ReviewJournal of clinical oncology : official journal of the American Society of Clinical Oncology2011
Unraveling the molecular pathophysiology of myelodysplastic syndromes.
Review in Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 3 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
131 citing papers in PubMed, 3 syntheses or guidelines pooled it, 305 citations in OpenAlex.
- Association of Somatic Gene Mutations with Risk of Transformation into Acute Myeloid Leukemia in Patients with Myelodysplastic Syndrome: A Systematic Review and Meta-Analysis.Asian Pacific journal of cancer prevention : APJCP · 2022Pooled it
- Pooled it
- Prognostic value of isocitrate dehydrogenase mutations in myelodysplastic syndromes: a retrospective cohort study and meta-analysis.PloS one · 2014Pooled it
- Randomized phase 2 study of low-dose decitabine vs low-dose azacitidine in lower-risk MDS and MDS/MPN.Blood · 2017Trial
- Potential diagnostic, prognostic, and therapeutic implications of ferroptosis in myelodysplastic syndromes.Discover oncology · 2026Review
- Accelerated senescence of bone marrow erythrocyte precursors in myelodysplastic syndrome.Annals of medicine · 2025Article
- NAMPT haploinsufficiency is a collateral lethal therapeutic vulnerability in high-risk myeloid malignancies withBlood neoplasia · 2025Article
- Nucleophosmin 1 promotes mucosal immunity by supporting mitochondrial oxidative phosphorylation and ILC3 activity.Nature immunology · 2024Article
- CAR virus receptor mediates erythroid differentiation and migration and is downregulated in MDS.Leukemia · 2023Article
- Progressive disruption of hematopoietic architecture from clonal hematopoiesis to MDS.iScience · 2023Article
- Myelodysplastic syndromes: 2023 update on diagnosis, risk-stratification, and management.American journal of hematology · 2023Review
- Epigenetic regulation by ASXL1 in myeloid malignancies.International journal of hematology · 2023Review
- LEP promoter methylation in the initiation and progression of clonal cytopenia of undetermined significance and myelodysplastic syndrome.Clinical epigenetics · 2023Article
- Article
- Molecular Drivers of Myelodysplastic Neoplasms (MDS)-Classification and Prognostic Relevance.Cells · 2023Review
- Myelodysplastic syndromes.Nature reviews. Disease primers · 2022Review
- O-GlcNAcylation: an important post-translational modification and a potential therapeutic target for cancer therapy.Molecular medicine (Cambridge, Mass.) · 2022Review
- Immunohistochemical loss of enhancer of Zeste Homolog 2 (EZH2) protein expression correlates with EZH2 alterations and portends a worse outcome in myelodysplastic syndromes.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022Article
- The genetics of myelodysplastic syndromes and the opportunities for tailored treatments.Frontiers in oncology · 2022Review
- Cyclin-dependent kinase inhibitors in malignant hematopoiesis.Frontiers in oncology · 2022Review
71 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
Somatically acquired genetic abnormalities lead to the salient features that define myelodysplastic syndromes (MDS): clonal hematopoiesis, aberrant differentiation, peripheral cytopenias, and risk of progression to acute myeloid leukemia. Although specific karyotypic abnormalities have been linked to MDS for decades, more recent findings have demonstrated the importance of mutations within individual genes, focal alterations that are not apparent by standard cytogenetics, and aberrant epigenetic regulation of gene expression. The spectrum of genetic abnormalities in MDS implicates a wide range of molecular mechanisms in the pathogenesis of these disorders, including activation of tyrosine kinase signaling, genomic instability, impaired differentiation, altered ribosome function, and changes in the bone marrow microenvironment. Specific alterations present in individual patients with MDS may explain much of the heterogeneity in clinical phenotype associated with this disease and can predict prognosis and response to therapy. Elucidation of the full complement of genetic causes of MDS promises profound insight into the biology of the disease, improved classification and prognostic scoring schemes, and the potential for novel targeted therapies with molecular predictors of response.
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.