Why Cancer & Metabolism? Why now?
نویسندگان
چکیده
The identification of oncogenic driver mutations of many cancers by deep sequencing is validating the oncogene versus tumor suppressor paradigm of tumorigenesis. At the same time, 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. 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. Enzymes of key metabolic pathways are mutated in specific types of cancers, linking oncogenic alterations to perturbed metabolism. Newly identified metabolic pathways have also emerged as the flexibility of re-wired cancer cell metabolism is appreciated. Much of this development has been enabled by better tools to study the genome as well as cellular metabolism. 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. Improvements in metabolic imaging have also provided new glimpses of in vivo real-time metabolic changes. Both hyperpolarized 13C MRI and new positron emission tomography (PET) radiolabeled ligands provide remarkable insights into tumor metabolism in vivo. The journal Cancer & Metabolism provides a timely forum to report progress in cancer research spanning the entire spectrum including cell metabolism,
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