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Status |
Public on Jul 31, 2022 |
Title |
JAK inhibition selectively suppresses melanoma lacking IFN-γ pathway |
Organism |
Mus musculus |
Experiment type |
Expression profiling by high throughput sequencing
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Summary |
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.
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Overall design |
Scramble and IFNγR1KO B16 melanoma cells were sent for transcriptomic analysis by paired-end RNAseq analysis to find the activation of PI3K-Akt-mTOR pathway in IFNγR1 knocked out cells.
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Contributor(s) |
Shen H, Huang F, Gao M, Chong Z, Shi LZ |
Citation(s) |
36008408 |
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Submission date |
Apr 19, 2022 |
Last update date |
Aug 31, 2022 |
Contact name |
Min Gao |
E-mail(s) |
mgao@uabmc.edu
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Organization name |
University of Alabama at Birmingham
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Street address |
1900 University Blvd, THT Building Suite #130G
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City |
Birmingham |
State/province |
AL |
ZIP/Postal code |
35294 |
Country |
USA |
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Platforms (1) |
GPL17021 |
Illumina HiSeq 2500 (Mus musculus) |
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Samples (6)
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Relations |
BioProject |
PRJNA828250 |