ReviewInternational journal of clinical oncology2019
Genetic abnormalities and pathophysiology of MDS.
Review in International journal of clinical oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 2 syntheses or guidelines pooled it, 117 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
- Meta-analysis of the benefit of hypomethylating agents before allogeneic hematopoietic stem cell transplantation in myelodysplastic syndromes.Clinical and experimental medicine · 2021Pooled it
- Favorable Response to Immunosuppressive Therapy in Severe Aplastic Anemia With Trisomy 8 and BCOR Mutation: Sustained Hematologic Response Despite Evolving Mutational Profile-A Case Report.Clinical case reports · 2026Article
- Modulation of miRNA networks by exercise in muscular dystrophies: therapeutic insights and future directions.Molecular and cellular biochemistry · 2026Review
- Potential diagnostic, prognostic, and therapeutic implications of ferroptosis in myelodysplastic syndromes.Discover oncology · 2026Review
- Cell Lines in Myelodysplastic Syndromes/Neoplasms (MDS) Research: A Review of Existing Models and Their Applications.International journal of molecular sciences · 2026Review
- Reduced STAG2 expression in myelodysplastic neoplasms and acute myeloid leukemia myelodysplasia-related: a potential biomarker associated with aneuploidy and disease progression.Frontiers in cell and developmental biology · 2026Article
- Prognostic impact of lymphocyte to monocyte ratio in patients with myelodysplastic neoplasms/syndromes.Blood research · 2025Article
- FDA approval of imetelstat: a new era in the treatment of lower-risk myelodysplastic syndrome.Annals of medicine and surgery (2012) · 2025Review
- Humanized mouse models in MDS.Cell death & disease · 2025Review
- Oxidative Stress and Mitochondrial Dysfunction in Myelodysplastic Syndrome: Roles in Development, Diagnosis, Prognosis, and Treatment.International journal of molecular sciences · 2025Review
- Myelodysplastic Neoplasms (MDS): Pathogenesis and Therapeutic Prospects.Biomolecules · 2025Review
- TET3 regulates hematopoietic stem cell homeostasis during embryonic and adult hematopoiesis.HemaSphere · 2025Article
- The Emerging Role of CD8Cancers · 2025Review
- Validation and improvement of the molecular international prognostic scoring system in Chinese patients with myelodysplastic syndromes.Annals of hematology · 2025Article
- Metabolic dysregulation in myelodysplastic neoplasm: impact on pathogenesis and potential therapeutic targets.Medical oncology (Northwood, London, England) · 2024Review
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- Rare Hematologic Malignancies and Pre-Leukemic Entities in Children and Adolescents Young Adults.Cancers · 2024Review
10 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 1 country.
Funding
Abstract
Myelodysplastic syndromes (MDS) are a heterogeneous group of myeloid malignancies characterized by peripheral blood cytopenia and dishematopoiesis and frequently progress to acute myeloid leukemia. Genetic defects play a major role in pathogenesis of MDS, including cytogenetic abnormalities, gene mutations, and abnormal gene expression. Chromosomal abnormalities have been detected in approximately 50-60% of MDS patients, including the deletions of chromosome 5q and 7q, trisomy 8, and complex karyotypes. Newer genomic technologies, such as single-nucleotide polymorphism array and next-generation sequencing, revealed the heterozygous deletions resulting in haploinsufficient gene expression (e.g., CSNK1A1, DDX41 on chromosome 5, CUX1, LUC7L2, EZH2 on chromosome 7) involved in the pathogenesis of MDS. In addition, recurrent somatic mutations in more than 50 genes have been identified in 80-90% of MDS. The most recurrent genetic mutations are involved in the RNA splicing (e.g., SF3B1, SRSF2, U2AF1, ZRSR2, LUC7L2, DDX41) and epigenetic modifications, such as histone modification (e.g., ASXL1, EZH2) and DNA methylation (e.g., TET2, DNMT3A, IDH1/IDH2). TP53 mutation is associated with aggressive disease and frequently coincides with deletion of chromosome 5q. This review summarizes the recent progress in molecular pathogenesis of MDS. A better understanding of the specific subgroups of MDS patients will also aid in the development of new therapeutic approach for MDS.
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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.