ReviewFrontiers in oncology2025
Overcoming the sorafenib resistance mechanism in FLT3-mutated acute myeloid leukemia: molecular basis and new targets.
Review in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 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
1 citing paper 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) originates from myeloid hematopoietic stem cells. Approximately 30% of patients exhibit FMS-like tyrosine kinase 3 (FLT3) mutations clinically, which is associated with a poor prognosis. FLT3 tyrosine kinase inhibitors (FLT3-TKIs), including sorafenib, demonstrate efficacy in FLT3-mutated AML, but resistance remains a significant challenge. However, various mechanisms have led to the rapid development of resistance to sorafenib treatment, including both primary and secondary drug resistance. Primary resistance refers to sorafenib's initial treatment failure due to redundant signaling pathways and tumor heterogeneity, while secondary resistance develops after prolonged therapy through new genetic mutations or activation of alternative pathways. This study systematically examines mechanisms of sorafenib resistance in AML, including tumor genetic changes and the bone marrow microenvironment. It outlines classic mechanisms, such as FLT3 functions, kinase mutations, and cellular signaling pathways, while also addressing gaps in knowledge regarding resistance driven by metabolic factors and the bone marrow environment. Furthermore, the paper explores novel FLT3 inhibitors and combination therapies, while outlining future directions for precision intervention through dynamic monitoring of clonal evolution. This review provides a comprehensive framework for understanding and addressing sorafenib resistance, offering insights into future therapeutic strategies for FLT3-mutated AML.
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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.