A Drosophila Model Linking Diet-induced Obesity and Cancer (PQ 1)

将饮食引起的肥胖与癌症联系起来的果蝇模型 (PQ 1)

• 批准号: 8383704
• 负责人: Ross Leigh Cagan
• 金额: $ 35.17万
• 依托单位: ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI
• 依托单位国家: 美国
• 财政年份: 2012
• 资助国家: 美国
• 起止时间: 2012-08-20 至 2016-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8383704
• 关键词: Address; Animal Genetics; Animals; Biological Assay; Cancer Model; Carbohydrates; Chemicals; Collection; Colon Carcinoma; Complex; Data; Development; Diet; Dietary Sucrose; Dietary Sugars; Drosophila genus; Epidemiologic Studies; FDA approved; Fatty acid glycerol esters; Functional disorder; Genes; Genetic Screening; Goals; Hyperglycemia; In Situ; Insulin Resistance; Laboratories; Libraries; Link; Malignant Neoplasms; Malignant neoplasm of liver; Malignant neoplasm of pancreas; Mediating; Metabolic; Microarray Analysis; Modeling; Molecular; Molecular Profiling; Mutation; Neoplasm Metastasis; Obesity; Palate; Pathway interactions; Pharmaceutical Preparations; Property; Risk; Robotics; Screening procedure; Severities; Sucrose; System; TP53 gene; Testing; Therapeutic; Tissues; Tumor Suppressor Genes; base; cancer risk; cancer type; experience; feeding; fly; inhibitor/antagonist; response; tumor; tumor progression; tumorigenesis

DESCRIPTION (provided by applicant): Epidemiological studies have demonstrated that increased cancer risk is associated with obesity, but the underlying mechanism remains poorly understood. We have recently developed a Drosophila model of obesity; raising Drosophila on a diet high in carbohydrates led to metabolic dysfunction including hyperglycemia, insulin-resistance and accumulation of fat. Feeding a high dietary sucrose to Ras/Src co- activated Drosophila cancer model developed aggressive tumor with emergent metastasis in a diet-dependent manner. The goal of this Application is to further utilize Drosophila as a useful in situ model to explore mechanistic link between diet-induced obesity and tumor progression. PUBLIC HEALTH RELEVANCE: Epidemiological studies have long shown that obesity and other metabolic dysfunctions increase the risk and severity of tumor progression. In this Application we use fruit flies to explore the mechanisms by which high dietary sugar enhances tumorigenesis.

描述(由申请人提供)：流行病学研究表明，癌症风险增加与肥胖有关，但其潜在机制仍然知之甚少。我们最近建立了一个果蝇肥胖模型；用高碳水化合物饮食饲养果蝇会导致代谢功能障碍，包括高血糖、胰岛素抵抗和脂肪堆积。给Ras/Src共激活的果蝇肿瘤模型喂食高蔗糖可形成侵袭性肿瘤，并以饮食依赖的方式发生紧急转移。本申请的目标是进一步利用果蝇作为有用的原位 探索饮食诱导的肥胖和肿瘤进展之间的机制联系的模型。 公共卫生相关性：流行病学研究长期以来表明，肥胖和其他代谢功能障碍会增加肿瘤进展的风险和严重性。在本申请中，我们使用果蝇来探索高饮食糖促进肿瘤发生的机制。