ReviewBlood2019
Genetics of MDS.
Review in Blood, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 229 papers, 1 of them a synthesis 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
229 citing papers in PubMed, 1 synthesis or guideline pooled it, 363 citations in OpenAlex.
- Contemporary Approach to the Diagnosis and Classification of Myelodysplastic Neoplasms/Syndromes-Recommendations From the International Consortium for Myelodysplastic Neoplasms/Syndromes (MDS [icMDS]).Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2024Guideline
- Pevonedistat plus azacitidine vs azacitidine alone in higher-risk MDS/chronic myelomonocytic leukemia or low-blast-percentage AML.Blood advances · 2022Trial
- ELN vs. IPSS-M in MDS/AML: Which Prognostic System Should Guide Clinical Decision-Making?Cancers · 2026Review
- Therapeutic Silencing of Tmprss6 Reduces Iron-Induced Inflammation and Prolongs Survival in MDS Mice.American journal of hematology · 2026Article
- Article
- Genomic landscape, clinical correlates and prognostic implications of U2AF1 mutation subtypes in myelodysplastic neoplasms.Blood cancer journal · 2026Article
- Mapping the research landscape of myelodysplastic syndromes: a scientometric analysis (2014-2025).Clinical and experimental medicine · 2026Article
- High frequency of CD95British journal of haematology · 2026Article
- Critical Role of Molecular-Based Stratification in Low-Risk Myelodysplastic Syndrome with Direct Progression to Acute Myeloid Leukemia: A Case Report.International journal of molecular sciences · 2026Article
- Exposure to Agent Orange and association with myelodysplastic syndromes.Blood advances · 2026Article
- Impact of allogeneic stem cell transplantation in patients with higher risk myelodysplastic syndromes.Blood cancer journal · 2026Article
- BRD9 depletion-mediated ALOX5 upregulation via chromatin dysregulation induces ferroptosis in SF3B1-mutant hematopoiesis.International journal of hematology · 2026Article
- MDS/AML-associated DDX41 helicase facilitates homologous recombination repair by potentially resolving R-loops.Nucleic acids research · 2026Article
- Dynamic activity of Erg promotes maturation of the hematopoietic system.Blood advances · 2026Article
- Ultra-Sensitive Mutation Detection Technology in Myeloid Neoplasms: New Tools for Patient Monitoring.Journal of clinical medicine · 2026Review
- Autoimmune HLA alleles and neoantigens predict myelodysplastic syndrome outcomes after allogeneic HSCT: A CIBMTR analysis.iScience · 2026Article
- Myelodysplastic syndrome progress to acute myeloid leukemia: new insights and updates.Frontiers in immunology · 2026Review
- Genomic characterisation of Chinese myeloid malignancies and its clinical correlates: insights from targeted next-generation sequencing.Frontiers in medicine · 2026Article
- Base-resolution DNA methylome of human MDS hematopoietic stem cell reveals TET2-GFI1 epigenetic axis repressing MDS.Immunity & inflammation · 2026Article
- Prognostic impact of lymphocyte to monocyte ratio in patients with myelodysplastic neoplasms/syndromes.Blood research · 2025Article
169 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
1 author at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our knowledge about the genetics of myelodysplastic syndromes (MDS) and related myeloid disorders has been dramatically improved during the past decade, in which revolutionized sequencing technologies have played a major role. Through intensive efforts of sequencing of a large number of MDS genomes, a comprehensive registry of driver mutations recurrently found in a recognizable fraction of MDS patients has been revealed, and ongoing efforts are being made to clarify their impacts on clinical phenotype and prognosis, as well as their role in the pathogenesis of MDS. Among major mutational targets in MDS are the molecules involved in DNA methylations, chromatin modification, RNA splicing, transcription, signal transduction, cohesin regulation, and DNA repair. Showing substantial overlaps with driver mutations seen in acute myeloid leukemia (AML), as well as age-related clonal hematopoiesis in healthy individuals, these mutations are presumed to have a common clonal origin. Mutations are thought to be acquired and positively selected in a well-organized manner to allow for expansion of the initiating clone to compromise normal hematopoiesis, ultimately giving rise to MDS and subsequent transformation to AML in many patients. Significant correlations between mutations suggest the presence of functional interactions between mutations, which dictate disease progression. Mutations are frequently associated with specific disease phenotype, drug response, and clinical outcomes, and thus, it is essential to be familiar with MDS genetics for better management of patients. This review aims to provide a brief overview of the recent progresses in MDS genetics.
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.