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- W2891146170 abstract "Despite extensive efforts, oncogenic KRAS remains resistant to targeted therapy. Combined downstream RAL-TBK1 and MEK inhibition induces only transient lung tumor shrinkage in KRAS-driven genetically engineered mouse models (GEMMs). Using the sensitive KRAS;LKB1 (KL) mutant background, we identify YAP1 upregulation and a therapy-induced secretome as mediators of acquired resistance. This program is reversible, associated with H3K27 promoter acetylation, and suppressed by BET inhibition, resensitizing resistant KL cells to TBK1/MEK inhibition. Constitutive YAP1 signaling promotes intrinsic resistance in KRAS;TP53 (KP) mutant lung cancer. Intermittent treatment with the BET inhibitor JQ1 thus overcomes resistance to combined pathway inhibition in KL and KP GEMMs. Using potent and selective TBK1 and BET inhibitors we further develop an effective therapeutic strategy with potential translatability to the clinic." @default.
- W2891146170 created "2018-09-27" @default.
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- W2891146170 date "2018-09-01" @default.
- W2891146170 modified "2023-10-17" @default.
- W2891146170 title "Overcoming Resistance to Dual Innate Immune and MEK Inhibition Downstream of KRAS" @default.
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- W2891146170 doi "https://doi.org/10.1016/j.ccell.2018.08.009" @default.
- W2891146170 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6422029" @default.
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