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Gene expression changes caused by treatment of TPC1 cells with RET inhibitor BLU6864 in combination with FGFR inhibitor BGJ398 vs. BLU6864 alone [BGJ398_24H + BLU6864_24H vs BLU6864_24H]

ABSTRACT: NOT PROVIDED; REQUESTED

ORGANISM(S): Homo sapiens

PROVIDER: GSE199018 | GEO | 2022/03/23

REPOSITORIES: GEO

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Gene expression changes caused by treatment of TPC1 cells with RET inhibitor BLU6864 [BLU6864_6H vs DMSO]

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2022-03-23 | GSE199021 | GEO

Gene expression changes caused by treatment of TPC1 cells with FGFR inhibitor BGJ398 [BGJ398_6H and BGJ398_24H]

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Gene expression changes caused by treatment of TPC1 cells with RET, FGFR inhibitor

Project description:This SuperSeries is composed of the SubSeries listed below.

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Gene expression changes caused by treatment of TPC1 cells with RET inhibitor BLU6864 in combination with FGFR inhibitor BGJ398 vs. BLU6864 alone [BGJ398_24H + BLU6864_24H vs BLU6864_24H]

Project description:Gene expression changes caused by treatment of TPC1 cells with RET inhibitor BLU6864 in combination with FGFR inhibitor BGJ398 vs. BLU6864 alone [BGJ398_24H + BLU6864_24H vs BLU6864_24H]

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Gene expression changes caused by treatment of TPC1 cells with RET, FGFR inhibitor

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Gene expression changes caused by treatment of TPC1 cells with RET inhibitor BLU6864 [BLU6864_6H vs DMSO]

Project description:Gene expression changes caused by treatment of TPC1 cells with RET inhibitor BLU6864 [BLU6864_6H vs DMSO]

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Inhibitor repurposing reveals ALK, LTK, FGFR, RET and TRK kinases as the targets of AZD1480.

Project description:Many tyrosine kinase inhibitors (TKIs) have failed to reach human use due to insufficient activity in clinical trials. However, the failed TKIs may still benefit patients if their other kinase targets are identified by providing treatment focused on syndromes driven by these kinases. Here, we searched for novel targets of AZD1480, an inhibitor of JAK2 kinase that recently failed phase two cancer clinical trials due to a lack of activity. Twenty seven human receptor tyrosine kinases (RTKs) and 153 of their disease-associated mutants were in-cell profiled for activity in the presence of AZD1480 using a newly developed RTK plasmid library. We demonstrate that AZD1480 inhibits ALK, LTK, FGFR1-3, RET and TRKA-C kinases and uncover a physical basis of this specificity. The RTK activity profiling described here facilitates inhibitor repurposing by enabling rapid and efficient identification of novel TKI targets in cells.

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