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- W2012368803 abstract "Epidemiological studies have demonstrated that increased cancer risk is associated with metabolic disease including obesity and diabetes, but the underlying mechanism remains poorly understood. We have recently found that feeding Drosophila a high sugar‐containing diet leads to a series of metabolic dysfunctions seen in human diabetes including hyperglycemia, increased insulin levels, and accumulation of fat. Here we demonstrate that a high sugar diet enhanced cell migration and invasion within Src‐mediated tumor and massive overgrowth in multigenic Ras/Src‐based tumor models. These diet‐enhanced Ras/Src‐based tumors produced aggressive metastasis‐like behavior: transformed cells left the primary tumor to invade through the hemolymph to secondary sites that led to lethality of the animals. Genetic and inhibitor studies indicated that the insulin pathway plays a primary role in this diet‐induced enhanced overgrowth through regulation of dTor. We further show that tumors with insulin pathway activation are resistant to dietary effects. Moreover, utilizing the diet‐enhanced lethal phenotype, we developed a drug screening platform that relies on robotics as well as rescue‐from‐lethality. These studies should provide insights into mechanisms of the association between metabolic dysfunction and cancer progression and allow us to take the first steps towards identifying novel candidate therapeutic compounds. Citation Information: Cancer Res 2009;69(23 Suppl):C17." @default.
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- W2012368803 date "2009-12-01" @default.
- W2012368803 modified "2023-09-25" @default.
- W2012368803 title "Abstract C17: Diet‐mediated enhancement of tumorigenesis inDrosophila" @default.
- W2012368803 doi "https://doi.org/10.1158/0008-5472.fbcr09-c17" @default.
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