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)

A patient is reported who developed the first symptoms of spinal motor neuron affection 20 years prior to his death at the age of 79. In the course of the disease dementia and spasticity of the legs occurred. The patient died of metastasizing carcinoma of the colon. The autopsy revealed amyloid angiopathy of the brain and cervical spinal cord, corresponding to the clinical symptomatology. So far, 11 cases of amyloid angiopathy have been reported in which dementia was preceded by dysarthric speech, ataxia and/or spasticity of the legs. We assume that these cases represent a distinct nosological entity, different from a variant course of Alzheimer's disease. The atypical symptomatology may cause problems in the diagnosis of amyloid angiopathy of the CNS.
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PMID:Congophilic angiopathy with cerebrospinal symptoms. 365 49

We observed leukoencephalopathy in 1 patient, and progressive dementia in another, during the administration of 5-fluorouracil (5-FU) and levamisole. A retrospective search, among 80 other patients with resected colorectal cancer receiving 5-FU and levamisole as adjuvant therapy, 166 resected malignant melanoma patients receiving adjuvant levamisole, and 254 advanced colorectal cancer patients receiving 5-FU often combined with leucovorin, for other cases of encephalopathy was negative. The frequency of this neurotoxicity is low (about 2% of patients receiving 5-FU and levamisole), but it appears specific for this combination of drugs. The lack of complete reversibility on stopping the drugs is worrisome, as this therapy is used to improve the curability of resected colon cancer.
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PMID:Disabling encephalopathy during 5-fluorouracil and levamisole adjuvant therapy for resected colorectal cancer: a report of two cases. 758 11

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

Susceptibility to most common human diseases is, at least in part, determined by genetic factors. Rapid progress is being made in defining these genetic determinants for a range of diseases including breast cancer, colon cancer, diabetes, arthritis and dementia. The ability to define susceptibility in genetic terms has already led to a reclassification of some of these diseases on genetic and mechanistic grounds. This information is likely to have a profound effect on our approach to human diseases as it will allow a better definition of these disorders, permitting more effective therapeutic intervention, and will lead to both a more precise understanding of the natural history of these diseases and the possibility of identifying populations at risk. An understanding of the mechanisms underlying disease susceptibilty will also improve our ability to develop rational therapeutic interventions for many of these diseases. The role of genetic screening in these common diseases will be discussed, particularly in regard to the application of health care in populations.
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PMID:Genetics of common disease: implications for therapy, screening and redefinition of disease. 930 70

The benefits of oestrogen replacement therapy (ERT) in preventing vasomotor symptoms, cardiovascular disease, osteoporosis, and colon cancer are well documented. Other potential benefits i.e. dementia and macular degeneration are being investigated. Although oestrogen is said to be contraindicated in women previously treated for breast and endometrial cancer, there is no data to support this admonition. Preliminary data would suggest ERT can be used safely in women who have had these cancers. Prospective randomised studies are currently on going in the United States and Europe addressing ERT in previously treated breast and endometrial cancer. Informed consent, patients' desires, and benefit-risk considerations are all part of information the woman needs to make a decision concerning ERT.
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PMID:HRT and women who have had breast or endometrial cancer. 1069 60

The common 5,10-methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism causes decreased activity of this enzyme and can be associated with mild-to-moderate hyperhomocysteinemia in homozygotes, particularly when there is folic acid deficiency, as well as with vascular dementia, arterial thrombosis, venous thrombosis, neural-tube defects, and fetal loss. When folic acid intake is sufficient, homozygotes for MTHFR 677T appear to be protected against colon cancer and acute lymphatic leukemia, and fetuses bearing this genotype have an augmented survival. The distribution of MTHFR 677T is worldwide, but its frequency in different populations varies extensively. In the present study, we addressed the question of whether the MTHFR 677T alteration has an ancestral origin or has occurred repeatedly. We analyzed the frequency distribution of the previously described polymorphism A1298C in exon 7 and of three intronic dimorphisms, in white Israelis (Jews and Arabs), Japanese, and Ghanaian Africans. The 677T allele was, remarkably, associated with one haplotype, G-T-A-C, in white and Japanese homozygotes. Among the Africans, analysis of maximum likelihood also disclosed an association with the G-T-A-C haplotype, although none of the 174 subjects examined was homozygous for MTHFR 677T. These results suggest that the MTHFR 677T alteration occurred on a founder haplotype that may have had a selective advantage.
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PMID:The frequent 5,10-methylenetetrahydrofolate reductase C677T polymorphism is associated with a common haplotype in whites, Japanese, and Africans. 1178 70

Clinical trials show that hormone therapy (HT) is an effective treatment for vasomotor symptoms and vaginal dryness. HT improves other symptoms including sleep and quality of life in women who have menopause symptoms. In the Women's Health Initiative controlled clinical trials, both estrogen therapy (ET) and estrogen plus progestin therapy (EPT) reduced fracture risk, neither reduced the risk of heart disease, and both increased the risk of stroke, deep vein thrombosis, and dementia. EPT, but not ET, increased breast cancer risk and reduced colon cancer risk. Differences between EPT and ET may reflect chance, baseline differences between the EPT and ET cohorts, or a progestin effect. Studies of younger women and lower HT doses with intermediate endpoints are beginning.
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PMID:The rise and fall of menopausal hormone therapy. 1576 Feb 83

In contrast to observational studies, clinical trials examining the efficacy of hormone replacement therapy (HRT) have shown the overall negative or deteriorating effects of HRT in postmenopausal women. Particularly, the results of Women's Health Initiative (WHI) demonstrated that HRT was preventive of fractures and colon cancer but increased the risk of myocardial infarction, stroke and dementia in addition to breast cancer and venous thromboembolism. Conversely, recent progress in androgen research suggests the efficacy of androgen replacement therapy in elderly men, pending clinical trials.
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PMID:[Risks and benefits of hormone replacement therapy]. 1818 60

This special issue of AJP is focused on research using nonhuman primates as models to further the understanding of women's health. Nonhuman primates play a unique role in translational science by bridging the gap between basic and clinical investigations. The use of nonhuman primates in biomedical research challenges our resolve to treat all life as sacred. The scientific community has responded by developing ethical guidelines for the care and the use of primates and clarifying the responsibility of investigators to insure the physical and psychological well-being of nonhuman primates used in research. Preclinical investigations often involve the use of animal models. Rodent models have been the mainstay of biomedical science and have provided enormous insight into the workings of many mammalian systems that have proved applicable to human biological systems. Rodent models are dissimilar to primates in numerous ways, which may limit the generalizability to human biological systems. These limitations are much less likely in nonhuman primates and in Old World primates, in particular, Macaques are useful models for investigations involving the reproductive system, bioenergetics, obesity and diabetes, cardiovascular health, central nervous system function, cognitive and social behavior, the musculoskeletal system, and diseases of aging. This issue considers primate models of polycystic ovary syndrome; diet effects on glycemic control, breast and endometrium; estrogen, reproductive life stage and atherosclerosis; estrogen and diet effects on inflammation in atherogenesis; the neuroprotective effects of estrogen therapy; social stress and visceral obesity; and sex differences in the role of social status in atherogenesis. Unmet research needs in women's health include the use of diets in nonhuman primate studies that are similar to those consumed by human beings, primate models of natural menopause, dementia, hypertension, colon cancer, and frailty in old age, and dedicated colonies for the study of breast cancer.
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PMID:The unique value of primate models in translational research. Nonhuman primate models of women's health: introduction and overview. 1950 47


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