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Abstract

Many of the links between diet and cancer are controversial and over simplified. To date,human epidemiological studies consistently reveal that patients who suffer diet-related obesityand/or type II diabetes have an increased risk of cancer, suffer more aggressive cancers, and respondpoorly to current therapies. However, the underlying molecular mechanisms that increase cancerrisk and decrease the response to cancer therapies in these patients remain largely unknown. Here,we review studies in mouse cancer models in which either dietary or genetic manipulation has beenused to model obesity and/or type II diabetes. These studies demonstrate an emerging role for theconserved insulin and insulin-like growth factor signaling pathways as links between diet and cancerprogression. However, these models are time consuming to develop and expensive to maintain.As the world faces an epidemic of obesity and type II diabetes we argue that the development of novelanimal models is urgently required. We make the case for Drosophila as providing an unparalleledopportunity to combine dietary manipulation with models of human metabolic disease and cancer.Thus, combining diet and cancer models in Drosophila can rapidly and significantly advance ourunderstanding of the conserved molecular mechanisms that link diet and diet-related metabolicdisorders to poor cancer patient prognosis.

Item Type:	Article
Authors/Creators:	Warr, CG and Shaw, KH and Azim, A and Piper, MDW and Parsons, LM
Keywords:	cancer, diet, obesity, type II diabetes mellitus, Drosophila
Journal or Publication Title:	International Journal of Molecular Sciences
Publisher:	MDPI
ISSN:	1661-6596
DOI / ID Number:	https://doi.org/10.3390/ijms19124110
Copyright Information:	© 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
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