Abstract
Inhibitors of tropomyosin receptor kinase (TRK) have shown promising activity against neurotrophic TRK (NTRK) fusion-driven cancers. NTRK gene fusions are observed in less than 1% of colorectal cancers (CRCs). CRCs harboring wild-type BRAF, KRAS and MisMatch Repair deficiency (dMMR)/MicroSatellite Instability (MSI) due to MLH1 hypermethylation have been associated with NTRK fusions in small cohorts of non-metastatic tumors. We evaluated the frequency and associated clinical characteristics of NTRK fusions among dMMR/MSI metastatic CRCs (mCRCs) patients (pts).
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