Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review article touches on various categories of research that have been expanded or made possible predominantly by funding through the National Cancer Program of the National Cancer Institute and the American Cancer Society. Under diagnosis, categories mentioned are biological markers, chromosome banding techniques, fluorescent-activated cell sorter identification of cell surface antigens, ultrastructural studies with electron microscopy, histochemical, radiologic, ultrasonographic, thermographic, angiographic techniques, nuclear magnetic resonance imaging, radioactively labeled compounds that attach to specific tumor cell surface receptors, and other agents that are preferentially taken up by tumor tissues. Predictive tests include human tumor stem cell assays, sister chromatid exchange assay, and hormone receptor assays. The techniques listed under therapy include hyperthermia, immunotherapy, chemotherapy, radiosensitizing compounds, and the supportive measures of hyperalimentation and other nutritional manipulations, psychological reinforcement, rehabilitative efforts, bone marrow transplants, blood component therapy, protective "germ-free" environments, and pain control. Drug delivery systems, animal and cell culture models, and prevention of carcinogenesis are also mentioned.
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PMID:Cancer 1980: achievements, challenges, and prospects. 617 12

Feeding of retinyl acetate (0.2 mM) or N-(4-hydroxyphenyl) retinamide (4-HPR) (1.0 mM) for 27 weeks to female BD2F1 mice previously treated with a series of gastric intubations of 7,12-dimethylbenzanthracene (DMBA), did not significantly affect the incidence of mammary tumors. In the retinyl acetate study, 75 retinyl acetate fed mice developed 31 mammary adenocarcinomas and 19 mammary adenoacanthomas (50 total mammary tumors) while 75 control mice developed 22 mammary adenocarcinomas and 20 mammary adenoacanthomas (42 total mammary tumors). In the 4-HPR study, 74 4-HPR fed mice developed 45 mammary adenocarcinomas and 41 mammary adenoacanthomas (86 total mammary tumors) while 74 control mice developed 29 mammary adenocarcinomas and 44 mammary adenoacanthomas (73 total mammary tumors). Retinoid treatments did not significantly affect body weight gains or mortality rates. These results provide evidence that carcinogen induced mouse mammary gland tumorigenesis in vivo is not influenced by hyperalimentation of dietary retinoids.
Carcinogenesis 1984 Oct
PMID:Lack of an effect of dietary retinoids in chemical carcinogenesis of the mouse mammary gland: inverse relationship between mammary tumor cell anaplasia and retinoid efficacy. 623 6

Epigenetic gene silencing through DNA methylation is one of the important steps in the mechanism underlying tumorigenesis, including in the stomach. Past lifestyle factors of cancer patients, such as intake of vegetables, are very important in affecting gastric carcinogenesis. However, the relationship between DNA methylation and past dietary habits in cancer patients remains largely unknown. The CDX2 homeobox transcription factor plays a key role in intestinal development, but CDX2 is also expressed in most of the intestinal metaplasia and part of the carcinomas of the stomach. We analyzed the methylation status of the CDX2 5' CpG island in gastric cancer cell lines by methylation-specific PCR (MSP), and then CDX2 mRNA was found to be activated after 5-aza-2'-deoxycytidine treatment of the methylation-positive cells. We further examined the methylation status of CDX2 in primary gastric carcinomas by MSP and compared it with the past lifestyle of the patients, including dietary habits. Methylation of CDX2 was found in 20 (34.5%) of the 58 male patients and one (6.7%) of the 15 female patients. Since the methylation frequency was low in the female patients, the analysis was performed only on the male cases. CDX2 methylation was correlated with the decreased intake of green tea and cruciferous vegetables, and also with full or overeating habits. These findings are consistent with epidemiological observations on gastric cancer. We also analyzed the methylation status of p16/INK4a and hMLH1, but their frequencies were not associated with dietary factors or other lifestyle factors. Thus, diet could be an important factor determining the methylation status of genes such as CDX2 and the resultant aberrant expression of genes involved in carcinogenesis.
Carcinogenesis 2005 Jan
PMID:Relationship between CDX2 gene methylation and dietary factors in gastric cancer patients. 1549 92

