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• W2913774804 abstract "Anti-EGFR therapy is used to treat metastatic colorectal cancer (CRC) patients, for which initial response rates of 10-20% have been achieved. Although the presence of HER2 amplifications and oncogenic mutations in KRAS, NRAS, and BRAF are associated with EGFR-targeted therapy resistance, for a large population of CRC patients the underlying mechanism of RAS-MEK-ERK hyperactivation is not clear. Loss-of-function mutations in RASGAPs are often speculated in literature to promote CRC growth as being negative regulators of RAS, but direct experimental evidence is lacking. We generated a CRISPR-mediated knock out panel of all RASGAPs in patient-derived CRC organoids and found that only loss of NF1, but no other RASGAPs e.g. RASA1, results in enhanced RAS-ERK signal amplification and improved tolerance towards limited EGF stimulation. Our data suggests that NF1-deficient CRCs are likely not responsive to anti-EGFR monotherapy and can potentially function as a biomarker for CRC progression." @default.
• W2913774804 created "2019-02-21" @default.
• W2913774804 creator A5012633181 @default.
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• W2913774804 date "2019-02-15" @default.
• W2913774804 modified "2023-10-12" @default.
• W2913774804 title "CRISPR-induced RASGAP deficiencies in colorectal cancer organoids reveal that only loss of NF1 promotes resistance to EGFR inhibition" @default.
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• W2913774804 doi "https://doi.org/10.18632/oncotarget.26677" @default.
• W2913774804 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6402720" @default.
• W2913774804 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30858928" @default.
• W2913774804 hasPublicationYear "2019" @default.
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