Trial reportLeukemia2022
Genomic landscape of patients with FLT3-mutated acute myeloid leukemia (AML) treated within the CALGB 10603/RATIFY trial.
Trial report in Leukemia, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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
20 citing papers in PubMed, 32 citations in OpenAlex.
- Quizartinib and omacetaxine mepesuccinate combination therapy in FLT3-ITD AML: a phase II trial.Nature communications · 2026Trial
- Guadecitabine vs treatment choice in newly diagnosed acute myeloid leukemia: a global phase 3 randomized study.Blood advances · 2023Trial
- Clinical outcomes of combination treatment with FMS-like tyrosine kinase 3 (FLT3) and isocitrate dehydrogenase 1/2 (IDH1/2) inhibitors in patients with acute myeloid leukaemia.British journal of haematology · 2026Article
- Article
- Impact of clinical characteristics and genetic profiles on outcomes of allogeneic stem cell transplantation with sorafenib maintenance inChinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2025Article
- NPM1 Measurable Residual Disease: A Narrative Review.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2025Review
- ARF6 Promotes AML Progression via Activation of PI3K/AKT/mTOR Signaling.Cancer medicine · 2025Article
- Significance of targeting DNMT3A mutations in AML.Annals of hematology · 2025Review
- Chronic myelomonocytic leukemia with NPM1 mutation or acute myeloid leukemia?The oncologist · 2025Review
- AML typical mutations (CEBPA, FLT3, NPM1) identify a high-risk chronic myelomonocytic leukemia independent of CPSS molecular.Blood advances · 2025Article
- Impact of myelodysplasia-related and additional gene mutations in intensively treated patients withHemaSphere · 2025Article
- Menin inhibitors for the treatment of acute myeloid leukemia: challenges and opportunities ahead.Journal of hematology & oncology · 2024Review
- FLT3 targeting in the modern era: from clonal selection to combination therapies.International journal of hematology · 2024Review
- DistinctInternational journal of molecular sciences · 2024Article
- CoHIT: a one-pot ultrasensitive ERA-CRISPR system for detecting multiple same-site indels.Nature communications · 2024Article
- Current knowledge about FLT3 gene mutations, exploring the isoforms, and protein importance in AML.Molecular biology reports · 2024Review
- Very short insertions in the FLT3 gene are of therapeutic significance in acute myeloid leukemia.Blood advances · 2023Article
- Impact of genetic patterns on sorafenib efficacy in patients with FLT3-ITD acute myeloid leukemia undergoing allogeneic hematopoietic stem cell transplantation: a multi-center, cohort study.Signal transduction and targeted therapy · 2023Article
- Clinical and molecular response of acute myeloid leukemia harboring non-canonicalHaematologica · 2023Article
- FMS-Like Tyrosine Kinase 3 Inhibitors in the Treatment of Acute Myeloid Leukemia: An Update on the Emerging Evidence and Safety Profile.OncoTargets and therapy · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
24 authors at 15 institutions in 5 countries.
Funding
Abstract
The aim of this study was to characterize the mutational landscape of patients with FLT3-mutated acute myeloid leukemia (AML) treated within the randomized CALGB 10603/RATIFY trial evaluating intensive chemotherapy plus the multi-kinase inhibitor midostaurin versus placebo. We performed sequencing of 262 genes in 475 patients: mutations occurring concurrently with the FLT3-mutation were most frequent in NPM1 (61%), DNMT3A (39%), WT1 (21%), TET2 (12%), NRAS (11%), RUNX1 (11%), PTPN11 (10%), and ASXL1 (8%) genes. To assess effects of clinical and genetic features and their possible interactions, we fitted random survival forests and interpreted the resulting variable importance. Highest prognostic impact was found for WT1 and NPM1 mutations, followed by white blood cell count, FLT3 mutation type (internal tandem duplications vs. tyrosine kinase domain mutations), treatment (midostaurin vs. placebo), ASXL1 mutation, and ECOG performance status. When evaluating two-fold variable combinations the most striking effects were found for WT1:NPM1 (with NPM1 mutation abrogating the negative effect of WT1 mutation), and for WT1:treatment (with midostaurin exerting a beneficial effect in WT1-mutated AML). This targeted gene sequencing study provides important, novel insights into the genomic background of FLT3-mutated AML including the prognostic impact of co-mutations, specific gene-gene interactions, and possible treatment effects of midostaurin.
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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.