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carcinogenesis/obesity

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Paj 1 soti nan 1073 rezilta yo
Colon cancer strikes more than 1 million people annually and is responsible for more than 500,000 cancer deaths worldwide. Recent evidence suggests that the majority of malignancies, including colon cancer are driven by cancer stem cells (CSCs) that are resistant to current chemotherapeutic
BACKGROUND The authors recently reported that gastrin gene knockout (GAS-KO) mice had an increased risk for colon carcinogenesis in response to azoxymethane (AOM) compared with their wild type (WT) littermates. In the current report, the authors discuss the predisposition of GAS-KO mice to develop

Citrus compounds inhibit inflammation- and obesity-related colon carcinogenesis in mice.

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Dietary polyphenols are important potential chemopreventive natural agents. Other agents, such as citrus compounds, are also candidates for cancer chemopreventives. They act on multiple key elements in signal transduction pathways related to cellular proliferation, differentiation, apoptosis,

Eicosapentaenoic acid attenuates obesity-related hepatocellular carcinogenesis.

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Non-alcoholic fatty liver disease (NAFLD), the hepatic manifestation of obesity, is an emerging risk factor for hepatocellular carcinoma (HCC). Accumulating evidence has shown that chronic inflammation represents a plausible link between obesity and HCC and that the pro-inflammatory cytokine
Orlistat is an anti-obesity agent that increases the fecal fat excretion, which promotes colon carcinogenesis. Therefore, the present study was designed to verify the effects of Orlistat on the formation of rat colonic aberrant crypt foci (ACF) and cell proliferation evaluated by the PCNA method.

Role of adiponectin in obesity related gastrointestinal carcinogenesis.

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Adiponectin is produced in the white adipose tissue and is known to have anti-metabolic and anti-inflammatory properties. Serum/plasma adiponectin levels depend on diet, physical activity, and inheritance. Epidemiologic observations suggest a potential link between obesity and gastrointestinal

4-Nitroquinoline 1-Oxide-Induced Tongue and Esophagus Carcinogenesis in Obese and Diabetic TSOD Mice.

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UNASSIGNED Obesity and diabetes mellitus are associated with lifestyle-related carcinogenesis. They are also risk factors of esophageal adenocarcinoma, but there are only a few reports on association between obesity/diabetes and development of squamous cell carcinoma in the oral cavity and

Susceptibility to induced and spontaneous carcinogenesis is increased in fatless A-ZIP/F-1 but not in obese ob/ob mice.

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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

A Rat Model to Study the Effects of Diet-Induced Obesity on Radiation-Induced Mammary Carcinogenesis.

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A detailed understanding of the relationship between radiation-induced breast cancer and obesity is needed for appropriate risk management and to prevent the development of a secondary cancer in patients who have been treated with radiation. Our goal was to develop an animal model to study the

A Screening Study of Potential Carcinogen Biomarkers After Surgical Treatment of Obesity.

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BACKGROUND Obesity has been associated with the development of various types of cancer. Biomarker studies may provide molecular level knowledge of the factors involved in this association, improving clinical practice through new methods of prevention and treatment. OBJECTIVE The present study aimed

Obesity provides a permissive milieu in inflammation-associated carcinogenesis: analysis of insulin and IGF pathways.

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Current dogma suggests that the positive correlation between obesity and cancer is driven by white adipose tissue that accompanies obesity, possibly through excess secretion of adipokines. However, recent studies in fatless A-Zip/F-1 mice, which have undetectable adipokine levels but display

The effects of dehydroepiandrosterone on carcinogenesis, obesity, the immune system, and aging.

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With the passage of the U.S. Dietary Supplement Health and Education Act of 1994, dehydroepiandrosterone (DHEA, 5-androsten-3beta-ol-17-one) has become widely available, and a large and growing market has developed for this "fountain of youth." DHEA has been shown to have significant beneficial

Obesity enhances carcinogen 7, 12-Dimethylbenz [a] anthracene -induced tumorigenesis in vitro and in vivo.

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Growing body of evidence shows that extra adiposity influences on the progression of multiple cancers, including breast cancer. The aim of this study is to investigate whether obesity correlates with mammary tumor development in vitro and in vivo. We found that obesity-related mediators, 3T3-L1
Obesity is associated with an increased risk of cancer. To study the promotion of dietary carcinogen-induced gastrointestinal cancer by obesity, we employed 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) to induce intestinal tumorigenesis in CYP1A-humanized (hCYP1A) mice, in which mouse
Obesity is highly associated with colon cancer development. Whereas it is generally attributed to pro-tumorigenic effects of high fat diet (HFD), we here show that a common genetic basis for predisposition to obesity and colon cancer might also underlie the close association. Comparison across
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