Abstract
Why Cancer & Metabolism? Why now?
Highlights
At the organismal level, the clinical association of obesity with increased cancer risk, the classic observations that caloric restriction can inhibit carcinogenesis in rodent models, and experimental models that suggest that the behavior of a subset of cancers is influenced by drugs such as metformin, that may act at least in part by perturbing whole organism energy metabolism, further tie altered metabolic states with tumorigenesis and cancer progression
The identification of oncogenic driver mutations of many cancers by deep sequencing is validating the oncogene versus tumor suppressor paradigm of tumorigenesis
The rapid expansion of research on metabolic aspects of neoplasia has improved our understanding of how oncogenes and tumor suppressors are linked to altered cancer cell metabolism, and how altered metabolism, in turn, affect the cancer epigenome
Summary
The clinical association of obesity with increased cancer risk, the classic observations that caloric restriction can inhibit carcinogenesis in rodent models, and experimental models that suggest that the behavior of a subset of cancers is influenced by drugs such as metformin, that may act at least in part by perturbing whole organism energy metabolism, further tie altered metabolic states with tumorigenesis and cancer progression. There is a profound resurgence of interest in metabolism in the context of neoplasia, both at the whole-organism level with respect to the influence of caloric intake on cancer behavior, and at the cellular level, with respect to possible therapeutic exploitation of differences between the metabolism of normal and cancer cells.
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