Journal
AUTOPHAGY
Volume 10, Issue 11, Pages 2077-2078Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/auto.36138
Keywords
brain tumors; pediatric; autophagy; BRAF; chloroquine
Categories
Funding
- NCATS NIH HHS [UL1 TR001082] Funding Source: Medline
- NCI NIH HHS [CA111421, R01CA150925, P30CA046934, P30 CA046934, R01 CA150925, R01 CA111421] Funding Source: Medline
- NCRR NIH HHS [UL1 RR025780] Funding Source: Medline
- NICHD NIH HHS [K12 HD068372] Funding Source: Medline
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Autophagy inhibition is a potential therapeutic strategy in central nervous system (CNS) tumors. The BRAF(V600E) mutation is known to affect autophagy. Our studies indicate CNS tumor cells with BRAF(V600E) mutant cells (but not wild type) display high rates of induced autophagy, are sensitive to autophagy inhibition, and display synergy when chloroquine is combined with the RAF kinase inhibitor vemurafenib or standard chemotherapeutics. Our studies also indicate chloroquine can improve vemurafenib sensitivity in intrinsically resistant cells and in a patient with induced-vemurafenib resistance. These findings suggest CNS tumors with BRAF(V600E) are autophagy-dependent and that identification of BRAF(V600E) may be a marker to identify pediatric patients with the best potential response to autophagy inhibition.
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