期刊
NATURE NEUROSCIENCE
卷 19, 期 1, 页码 10-19出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.4190
关键词
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资金
- Banting Fellowship
- James S. McDonnell Foundation
- US National Institutes of Health [F32 CA189647, F30 CA183510, T32 GM007250 MSTP, R35 CA197718, CA154130, R01 CA169117, R01 CA171652, R01 NS087913, R01 NS089272, R01CA159859, R01CA148699]
- Canadian Institutes of Health Research Clinician Scientist Phase II award
- Garron Family Chair in Childhood Cancer Research at The Hospital for Sick Children
- University of Toronto
- Canadian Institutes of Health Research
- Pediatric Brain Tumor Foundation
- NATIONAL CANCER INSTITUTE [R01CA171652, F32CA189647, R01CA169117, R01CA148699, R01CA159859, F30CA183510, R35CA197718, R01CA154130] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM007250] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS087913, R01NS089272] Funding Source: NIH RePORTER
Precise targeting of genetic lesions alone has been insufficient to extend brain tumor patient survival. Brain cancer cells are diverse in their genetic, metabolic and microenvironmental compositions, accounting for their phenotypic heterogeneity and disparate responses to therapy. These factors converge at the level of the epigenome, representing a unified node that can be disrupted by pharmacologic inhibition. Aberrant epigenomes define many childhood and adult brain cancers, as demonstrated by widespread changes to DNA methylation patterns, redistribution of histone marks and disruption of chromatin structure. In this Review, we describe the convergence of genetic, metabolic and microenvironmental factors on mechanisms of epigenetic deregulation in brain cancer. We discuss how aberrant epigenetic pathways identified in brain tumors affect cell identity, cell state and neoplastic transformation, as well as addressing the potential to exploit these alterations as new therapeutic strategies for the treatment of brain cancer.
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