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Genome-Wide CRISPR Screen Identifies Multiple Synthetic Lethal Targets That Enhance KRAS (G12C) Inhibitor Efficacy

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE240120 | GEO | 2023/09/11

REPOSITORIES: GEO

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Genome-Wide CRISPR Screen Identifies Multiple Synthetic Lethal Targets That Enhance KRAS (G12C) Inhibitor Efficacy [CRISPR]

Project description:KRAS G12C inhibitors (G12Ci) alone and in various combinations are being tested in multiple tumors with over-activation of the RAS/ERK pathway. KRAS plays a critical role in normal cell signaling; hence, G12Cis has been reported to create resistance. We found several novel pathways, including Hippo pathways, are enriched from significant dropouts upon MRTX849 treatment. Our results argue for testing KRAS G12C and TEAD inhibitor combinations in NSCLC patients.

2023-09-11 | GSE240110 | GEO

Genome-Wide CRISPR Screen Identifies Multiple Synthetic Lethal Targets That Enhance KRAS (G12C) Inhibitor Efficacy [scRNA-seq]

Project description:KRAS G12C inhibitors (G12Ci) alone and in various combinations are being tested in multiple tumors with over-activation of the RAS/ERK pathway. KRAS plays a critical role in normal cell signaling; hence, G12Cis could influence the signaling pathways. We found that several novel pathways including Hippo pathways are upregulated upon MRTX849 treatment. Our results argue for testing KRAS G12C and TEAD inhibitor combinations in NSCLC patients.

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Genome-Wide CRISPR Screen Identifies Multiple Synthetic Lethal Targets That Enhance KRAS (G12C) Inhibitor Efficacy [RNA-seq-mm10]

Project description:KRAS G12C inhibitors (G12Ci) alone and in various combinations are being tested in multiple tumors with over-activation of the RAS/ERK pathway. KRAS plays a critical role in normal cell signaling; hence, G12Cis could influence the signaling pathways. We found that several novel pathways including Hippo pathways are upregulated upon MRTX849 treatment. Our results argue for testing KRAS G12C and TEAD inhibitor combinations in NSCLC patients.

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Genome-Wide CRISPR Screen Identifies Multiple Synthetic Lethal Targets That Enhance KRAS (G12C) Inhibitor Efficacy [RNA-seq-human]

Project description:Transcriptomic analysis of NSCLC cells either under MRTX849 treatment or Ctrl (DMSO) to identify key pathways causing resistance.

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In vivo CRISPR/Cas9 screen to identify candidate therapeutic gene targets to enhance docetaxel efficacy in prostate cancer

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Novel Treatments of Uveal Melanoma Identified with a Synthetic Lethal CRISPR/Cas9 Screen.

Project description: Not available

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Synthetic lethal and resistance interactions with BET bromodomain inhibitors [CRISPR screen]

Project description:BET bromodomain inhibitors (BBDI) are promising therapeutic agents in triple-negative breast cancer (TNBC). However, not all tumors respond and acquired resistance emerges rapidly even in the responders. Using CRISPR and small molecule inhibitor screens combined with comprehensive molecular profiling of BBDI response and resistance in TNBC cell lines, we identified numerous synthetic lethal interactions with BBDIs as well as genes that when deleted confer resistance. The most prominent and consistent synergy was observed with CDK4/6 inhibitors and paclitaxel. We also uncovered functional similarities and differences between BBD proteins BRD2, BRD4, and BRD7, whereas deletion of BRD2 and BRD4 enhances sensitivity to BBDIs, BRD7 loss leads to resistance. Lastly, single cell RNA-seq and cellular barcoding analysis of BBDI responses in sensitive and resistant cell lines highlight heterogeneity among samples and demonstrate that BBDI resistance can be both pre-existing and acquired.

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