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)

Mortality rates from multiple sclerosis show a well-known north-south gradient, both within the United States and internationally. Mortality rates from prostate cancer show a similar gradient and are significantly correlated with multiple sclerosis (MS) mortality and MS prevalence. This finding adds prostate cancer to the set of diseases whose geographic distributions are significantly correlated with MS and whose members include colon cancer, dental caries, and Parkinson's disease. Review of the literature indicates that these clinically dissimilar diseases may share an aberration in vitamin (hormone) D. Recent evidence demonstrating a multi-faceted role for vitamin D in immunoregulation suggests that a vitamin D aberration may also contribute to the etiology of MS. A vitamin D hypothesis can illuminate several unexplained features of the epidemiology of MS and suggests opportunities for epidemiologic, laboratory, and clinical investigation.
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PMID:Multiple sclerosis and prostate cancer: what do their similar geographies suggest? 129 88

Between 1992 and 2040, the United States nonwhite elderly population is expected to grow from 3.3 to 14.1 million. In order to assess the implications of this increase on the mortality from neurodegenerative diseases in the United States, we used Census Bureau population estimates to formulate projections of the annual number of deaths from neurodegenerative diseases and from six comparison conditions (liver cirrhosis, colon cancer, lung cancer, cancer of the female breast, multiple sclerosis, and malignant melanoma), assuming that the United States disease-age-gender-specific death rates for 1985-1988 remain constant between 1990 and 2040. We find that neurodegenerative disease mortality increases by 281-524%, depending on the model of population growth used. For the 'middle' population growth model, the increase in annual neurodegenerative disease mortality is 373%. The major component of this increase is the rise in deaths attributed to dementia. For the six comparison diseases, the increases in mortality range from 130 (multiple sclerosis) to 288% (colon cancer). Given the current level of underascertainment of neurodegenerative disease mortality, particularly among minorities, and the conservative nature of the Census Bureau estimates of future population, it is likely that these projections are under-estimates. The implications of these data are discussed.
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PMID:Projected neurodegenerative disease mortality among minorities in the United States, 1990-2040. 809 Feb 60

Between 1990 and 2040, the United States elderly population is expected to grow from 31.6 to 68.1 million. In order to assess the implications of this increase on the mortality from neurodegenerative diseases in the United States, we used Census Bureau population estimates to formulate projections of the annual number of deaths from neurodegenerative diseases and from six comparison conditions (liver cirrhosis, colon cancer, lung cancer, cancer of the female breast, multiple sclerosis, and malignant melanoma), assuming that the United States disease-age-gender-race-specific death rates for 1985-1988 remain constant between 1990 and 2040. We find that neurodegenerative disease mortality increases by 119-231%, depending on the model of population growth used. For the 'middle' population growth model, the increase in annual neurodegenerative disease mortality is 166%. The major component of this increase is the rise in deaths attributed to dementia. For the six comparison diseases, the increases in mortality range from 52 (multiple sclerosis) to 130% (colon cancer). Given the current level of under ascertainment of neurodegenerative disease mortality and the conservative nature of the Census Bureau estimates of future population, it is likely that these projections are underestimates. The implications of these data are discussed.
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PMID:Projected neurodegenerative disease mortality in the United States, 1990-2040. 827 81

A multifocal inflammatory leukoencephalopathy is associated with the administration of 5-fluorouracil (5-FU), a pyrimidine analogue, and levamisole (LE), an immunomodulator, in patients receiving adjuvant therapy for colon cancer. Cerebral biopsy demonstrated features indistinguishable from multiple sclerosis. We tested whether administration of these agents directly resulted in inflammatory demyelination in mice or whether they exacerbated demyelination in a host predisposed to myelin injury. We used mice intracerebrally infected with Theiler's murine encephalomyelitis virus (TMEV) which serves as an excellent model for multiple sclerosis. Varying dosages of 5-FU (240 micrograms-2.4 mg) and LE (40 micrograms-1 mg) were administered alone or in combination on a fixed schedule to 52 normal SJL mice and 61 Theiler's virus-infected mice (51 SJL/J mice susceptible to demyelination; 10 C57BL10 mice resistant to demyelination). Controls included 6 noninfected SJL and 26 infected mice (16 susceptible; 10 resistant) treated with phosphate-buffered saline (PBS). Inflammation or demyelination was not detected in brains or spinal cords of noninfected SJL mice treated with 5-FU and/or LE. TMEV-susceptible SJL mice treated with LE alone or in combination with 5-FU demonstrated more extensive inflammation and demyelination at Day 45 than mice treated with PBS. Demyelination was accelerated in infected animals treated with these agents at 45 days but at 70 days a significant difference in extent of demyelination was no longer appreciated between treatment and control groups. Treatment with 5-FU and LE did not convert normally resistant TMEV-infected C57BL/10 mice to demyelination. These experiments support the hypothesis that 5-FU and LE may exacerbate inflammatory demyelination in a susceptible host.
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PMID:5-Fluorouracil and levamisole exacerbate demyelination in susceptible mice infected with Theiler's virus. 929 9

JC polyoma virus (JCV) is known to be the cause of the degenerative central nervous system white matter disease progressive multifocal leucoencephalopathy. Recently, JCV DNA has unexpectedly been found in significant quantity in normal colon mucosa and in tissue from colonic carcinomas, with increased quantities in the cancerous tissues. The yield of JCV DNA was increased by use of topoisomerase I, possibly because the JCV DNA was negatively supercoiled. The causes of ulcerative colitis (in which colon cancer is common) and multiple sclerosis are not known. Here I suggest that JCV may play a role in the pathogenesis of these diseases, and discuss methods for testing this hypothesis.
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PMID:Is JC polyoma virus the cause of ulcerative colitis and multiple sclerosis? 1100 63

