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MYC and metabolism on the path to cancer.
Hsieh, Annie L; Walton, Zandra E; Altman, Brian J; Stine, Zachary E; Dang, Chi V.
Afiliação
  • Hsieh AL; Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA; Abramson Cancer Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA; Department of Pathology, Johns Hopkins University School of Medicine, Bal
  • Walton ZE; Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA; Abramson Cancer Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
  • Altman BJ; Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA; Abramson Cancer Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
  • Stine ZE; Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA; Abramson Cancer Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
  • Dang CV; Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA; Abramson Cancer Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA; Division of Hematology-Oncology, Department of Medicine, Perelman School
Semin Cell Dev Biol ; 43: 11-21, 2015 Jul.
Article em En | MEDLINE | ID: mdl-26277543
The MYC proto-oncogene is frequently deregulated in human cancers, activating genetic programs that orchestrate biological processes to promote growth and proliferation. Altered metabolism characterized by heightened nutrients uptake, enhanced glycolysis and glutaminolysis and elevated fatty acid and nucleotide synthesis is the hallmark of MYC-driven cancer. Recent evidence strongly suggests that Myc-dependent metabolic reprogramming is critical for tumorigenesis, which could be attenuated by targeting specific metabolic pathways using small drug-like molecules. Understanding the complexity of MYC-mediated metabolic re-wiring in cancers as well as how MYC cooperates with other metabolic drivers such as mammalian target of rapamycin (mTOR) will provide translational opportunities for cancer therapy.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Transformação Celular Neoplásica / Proteínas Proto-Oncogênicas c-myc / Glucose / Glicólise / Homeostase / Neoplasias Limite: Humans Idioma: En Revista: Semin Cell Dev Biol Assunto da revista: EMBRIOLOGIA Ano de publicação: 2015 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Transformação Celular Neoplásica / Proteínas Proto-Oncogênicas c-myc / Glucose / Glicólise / Homeostase / Neoplasias Limite: Humans Idioma: En Revista: Semin Cell Dev Biol Assunto da revista: EMBRIOLOGIA Ano de publicação: 2015 Tipo de documento: Article