ArticleBlood advances2021
Deletions in FLT-3 juxtamembrane domain define a new class of pathogenic mutations: case report and systematic analysis.
Article in Blood advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Review
- Gilteritinib response in acute myeloid leukemia harboring a rare FLT3 juxtamembrane domain mutation with subsequent clonal evolution.Annals of hematology · 2026Article
- Article
- FLT3 targeting in the modern era: from clonal selection to combination therapies.International journal of hematology · 2024Review
- The Clinical Utility ofCurrent oncology (Toronto, Ont.) · 2023Article
- Clinical and molecular features of FLT3 juxtamembrane domain missense mutations in acute myeloid leukaemia.Journal of cellular and molecular medicine · 2022Article
- "FLipping" the Story: FLT3-Mutated Acute Myeloid Leukemia and the Evolving Role of FLT3 Inhibitors.Cancers · 2022Review
- Point Mutations in theFrontiers in oncology · 2022Article
- Genomic Abnormalities as Biomarkers and Therapeutic Targets in Acute Myeloid Leukemia.Cancers · 2021Review
- Case Report: A Novel Activating FLT3 Mutation in Acute Myeloid Leukemia.Frontiers in oncology · 2021Article
- Identification of Novel Insertions and Deletions in Haematopoietic Stem/Progenitor Cells in de novo Myelodysplastic Syndromes.International journal of molecular and cellular medicine · 2021Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The FMS-like tyrosine kinase 3 (FLT-3) is the most frequently mutated gene in acute myeloid leukemia (AML), a high-risk feature, and now the target of tyrosine kinase inhibitors (TKIs), which are approved and in development. The most common mutation is the internal tandem duplication (ITD). We present a novel mutation, FLT-3/Q575Δ, identified in a patient with AML through next-generation sequencing (NGS). This mutation is activating, drives downstream signaling comparable to FLT-3/ITD, and can be targeted using available FLT-3 TKIs. We present the results of a systematic analysis that identified Y572Δ, E573Δ, and S574Δ as similarly activating and targetable deletions located in the FLT-3 juxtamembrane domain (JMD). These mutations target key residues in the JMD involved in the interactions within FLT-3 that regulate its activation. Our results suggest a new class of FLT-3 mutations that may have an impact on patient care and highlight the increasing importance of a systematic understanding of FLT-3 mutations other than ITD. It is likely that, as NGS becomes more commonly used in the diagnosis of patients with AML, these and other activating mutations will be discovered with increasing frequency.
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