ReviewCells2025
Counter-Therapeutic Strategies for Resistance of FLT3 Inhibitors in Acute Myeloid Leukemia.
Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Efficacy and safety of FLT3 inhibitors for acute myeloid leukemia: a network meta-analysis.Frontiers in oncology · 2026Pooled it
- Targeting FLT3 in Acute Myeloid Leukemia: Structural Insights and Key Challenges.ACS bio & med chem Au · 2026Review
- Review
- The Mutational Landscape of Acute Myeloid Leukemia and Its Impact.International journal of molecular sciences · 2026Review
- 7-Ketocholesterol Links Sterol Homeostasis to Hedgehog Signaling and Stress-Survival Responses in MSCs from Patients with Acute Myeloid Leukemia.International journal of molecular sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FMS-like tyrosine kinase 3 (FLT3) mutations in acute myeloid leukemia (AML) are associated with an increased risk of relapse and a poor prognosis. Several FLT3 inhibitors that have been developed demonstrated efficacy against the FLT3 tyrosine kinase domain and/or internal tandem duplication mutations. Nevertheless, remission rates for these agents remain in the range of 30~40% of patients, attributed to both primary and secondary mechanisms of resistance, with relapse rates varying from ~30 to 50%. The mechanisms underlying resistance to FLT3 inhibitors have been characterized, offering valuable insights that can guide the development of clinical trials aimed at discovering novel FLT3 tyrosine kinase inhibitors (TKIs) that can overcome resistance. Additionally, elucidating resistance signaling pathways may facilitate the identification of other TKIs, rational combination therapies or multiple targeted TKIs to address alternative pathways, potentially helping overcome resistance in AML patients with refractory clones.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.