Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

BMX kinase mediates gilteritinib resistance in FLT3-mutated AML through microenvironmental factors.

Blood advances - 13 Sept 2022

Buelow Daelynn R, Bhatnagar Bhavana, Orwick Shelley J, Jeon Jae Yoon, Eisenmann Eric D, Stromatt Jack C, Pabla Navjot Singh, Blachly James S, Baker Sharyn D, Blaser Bradley W

Abstract excerpt

Despite the clinical benefit associated with gilteritinib in relapsed/refractory acute myeloid leukemia (AML), most patients eventually develop resistance through unknown mechanisms. To delineate the mechanistic basis of resistance to gilteritinib, we performed targeted sequencing and scRNASeq on primary FLT3-ITD-mutated AML samples. Co-occurring mutations in RAS pathway genes were the most common genetic...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Aniline Compounds
Share to fms-Like Tyrosine Kinase 3

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Leukemia, Myeloid, Acute

Share to Mutation

Share to Protein-Tyrosine Kinases

Share to Pyrazines

Share to Tumor Microenvironment

Source

Open in PubMed Open full text

Identifiers

PMID: 35797240
DOI: 10.1182/bloodadvances.2022007952
PMCID: PMC9631628

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

BMX kinase mediates gilteritinib resistance in FLT3-mutated AML through microenvironmental factors.PMID 35797240Read ↗

The AML microenvironment catalyzes a stepwise evolution to gilteritinib resistanceSemantic proximity Read ↗

A noncanonical FLT3 gatekeeper mutation disrupts gilteritinib binding and confers resistanceSemantic proximity Read ↗

Gilteritinib: An FMS-like tyrosine kinase 3/AXL tyrosine kinase inhibitor for the treatment of relapsed or refractory acute myeloid leukemia patients.Semantic proximity Read ↗

Expression of myeloid Src-family kinases is associated with poor prognosis in AML and influences Flt3-ITD kinase inhibitor acquired resistanceSemantic proximity Read ↗

Protein tyrosine kinase 2b inhibition reverts niche-associated resistance to tyrosine kinase inhibitors in AML.Semantic proximity Read ↗

Multi-omics integration reveals immune hallmarks and biomarkers associated with FLT3 inhibitor sensitivity in FLT3-mutated AMLSemantic proximity Read ↗

Gilteritinib monotherapy for relapsed/refractory FLT3 mutated acute myeloid leukemia: a real-world, multi-center, matched analysis.Semantic proximity Read ↗

Effectiveness of Gilteritinib Beyond Second-Line Therapy in Relapsed/Refractory FLT3 -Mutated Acute Myeloid Leukemia: A Real-World Multicenter Study of 171 Patients.Semantic proximity Read ↗

The European Medicines Agency Review of Gilteritinib (Xospata) for the Treatment of Adult Patients with Relapsed or Refractory Acute Myeloid Leukemia with an FLT3 Mutation.Semantic proximity Read ↗

The Dual PIM/FLT3 Inhibitor MEN1703 Combines Synergistically With Gilteritinib in FLT3-ITD-Mutant Acute Myeloid Leukaemia.Semantic proximity Read ↗

Outcomes with single-agent gilteritinib for relapsed or refractory FLT3-mutant AML after contemporary induction therapy.Semantic proximity Read ↗

Clinical and molecular response of AML harboring non-canonical <i>FLT3</i> N676K driver mutations to contemporary FLT3 inhibitorsSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.