For the last 15 yr, a great deal of knowledge has been accumulated on health beneficial factors, protein and nonprotein, of bovine milk fat globule membrane (MFGM). Among the health-beneficial components of the MFGM are cholesterolemia-lowering factor, inhibitors of cancer cell growth, vitamin binders, inhibitor of Helicobacter pylori, inhibitor of beta-glucuronidase of the intestinal Escherichia coli, xanthine oxidase as a bactericidal agent, butyrophilin as a possible suppressor of multiple sclerosis, and phospholipids as agents against colon cancer, gastrointestinal pathogens, Alzheimer's disease, depression, and stress. All of the above compel us to consider bovine MFGM as a potential nutraceutical.
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PMID:Invited review: Bovine milk fat globule membrane as a potential nutraceutical. 1595 91

Cytokines (interleukins, chemokines, and some growth factors) play an important role in cancer, metabolic disorders, autoimmune disorders and inflammatory diseases, such as rheumatoid arthritis, asthma, Crohn's disease, psoriasis, multiple sclerosis and asthma. Cytokine-based drugs and anticytokine therapies are an increasingly important class of drugs in the treatment and management of many diseases. Interferons are being used to treat viral diseases and cancers. Anti-tissue necrosis factor therapies, such as Enbrel (etanercept; Immunex Corp) and Remicade (infliximab; Centocor) have demonstrated clinical efficacy in rheumatoid arthritis and Crohn's disease. In addition, thalidomide (Celgene) is being used to treat erythema nodosum in leprosy, cancers (multiple myeloma and colon cancer) and autoimmune diseases. This conference focused on new developments in basic research, drug discovery and clinical development of cytokine-based drugs.
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PMID:Cytokines as drug targets. 1601 67

Vitamin D from ultraviolet-B (UVB) irradiance, food, and supplements is receiving increased attention lately for its role in maintaining optimal health. Although the calcemic effects of vitamin D have been known for about a century, the non-calcemic effects have been studied intently only during the past two-three decades. The strongest links to the beneficial roles of UVB and vitamin D to date are for bone and muscle conditions and diseases. There is also a preponderance of evidence from a variety of studies that vitamin D reduces the risk of colon cancer, with 1000 IU/day of vitamin D or serum 25-hydroxyvitamin D levels >33 ng/mL (82 nmol/L) associated with a 50% lower incidence of colorectal cancer. There is also reasonable evidence that vitamin D reduces the risk of breast, lung, ovarian, and prostate cancer and non-Hodgkin's lymphoma. There is weaker, primarily ecologic, evidence for the role of vitamin D in reducing the risk of an additional dozen types of cancer. There is reasonably strong ecologic and case-control evidence that vitamin D reduces the risk of autoimmune diseases including such as multiple sclerosis and type 1 diabetes mellitus, and weaker evidence for rheumatoid arthritis, osteoarthritis, type 2 diabetes mellitus, hypertension and stroke. It is noted that mechanisms whereby vitamin D exerts its effect are generally well understood for the various conditions and diseases discussed here.
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PMID:Epidemiology of disease risks in relation to vitamin D insufficiency. 1654 42

The sun is our most important source of vitamin D. Exposure to solaria, in sub-erythemogenic doses, also gives large amounts of this vitamin. The ultraviolet radiation in these sources converts 7-dihydrocholesterol to previtamin D3 in the skin. Furthermore, heat isomerization to vitamin D3 takes place, then transport to the liver and hydroxylation to calcidiol, which is transported to the kidneys and hydroxylated to the active hormone calcitriol. The vitamin D3 status of the body is supposed to be reliably imaged by calcidiol measurements. Calcidiol levels above 12.5 nmol/l prevent rickets and osteomalacia, but optimal levels are probably higher, in the range 100-250 nmol/l. A daily food intake of 100-200 microg vitamin D3 (50-100 g cod-liver oil), or a weekly exposure to two minimal erythemal doses of ultraviolet radiation (20 to 40 minutes whole body exposure to midday midsummer sun in Oslo, Norway), will give this level. An adequate supply of vitamin D3 seems to reduce the incidence rates or improve the prognosis of several cancer forms, including prostate, breast and colon cancer, as well as of lymphomas. Several other diseases are related to a low vitamin D3 status: heart diseases, multiple sclerosis, diabetes, and arthritis. The action mechanisms of vitamin D are thought to be mainly related to its known cell-differentiating and immuno-modulating effects. Even though most of the 250 annual death cases from skin cancer in Norway are caused by sun exposure, we should, in view of the health effects of ultraviolet radiation, consider modifying our restrictive attitude towards sun exposure and use of solaria.
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PMID:[The photobiology of vitamin D--a topic of renewed focus]. 1677 Mar 83

Adjuvants are essential components of vaccines that augment an immunological reaction of organism. New vaccines based on recombinant proteins and DNA, are more save than traditional vaccines but they are less immunogenic. Therefore, there is an urgent need for the development of new, improved vaccine adjuvants. There are two classes of adjuvants: vaccine delivery systems (e.g. emulsions, microparticles, immune-stimulating complexes ISCOMs, liposomes) and immunostimulatory adjuvants (e.g. lipopolysaccharide, monophosphoryl lipid A, CpG DNA, or muramylpeptides). The discovery of more potent and safer adjuvants may allow to development better prophylactic and therapeutic vaccines against chronic infectious (e.g., HSV, HIV, HCV, HBV, HPV, or Helicobacter pylori) and noninfectious diseases as multiple sclerosis, insulin-dependent diabetes, rheumatoid arthritis, allergy and tumors (e.g., melanoma, breast, or colon cancer).
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PMID:[Adjuvants--essential components of new generation vaccines]. 1707 10


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