ArticleLeukemia2017
Subtype-specific patterns of molecular mutations in acute myeloid leukemia.
Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 98 citations in OpenAlex.
- Synthetic lethality of decitabine plus ATR inhibition for TP53-mutated AML.Blood advances · 2026Article
- Hypermethylation of microRNA-34c CpG Island predicts unfavorable prognosis in acute myeloid leukemia.Scientific reports · 2025Article
- Review
- Use of Human Acute Myeloid Leukemia Cells to Study Graft-Versus-Leukemia Immunity in Xenogeneic Mouse Models of Graft-Versus-Host Disease.Methods in molecular biology (Clifton, N.J.) · 2025Article
- NK cell-based immunotherapy strategies for myeloid leukemia.Frontiers in immunology · 2025Review
- From regulation to deregulation of p53 in hematologic malignancies: implications for diagnosis, prognosis and therapy.Biomarker research · 2024Review
- An unusual case of pure erythroid leukemia with normal karyotype and NPM1 mutation.Journal of hematopathology · 2024Article
- A network-based trans-omics approach for predicting synergistic drug combinations.Communications medicine · 2024Article
- A Chronological Overview of Using Deep Learning for Leukemia Detection: A Scoping Review.Cureus · 2024Article
- T cell-mediated tumor killing sensitivity gene signature-based prognostic score for acute myeloid leukemia.Discover oncology · 2024Article
- p53 biology and reactivation for improved therapy in MDS and AML.Biomarker research · 2024Review
- Simvastatin Preferentially Targets FLT3/ITD Acute Myeloid Leukemia by Inhibiting MEK/ERK and p38-MAPK Signaling Pathways.Drugs in R&D · 2023Article
- Reverse Phase Protein Array Profiling Identifies Recurrent Protein Expression Patterns of DNA Damage-Related Proteins across Acute and Chronic Leukemia: Samples from Adults and the Children's Oncology Group.International journal of molecular sciences · 2023Article
- "Losing the Brakes"-Suppressed Inhibitors Triggering UncontrolledCurrent issues in molecular biology · 2023Article
- Emerging bone marrow failure syndromes- new pieces to an unsolved puzzle.Frontiers in oncology · 2023Review
- Are We Moving the Needle for Patients withCancers · 2022Review
- TargetingOncoTargets and therapy · 2022Review
- A Novel BRD Family PROTAC Inhibitor dBET1 Exerts Great Anti-Cancer Effects by Targeting c-MYC in Acute Myeloid Leukemia Cells.Pathology oncology research : POR · 2022Article
- Review
- Anti-CD19 CAR T Cells That Secrete a Biparatopic Anti-CLEC12A Bridging Protein Have Potent Activity Against Highly Aggressive Acute Myeloid LeukemiaMolecular cancer therapeutics · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) can be grouped into morphologically or genetically defined subtypes. Today, the AML phenotype-genotype associations, that is, FAB/WHO (French-American-British/World Health Organization) definitions and recurrent molecular mutations, are not fully understood. Therefore, we evaluated the impact of molecular mutations on the AML differentiation stage by molecular profiling of 4373 adult de novo AML patients in 7 cytomorphological subtypes. We investigated mutations in 20 genes, including myeloid transcription factors (CEBPA, RUNX1), tumor suppressors (TP53, WT1), DNA modifiers (DNMT3A, IDH1/2, TET2), chromatin modifiers (ASXL1, MLL), signal transduction genes (FLT3, KRAS, NRAS) and NPM1. The most frequently mutated genes per cytomorphological subtype were RUNX1 in M0 (43%), NPM1 in M1 (42%), DNMT3A in M2 (26%), NPM1 in M4 (57%), M5a (49%) and M5b (70%) and TP53 in M6 (36%). Although some gene mutations were frequent in several cytomorphological subtypes, a series of associations of co-occurring mutations with distinct phenotypes were identified for molecularly defined subcohorts. FLT3, NPM1 and WT1 mutations were associated with an immature phenotype in myeloblastic AML, whereas other combinations involving ASXL1, RUNX1, MLL-PTD, CEBPA or KRAS were more frequent in myeloblastic AML with maturation. Within the NPM1 mutated subcohort, ASXL1 mutations were significantly associated with a monoblastic differentiation and DNMT3A mutations with a monocytic phenotype.
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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.