ReviewLeukemia2008
Cooperating gene mutations in acute myeloid leukemia: a review of the literature.
Review in Leukemia, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 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
137 citing papers in PubMed, 346 citations in OpenAlex.
- Trial
- Genetic abnormalities predict outcomes in patients with core binding factor acute myeloid leukemia.Annals of hematology · 2025Article
- APIR: Aggregating Universal Proteomics Database Search Algorithms for Peptide Identification with FDR Control.Genomics, proteomics & bioinformatics · 2024Article
- PRL2 inhibition elevates PTEN protein and ameliorates progression of acute myeloid leukemia.JCI insight · 2023Article
- Cytogenetics analysis as the central point of genetic testing in acute myeloid leukemia (AML): a laboratory perspective for clinical applications.Clinical and experimental medicine · 2023Review
- The Therapeutic Potential of a Strategy to Prevent Acute Myeloid Leukemia Stem Cell Reprogramming in Older Patients.International journal of molecular sciences · 2023Review
- The Question of Survival or Death: What Is the Role of Autophagy in Acute Myeloid Leukemia (AML)?International journal of hematology-oncology and stem cell research · 2022Review
- Quantification of mutant-allele expression at isoform level in cancer from RNA-seq data.NAR genomics and bioinformatics · 2022Article
- NF-κB: A Druggable Target in Acute Myeloid Leukemia.Cancers · 2022Review
- Leukotrienes promote stem cell self-renewal and chemoresistance in acute myeloid leukemia.Leukemia · 2022Article
- Article
- Whole exome sequencing of pediatric leukemia reveals a novel InDel within FLT-3 gene in AML patient from Mizo tribal population, Northeast India.BMC genomic data · 2022Article
- Straight to the Point-The Novel Strategies to Cure Pediatric AML.International journal of molecular sciences · 2022Review
- Molecular Systems Architecture of Interactome in the Acute Myeloid Leukemia Microenvironment.Cancers · 2022Review
- Article
- Using Cryo-ET to distinguish platelets during pre-acute myeloid leukemia from steady state hematopoiesis.Communications biology · 2022Article
- Proviral Integration of Moloney Virus-2 (PIM-2) Expression Level as a Prognostic Marker in Patients with Acute Myeloid Leukemia.International journal of general medicine · 2022Article
- Rapid Detection of N-RAS Gene Common Mutations in Acute Myeloid Leukemia (AML) Using High Resolution Melting (HRM) Method.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- RUNX1 can mediate the glucose and O-GlcNAc-driven proliferation and migration of human retinal microvascular endothelial cells.BMJ open diabetes research & care · 2021Article
- Thiazolidinedione "Magic Bullets" Simultaneously Targeting PPARγ and HDACs: Design, Synthesis, and Investigations of theirJournal of medicinal chemistry · 2021Article
77 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
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) is a heterogeneous group of neoplastic disorders with great variability in clinical course and response to therapy, as well as in the genetic and molecular basis of the pathology. Major advances in the understanding of leukemogenesis have been made by the characterization and the study of acquired cytogenetic abnormalities, particularly reciprocal translocations observed in AML. Besides these major cytogenetic abnormalities, gene mutations also constitute key events in AML pathogenesis. In this review, we describe the contribution of known gene mutations to the understanding of AML pathogenesis and their clinical significance. To gain more insight in this understanding, we clustered these alterations in three groups: (1) mutations affecting genes that contribute to cell proliferation (FLT3, c-KIT, RAS, protein tyrosine standard phosphatase nonreceptor 11); (2) mutations affecting genes involved in myeloid differentiation (AML1 and CEBPA) and (3) mutations affecting genes implicated in cell cycle regulation or apoptosis (P53, NPM1). This nonexhaustive review aims to show how gene mutations interact with each other, how they contribute to refine prognosis and how they can be useful for risk-adapted therapeutic management of AML patients.
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.