{"database":"ENA","file_versions":[],"scores":null,"additional":{"omics_type":["Genomics"],"center_name":["OREGON HEALTH & SCIENCE UNIVERSITY"],"full_dataset_link":["https://www.ebi.ac.uk/ena/browser/view/PRJNA476391"],"scientific_name":["Homo sapiens"],"long_description":["FLT3 mutations are commonly detected in Acute Myeloid Leukemia (AML) patients and are associated with poor prognosis. Crenolanib, a potent type I pan-FLT3 ( GeneID:2322) inhibitor, is effective against both internal tandem duplications (ITD) and resistance-conferring tyrosine kinase domain (TKD) mutations. While crenolanib monotherapy has demonstrated significant clinical benefit in heavily pretreated relapsed/refractory AML patients, responses are transient and relapse eventually occurs. To investigate the mechanisms of crenolanib resistance, we performed whole exome sequencing of AML patient samples before and after crenolanib treatment (122 samples from 59 patients). Unlike other FLT3 inhibitors, crenolanib did not induce FLT3 activation loop mutations, and mutations of the FLT3 \"gatekeeper\" residue were infrequent. Instead, mutations of NRAS ( GeneID:4893) and IDH2 ( GeneID:3418) arose, mostly as FLT3-independent subclones, while TET2 ( GeneID:54790... (for more see dbGaP study page.)"],"repository":["ENA"],"additional_accession":[]},"is_claimable":false,"name":"Clinical Resistance to Crenolanib in Acute Myeloid Leukemia Due to Diverse Molecular Mechanisms","description":"Clinical Resistance to Crenolanib in Acute Myeloid Leukemia Due to Diverse Molecular Mechanisms","dates":{"last_updated":"2025-09-24","first_public":"2018-06-17"},"accession":"PRJNA476391","cross_references":{"taxon":["9606"]}}