A Drosophila model linking diet-induced metabolic disease and cancer

Results We demonstrate that high dietary sucrose, but not high dietary fat transforms Ras/Src-activated cells from localized growths to aggressive tumors with emergent metastases. Surprisingly, while most tissues displayed aspects of metabolic dysfunction including insulin resistance, Ras/Src-activated tumors retained insulin pathway sensitivity and exhibited an increased ability to import glucose. We provide evidence that this reflects increased insulin signaling, which in turn acts through Wingless/ Wnt signaling to promote diet-mediated malignant phenotypes within Ras/Src-activated tumors [3]. These fly models should provide useful paradigms to study the link between metabolic dysfunction and tumorigenesis in the context of a whole animal.