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: 8534067
• 负责人: Ross Leigh Cagan
• 金额: $ 33.06万
• 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/8534067
• 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; Severities; Sucrose; System; TP53 gene; Testing; Therapeutic; Tissues; Tumor Suppressor Genes; base; cancer risk; cancer type; experience; feeding; fly; inhibitor/antagonist; response; screening; 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.

描述（由申请人提供）：流行病学研究表明，增加的癌症风险与肥胖有关，但潜在的机制仍然鲜为人知。我们最近开发了肥胖的果蝇模型。在高碳水化合物的饮食中提高​​果蝇，导致代谢功能障碍，包括高血糖，胰岛素抵抗和脂肪的积累。喂养高饮食中的饮食蔗糖，以RAS/SRC共同激活的果蝇癌模型以饮食依赖性方式产生了侵袭性肿瘤，并以饮食依赖性的方式产生了侵袭性肿瘤。该应用程序的目的是进一步利用果蝇作为原位 探索饮食引起的肥胖与肿瘤进展之间的机械联系的模型。