches include factorial analysis to evaluate dietary patterns and cluster analysis to examine nutrient intake, gender, and weight status across food-pattern clusters. These methods work best within groups to identify major dietary patterns, but not necessarily ideal diets. They may also differ across population groups. The success of the Dietary Approaches to Stop Hypertension and Lyon Diet Heart studies supports the value of dietary pattern analysis. At the same time, the relative failure of single-nutrient studies underscores the need for new methodologies and directions in research.
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PMID:Treatment approaches: food first for weight management and health. 1170 45

The discovery of the isoenzymes cyclooxygenase-(COX-) 1 and COX-2 led to the development of newer nonsteroidal anti-inflammatory drugs (NSAIDs) designed to block COX-2, such as rofecoxib, celecoxib, and valdecoxib. Because of the specificity of COX-2 expression, COX-2 inhibitors have the potential to reduce the risk of gastrointestinal bleeding experienced with the use of classic NSAIDs. With their crucial role in the control of inflammation, the COX-2 agents originally were marketed for the treatment of rheumatoid and osteoarthritis. However, promising new indications for COX-2 agents in the prevention and treatment of cancer are under investigation. The role of aberrant COX-2 expression in the development of cancer has been studied most widely in patients with colon cancer and adenomas. Recent studies suggest that COX-2-derived prostaglandins may play an important role in tumor viability, growth, and control of metastasis. Possible new indications for the use of COX-2 inhibitors to prevent and treat cancers may be monumental. However, therapy with these agents is not without risk. Oncology nurses must be aware of the potential problems inherent in the use of COX-2 as well as COX-2 agents for chemoprevention in certain cancers.
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PMID:Cyclooxygenase-2: from arthritis treatment to new indications for the prevention and treatment of cancer. 1262 31


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