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Expression data from tumor lungs after continuous vs. pulsatile selumetinib treatment in KRASG12C GEMM

ABSTRACT: KRAS is one of the driver oncogenes in non-small cell lung cancer (NSCLC), but remains refractory to current modalities of targeted pathway inhibition, which include inhibiting downstream kinase MEK to circumvent KRAS activation. Here, we show that pulsatile, rather than continuous, treatment with MEK inhibitors (MEKis) maintains T cell activation and better control tumor growth and survival. We used microarrays to examine the MAPK signaling pathway suppression from tumor lungs of KRASG12C GEMM after continuous vs. pulsatile treatment of selumetinib.

ORGANISM(S): Mus musculus

PROVIDER: GSE126202 | GEO | 2019/09/11

REPOSITORIES: GEO

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