Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new medium-term in vivo model was tried using pulmonary adenoma induced by benzo(a)pyrene (BP) in newborn mice. Both inbred mice such as C57BL/5J, C57BR/cdJ. A/J mice and non inbred N:GP(S) mice were used. Benzo(a)pyrene was injected in the subscapular region of newborn mice within 24 hours after birth at a dose of 0.5 mg and 1 mg per mouse, respectively. After 9 weeks lung tumor induced in N:GP(S) and A/J mice but in the other mice. The dose showing a 50% tumor incidence was found in N:GP(S) mice to be 0.5 mg of BP but the tumor incidence was very high in A/J mice even at 40 micrograms of BP, the lowest dose in this experiment. To verify the utility of this model, ascorbic acid, carrot, beta carotene, soybean lecithin, spinach, Sesamum indicum, Ganoderma lucidum, caffeine, red ginseng extract, fresh ginseng and 13-cis retinoic acid, some of which are known to have anticarcinogenic activity in various animal models, were tried with this system. Ascorbic acid, soybean lecithin, Ganoderma lucidum, caffeine and red ginseng extract showed inhibition of lung tumor incidence, while fresh ginseng, carrot, beta carotene, spinach and 13-cis retinoic acid did not. This result suggested that the 9-week medium-term model using lung tumor induced by 0.5 mg of BP was useful for the screening of cancer preventive agents.
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PMID:Trial of a new medium-term model using benzo(a)pyrene induced lung tumor in newborn mice. 764 68

In many large bowel chemoprevention trials adenomas have a double duty: they are used to identify subjects at risk for large bowel neoplasia, and also serve as endpoints. Many features of adenomas make them suitable for these tasks. Patients with adenomas are fairly numerous and easy to identify; further, the 'adenoma-carcinoma' sequence suggests that adenomas are logical endpoints. The high recurrence risk among adenoma patients means that a relatively modest number of subjects will suffice for adequate statistical power. The are some limitations to the use of adenomas, however. There is clearly heterogeneity of risk for subsequent cancer. Patients with only small adenomas may have rates of colorectal cancer that are not much greater than those of the general population. Certainly subjects with large adenomas, and those with villous or highly dysplastic adenomas have a higher risk. Often, one would chose the high-risk patients for preventive interventions. Such a strategy makes sense from a risk-benefit point of view. However, from a population perspective, such a strategy may well have only a minor impact on the overall colorectal cancer burden. For more complete population-based prevention, efforts will have to be directed to the numerous individuals who are each at small risk, but who collectively account for most colorectal cancer. For this preventive approach, patients with any adenoma would certainly be part of the target population, and so are sensible subjects in chemoprevention trials. There are similar complexities in consideration of the use of adenomas as endpoints of chemoprevention trials. The adenomas that occur in prevention trials are generally small, and may not be associated with a greatly increased cancer risk. The issue for chemoprevention trials however, is not whether the endpoints are truly intermediate in the causal chain-but whether the intervention under study alters the adenoma recurrence risk to the same extent as it does for colorectal cancer risk. This is a difficult matter to verify, but the limited data available are encouraging. The epidemiology of colorectal adenomas (largely small adenomas) is similar in many regards to that for colorectal cancer itself. Thus to the extent that data are available, one can tentatively conclude that external influences affect adenomas and colorectal cancer similarly. To date, more than ten adenoma prevention trials have reported results. The data have been fairly consistent. Vitamin C (with or without vitamin E) has provided at most a modest protective benefit, except in one small trial in which it was combined with vitamin E and preformed vitamin A. beta-Carotene seems to be without any effect, and interventions to increase fiber and decrease fat intake have not indicated substantial effects. On the other hand, trials among familial polyposis patients have provided evidence for an impact of nonsteroidal anti-inflammatory drugs. Studies in progress have the potential to clarify greatly the preventive potential of the currently promising-but yet unproven-chemopreventive regimens.
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PMID:Large bowel adenomas: markers of risk and endpoints. 902 11

Apoptosis, or programmed cell death, may lower the risk of neoplasia by removing genetically damaged or mutated cells. A high rate of apoptosis has been linked to a reduced risk of colorectal adenomas; therefore, it is important to understand factors that impact apoptosis. Antioxidants (e.g., vitamin C) protect cells from harmful oxidation processes but may interfere with apoptosis by protecting genetically damaged cells from reactive oxygen species-dependent cell death. The objective of this study was to evaluate the association between vitamin C intake and apoptosis in normal rectal mucosa. Study participants were part of a large, cross-sectional study, the Diet and Health Study III. Participants were recruited from consecutive, consenting patients who underwent colonoscopy at University of North Carolina Hospitals between August 1, 1998 and March 4, 2000. Vitamin C intake, obtained from a food frequency questionnaire, included both dietary sources and vitamin supplements. Apoptosis was measured by morphological evaluation of H&E-stained sections obtained from pinch biopsy samples of normal rectal mucosa in consenting participants (n = 503). The relationship between vitamin C and apoptosis varied by adenoma status. Among individuals with adenomas, there was an inverse linear association between apoptosis and total vitamin C intake. Similarly, individuals with adenomas in the highest quintile of total vitamin C intake were substantially less likely than those in the lowest quintile to have increased colonic apoptosis (odds ratio, 0.05; 95% confidence interval, 0.01-0.46). Vitamin C was not significantly associated with apoptosis in adenoma-free patients. High vitamin C intake was associated with reduced colorectal apoptosis among individuals with adenomas in this study population. Given that high apoptosis may lower colorectal cancer risk, vitamin C supplements may be contraindicated for patients with a history of adenomas.
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PMID:Vitamin C intake and apoptosis in normal rectal epithelium. 1281 3

Previous observational studies suggest that vitamin C may reduce risk of colorectal cancer. Vitamin C transport is facilitated by membrane bound sodium-dependent transporters, SVCT1 (encoded by SLC23A1) and SVCT2 (encoded by SLC23A2). To investigate if common genetic variants in these two genes are associated with risk of colorectal tumor development, we conducted a case-control study of 656 Caucasian advanced distal colorectal adenoma cases and 665 Caucasian sigmoidoscopy-negative controls nested within the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. The analysis of common single nucleotide polymorphisms in SLC23A1 revealed no association. For SLC23A2, overall, there was no association with haplotypes, but two SNPs located in intron 8 and exon 11 could be associated (odds ratio = 0.49, 95% confidence interval = 0.25-0.95 for haplotype G-C vs. haplotype C-C). The findings should be confirmed in follow-up studies, and further investigation is required to probe the functional basis of this finding.
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PMID:Genetic variation in sodium-dependent vitamin C transporters SLC23A1 and SLC23A2 and risk of advanced colorectal adenoma. 1879 29