ReviewLeukemia2008
Genetics of therapy-related myelodysplasia and acute myeloid leukemia.
Review in Leukemia, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 2 of them syntheses 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
98 citing papers in PubMed, 2 syntheses or guidelines pooled it, 229 citations in OpenAlex.
- TP53 Mutations Unfavorably Impact the Outcomes of Myelofibrosis Patients with or Without Hematopoietic Stem Cell Transplantation: A Single-Center Study and Meta-Analysis.International journal of molecular sciences · 2026Pooled it
- Association between RAD51 gene polymorphism (-135G/C) and susceptibility of myelodysplastic syndrome and acute leukemia: evidence based on a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Pooled it
- Trial
- Clinical effect of increasing doses of lenalidomide in high-risk myelodysplastic syndrome and acute myeloid leukemia with chromosome 5 abnormalities.Haematologica · 2011Trial
- Low WT1 Expression Identifies a Subset of Acute Myeloid Leukemia with a Distinct Genotype.Cancers · 2025Article
- Risk of secondary myeloid neoplasms following treatment in patients with grade I-II follicular lymphoma: a retrospective cohort study.Discover oncology · 2025Article
- Transcriptomic characterisation of acute myeloid leukemia cell lines bearing the same t(9;11) driver mutation reveals different molecular signatures.BMC genomics · 2025Article
- Emergence and Cytogenetic Clonal Evolution of Chromosome 7 Abnormalities in Myeloid Malignancies: Investigating the Role of Telomere Dysfunction.International journal of molecular sciences · 2025Article
- Therapy-Related Myeloid Neoplasms: Complex Interactions among Cytotoxic Therapies, Genetic Factors, and Aberrant Microenvironment.Blood cancer discovery · 2024Review
- Recent Advances towards the Understanding of Secondary Acute Myeloid Leukemia Progression.Life (Basel, Switzerland) · 2024Review
- Criteria for Diagnosis and Molecular Monitoring of NPM1-Mutated AML.Blood cancer discovery · 2024Review
- Vemurafenib induces senescence in acute myeloid leukemia and myelodysplastic syndrome by activating the HIPPO signaling pathway: implications for potential targeted therapy.Biology direct · 2024Article
- A gain-of-function p53 mutant synergizes with oncogenic NRAS to promote acute myeloid leukemia in mice.The Journal of clinical investigation · 2023Article
- Combined inhibition of BCL-2 and MCL-1 overcomes BAX deficiency-mediated resistance of TP53-mutant acute myeloid leukemia to individual BH3 mimetics.Blood cancer journal · 2023Article
- Progress toward Better Treatment of Therapy-Related AML.Cancers · 2023Review
- Therapy-selected clonal hematopoiesis and its role in myeloid neoplasms.Leukemia research · 2023Article
- Functional association of NR4A3 downregulation with impaired differentiation in myeloid leukemogenesis.Annals of hematology · 2022Article
- Recurrent Translocations in Topoisomerase Inhibitor-Related Leukemia Are Determined by the Features of DNA Breaks Rather Than by the Proximity of the Translocating Genes.International journal of molecular sciences · 2022Article
- Review
- Myelodysplastic syndrome in a case of new-onset pancytopenia.Clinical case reports · 2022Article
38 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
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myelodysplasia (MDS) and acute myeloid leukemia (AML) are heterogeneous, closely associated diseases arising de novo or following chemotherapy with alkylating agents, topoisomerase II inhibitors, or after radiotherapy. Whereas de novo MDS and AML are almost always subclassified according to cytogenetic characteristics, therapy-related MDS (t-MDS) and therapy-related AML (t-AML) are often considered as separate entities and are not subdivided. Alternative genetic pathways were previously proposed in t-MDS and t-AML based on cytogenetic characteristics. An increasing number of gene mutations are now observed to cluster differently in these pathways with an identical pattern in de novo and in t-MDS and t-AML. An association is observed between activating mutations of genes in the tyrosine kinase RAS-BRAF signal-transduction pathway (Class I mutations) and inactivating mutations of genes encoding hematopoietic transcription factors (Class II mutations). Point mutations of AML1 and RAS seem to cooperate and predispose to progression from t-MDS to t-AML. Recently, critical genetic effects underlying 5q-/-5 and 7q-/-7 have been proposed. Their association and cooperation with point mutations of p53 and AML1, respectively, extend the scenario of cooperating genetic abnormalities in MDS and AML. As de novo and t-MDS and t-AML are biologically identical diseases, they ought to be subclassified and treated similarly.
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.