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Series GSE201078 Query DataSets for GSE201078
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
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.
 
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.
 
Contributor(s) Shen H, Huang F, Gao M, Chong Z, Shi LZ
Citation(s) 36008408
Submission date Apr 19, 2022
Last update date Aug 31, 2022
Contact name Min Gao
E-mail(s) mgao@uabmc.edu
Organization name University of Alabama at Birmingham
Street address 1900 University Blvd, THT Building Suite #130G
City Birmingham
State/province AL
ZIP/Postal code 35294
Country USA
 
Platforms (1)
GPL17021 Illumina HiSeq 2500 (Mus musculus)
Samples (6)
GSM6050257 B16 melanoma cells, control 1
GSM6050258 B16 melanoma cells, control 2
GSM6050259 B16 melanoma cells, control 3
Relations
BioProject PRJNA828250

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SOFT formatted family file(s) SOFTHelp
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Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE201078_RAW.tar 1.2 Mb (http)(custom) TAR (of TXT)
SRA Run SelectorHelp
Raw data are available in SRA
Processed data provided as supplementary file

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