GSE201078
JAK inhibition selectively suppresses melanoma lacking IFN-? pathway
Immune checkpoint blockers (ICBs) showed unprecedented clinical benefits. But the overall efficacy of ICBs is limited to a small subset of cancer patients due to therapeutic resistance. Concerted efforts from our group and others have identified that loss of IFN-g signaling genes in melanoma is a major mechanism of resistance to ICBs. We therefore generated B16 melanoma model with IFNgR1 knocked out by CRISPR-Cas9. We sequenced the whole transcriptomes and identified activated PI3K-Akt-mTOR pathway in IFNgR1 knocked out cells. This may represent an attractive target for therapeutic interventions to bypassing ICB resistance in melanoma lacking functional IFN-g signaling. Overall design: Scramble and IFN?R1KO B16 melanoma cells were sent for transcriptomic analysis by paired-end RNAseq analysis to find the activation of PI3K-Akt-mTOR pathway in IFN?R1 knocked out cells.