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，肥胖与癌症风险增加有关，但其潜在机制仍知之甚少。我们最近开发了一种肥胖的果蝇模型;以高碳水化合物饮食饲养果蝇导致代谢功能障碍，包括高血糖症、胰岛素抵抗和脂肪积累。以高蔗糖饮食喂养Ras/Src共激活的果蝇癌症模型以饮食依赖的方式发展具有紧急转移的侵袭性肿瘤。本申请的目的是进一步利用果蝇作为有用的原位杂交技术， 模型，以探索饮食诱导的肥胖和肿瘤进展之间的机制联系。 公共卫生相关性：流行病学研究长期以来一直表明，肥胖和其他代谢功能障碍会增加肿瘤进展的风险和严重程度。在本申请中，我们使用果蝇来探索高膳食糖增强肿瘤发生的机制。