ReviewCurrent opinion in hematology2020
Driver mutations in acute myeloid leukemia.
Review in Current opinion in hematology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 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
61 citing papers in PubMed, 93 citations in OpenAlex.
- The Znf711-Phf8 complex functions as a transcriptional rheostat essential for neutrophil development.Haematologica · 2026Article
- Multiomic analysis of clonal development reveals new regulators of leukemic cell growth.Genes & development · 2026Article
- Preliminary evidence for the integration of CNAs, CN-LOH and mutational profiles into the prognostic stratification of elderly patients withOncology letters · 2026Article
- ELK1 promotes the progress of myeloid leukemia by hindering the differentiation of neutrophils.Experimental hematology & oncology · 2026Article
- Hereditary Predisposition to Acute Myeloid Leukemia: A Novel Germline CEBPA Mutation in a Multigenerational Family.Case reports in hematology · 2026Article
- Genomic characterisation of Chinese myeloid malignancies and its clinical correlates: insights from targeted next-generation sequencing.Frontiers in medicine · 2026Article
- GAB2 couples genetic drivers and signaling networks in acute myeloid leukemia.The Journal of clinical investigation · 2025Article
- Screening for Antileukemia Agents in FMS-like Tyrosine Kinase 3 (FLT3)-Mutated Acute Myeloid Leukemia Cells.ACS pharmacology & translational science · 2025Article
- DCPS is a synthetic lethal therapeutic target in acute myeloid leukemia expressing low levels of FHIT.Leukemia · 2025Article
- A single mutation may contribute to accelerated evolution of SARS-CoV-2 toward Omicron.Nature communications · 2025Article
- In Silico Drug Repurposing Against PSMB8 as a Potential Target for Acute Myeloid Leukemia Treatment.Molecular biotechnology · 2025Article
- Leukemogenic Kras mutation reprograms multipotent progenitors to facilitate its spread through the hematopoietic system.The Journal of experimental medicine · 2025Article
- METTL3/YTDHF1 Stabilizes CSRP1 mRNA to Regulate Glycolysis and Promote Acute Myeloid Leukemia Progression.Cell biochemistry and biophysics · 2025Article
- Molecular Mechanisms of Biochanin A in AML Cells: Apoptosis Induction and Pathway-Specific Regulation in U937 and THP-1.International journal of molecular sciences · 2025Article
- Epigenomic insights and computational advances in hematologic malignancies.Molecular cytogenetics · 2025Review
- CINner: Modeling and simulation of chromosomal instability in cancer at single-cell resolution.PLoS computational biology · 2025Article
- Double mutant DNMT3A AML: a unique subtype experiencing increased DNA damage and poor prognosis.Blood advances · 2025Article
- Article
- MutatedFrontiers in immunology · 2025Article
- Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
purpose of reviewThe mutational landscape of acute myeloid leukemia (AML) has revised diagnostic, prognostic, and therapeutic schemata over the past decade. Recurrently mutated AML genes have functional consequences beyond typical oncogene-driven growth and loss of tumor suppresser function. RECENT
findingsLarge-scale genomic sequencing efforts have mapped the complexity of AML and trials of mutation-based targeted therapy has led to several FDA-approved drugs for mutant-specific AML. However, many recurrent mutations have been identified across a spectrum from clonal hematopoiesis to myelodysplasia to overt AML, such as effectors of DNA methylation, chromatin modifiers, and spliceosomal machinery. The functional effects of these mutations are the basis for substantial discovery. SUMMARY: Understanding the molecular and pathophysiologic functions of key genes that exert leukemogenic potential is essential towards translating these findings into better treatment for AML.
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.