Obesity is typically associated with increased tumor susceptibility, whereas caloric restriction, a regimen resulting in leanness, inhibits carcinogenesis. The link between adiposity and malignancies suggests that adipose tissue may influence carcinogenesis. An adipose tissue hormone, leptin, could be procarcinogenic because it stimulates proliferation in various tissues and tumor cell lines. Leptin may contribute to the correlation between adiposity and malignancies as its levels are usually increased in obese subjects and reduced by caloric restriction. We hypothesized that leptin deficiency, despite obesity, would inhibit carcinogenesis in leptin-null ob/ob mice and tested this hypothesis in two models: (a) two-stage skin carcinogenesis initiated by 7,12-dimethylbenz(a)anthracene and promoted by phorbol 12-myristate 13-acetate (PMA) and (b) p53 deficiency. Contrary to a typical association between obesity and enhanced carcinogenesis, obese ob/ob mice developed induced skin papillomas and spontaneous p53-deficient malignancies, mostly lymphomas, similarly to their lean littermates. Surprisingly, lipodystrophic (ZIP) mice that had very little both adipose tissue and leptin were highly susceptible to carcinogenesis. Hyperphagia, hyperinsulinemia, and hyperglycemia are unlikely to have contributed significantly to the enhancement of carcinogenesis in ZIP mice because similarly hyperphagic, hyperinsulinemic, and hyperglycemic ob/ob mice had normal susceptibility to carcinogenesis. Our data suggest that, in contrast to a well-known correlation between obesity and cancer, the direct effect of adipose tissue may rather be protective.
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PMID:Susceptibility to induced and spontaneous carcinogenesis is increased in fatless A-ZIP/F-1 but not in obese ob/ob mice. 1695 Dec 7

Calorie restriction can inhibit or delay carcinogenesis, reportedly due to a reduction in calorie intake rather than by concurrent changes in body mass and/or composition. Our objective was to test the hypothesis that body mass and/or composition have an important effect, independent of energy intake, on the benefits or hazards associated with calorie restriction or overeating, respectively. In the first experiment, transgenic mice that spontaneously develop prostate cancer [transgenic adenocarcinoma of mouse prostate (TRAMP)] were housed at 27 degrees C or 22 degrees C and pair fed the same diet for 21 weeks (95% of ad libitum intake at 27 degrees C). In the second experiment, TRAMP mice were housed at 27 degrees C or 22 degrees C and fed the same diet ad libitum for 21 weeks. Despite a similar calorie intake, pair-fed mice at 27 degrees C (PF27) were heavier (28.3 +/- 3.3 versus 17.6 +/- 1.6 g at 21 weeks; P < 0.001; mean +/- SD) and had greater fat (6.4 +/- 2.1 versus 1.9 +/- 0.3 g; P < 0.001) and lean mass (P < 0.001) than pair-fed mice at 22 degrees C. Furthermore, PF27 mice had greater levels of serum leptin (P < 0.001), lower levels of adiponectin (P < 0.05), and a greater frequency of prostatic adenocarcinoma (P < 0.05). In contrast, ad libitum-fed mice housed at 22 degrees C consumed approximately 30% more calories than ad libitum-fed mice at 27 degrees C, but there was no difference between groups in body composition or cancer progression. These results imply that the ability of calorie restriction to inhibit or delay cancer incidence and progression is mediated in part by changes in energy balance, body mass, and/or body composition rather than calorie intake per se, suggesting that excess calorie retention, rather than consumption, confers cancer risk.
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PMID:Cancer progression in the transgenic adenocarcinoma of mouse prostate mouse is related to energy balance, body mass, and body composition, but not food intake. 1718 79