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Oncogenic BRAF regulates oxidative metabolism via PGC1a and MITF.
BCL2A1 is a lineage-specific antiapoptotic melanoma oncogene that confers resistance to BRAF inhibition.
Proto-Oncogene Proteins B-raf
Improving apoptotic responses to targeted therapy.
Metabolic dysregulation in melanoma: cause or consequence?
Molecular pathways: BRAF induces bioenergetic adaptation by attenuating oxidative phosphorylation.
Clinical profiling of BCL-2 family members in the setting of BRAF inhibition offers a rationale for targeting de novo resistance using BH3 mimetics.
A melanoma cell state distinction influences sensitivity to MAPK pathway inhibitors.
Point of care assessment of melanoma tumor signaling and metastatic burden from µNMR analysis of tumor fine needle aspirates and peripheral blood.
Trapping Cancers as They Adapt to Survive.
Destabilization of NOXA mRNA as a common resistance mechanism to targeted therapies.
Integrated molecular drivers coordinate biological and clinical states in melanoma.
Proto Oncogene Proteins B raf