| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 8300826 | Biochimica et Biophysica Acta (BBA) - General Subjects | 2018 | 7 Pages |
Abstract
Metabolism is a key component of the melanoma response to BRAF and/or MEK inhibitors. Mitochondrial targeting may offer novel therapeutic approaches to overwhelm the mitochondrial addiction that limits the efficacy of BRAF and/or MEK inhibitors. These therapeutic approaches might be quickly applicable to the clinical situation.
Keywords
EGFRLDHAPDKDrp-1PGC1αULK1v-raf murine sarcoma viral oncogene homolog B1MITFmTORC1BRAFUPRFDGHIF-1αCOTLKB1AMPKPI3KERKnuclear magnetic resonanceperoxisome proliferator-activated receptor gamma coactivator 1-alpha2-deoxy-2-[18F]fluoro-D-glucoseAMP activated protein kinaseMAPKPET/CTNMRDormancyTargeted therapyStem cellendoplasmic reticulumhypoxia inducible factor 1 alphaLactate dehydrogenase AMEKSynthetic lethalityMitochondriaMammalian target of rapamycin complex 1Unfolded protein responsedynamin-related protein 1mitogen-activated protein kinasePyruvate dehydrogenase kinaseextracellular signal-regulated kinaseliver kinase B1Epidermal growth factor receptor
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Authors
Philippe Marchetti, Anne Trinh, Raeeka Khamari, Jerome Kluza,