ArticleOncotarget2016
Somatic mutations predict outcomes of hypomethylating therapy in patients with myelodysplastic syndrome.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 4 of them syntheses that pooled it.
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Who cites it
42 citing papers in PubMed, 4 syntheses or guidelines pooled it, 68 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
- Role Of TP53 mutations in predicting the clinical efficacy of hypomethylating therapy in patients with myelodysplastic syndrome and related neoplasms: a systematic review and meta-analysis.Clinical and experimental medicine · 2020Pooled it
- Prognostic significance ofThe Journal of international medical research · 2020Pooled it
- Effect of RNA splicing machinery gene mutations on prognosis of patients with MDS: A meta-analysis.Medicine · 2019Pooled it
- Asia-inclusive global development of pevonedistat: Clinical pharmacology and translational research enabling a phase 3 multiregional clinical trial.Clinical and translational science · 2021Trial
- Treatment with a 5-day versus a 10-day schedule of decitabine in older patients with newly diagnosed acute myeloid leukaemia: a randomised phase 2 trial.The Lancet. Haematology · 2019Trial
- Myelodysplastic Syndromes: 2026 Update on Diagnosis, Risk-Stratification and Management.American journal of hematology · 2026Review
- Epigenetic Inhibitor 5-Azacytidine Triggers DIM-2/DIM-5-Dependent Mutagenesis in H3K9me3-Enriched Regions ofJournal of fungi (Basel, Switzerland) · 2026Article
- Article
- p53 status determines the epigenetic response to demethylating agents azacitidine and decitabine.EMBO reports · 2026Article
- From regulation to deregulation of p53 in hematologic malignancies: implications for diagnosis, prognosis and therapy.Biomarker research · 2024Review
- Enhanced ALOX12 Gene Expression Predicts Therapeutic Susceptibility to 5-Azacytidine in Patients with Myelodysplastic Syndromes.International journal of molecular sciences · 2024Article
- Real-World Outcome and Prognostic Factors in MDS Patients Treated with Azacitidine-A Retrospective Analysis.Cancers · 2024Article
- U2AF1 pathogenic variants in myeloid neoplasms and precursor states: distribution of co-mutations and prognostic heterogeneity.Blood cancer journal · 2023Article
- Real-world practice-based prognostic model for higher-risk myelodysplastic syndromes treated with azacitidine monotherapy: The Kyoto prognostic scoring system.International journal of hematology · 2023Article
- Myelodysplastic syndromes: 2023 update on diagnosis, risk-stratification, and management.American journal of hematology · 2023Review
- Postazacitidine clone size predicts long-term outcome of patients with myelodysplastic syndromes and related myeloid neoplasms.Blood advances · 2023Article
- Decitabine in patients with myelodysplastic syndromes: A multi-center, open-label, dose comparison trial.Cancer medicine · 2023Article
- TP53 mutations confer resistance to hypomethylating agents and BCL-2 inhibition in myeloid neoplasms.Blood advances · 2022Article
- TET2 Mutation and High miR-22 Expression as Biomarkers to Predict Clinical Outcome in Myelodysplastic Syndrome Patients Treated with Hypomethylating Therapy.Current issues in molecular biology · 2021Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although hypomethylating therapy (HMT) is the first line therapy in higher-risk myelodysplastic syndromes (MDS), predicting response to HMT remains an unresolved issue. We aimed to identify mutations associated with response to HMT and survival in MDS. A total of 107 Korean patients with MDS who underwent HMT (57 responders and 50 non-responders) were enrolled. Targeted deep sequencing (median depth of coverage 1,623X) was performed for 26 candidate MDS genes. In multivariate analysis, no mutation was significantly associated with response to HMT, but a lower hemoglobin level (<10g/dL, OR 3.56, 95% CI 1.22-10.33) and low platelet count (<50,000/μL, OR 2.49, 95% CI 1.05-5.93) were independent markers of poor response to HMT. In the subgroup analysis by type of HMT agents, U2AF1 mutation was significantly associated with non-response to azacitidine, which was consistent in multivariate analysis (OR 14.96, 95% CI 1.67-134.18). Regarding overall survival, mutations in DNMT1 (P=0.031), DNMT3A (P=0.006), RAS (P=0.043), and TP53 (P=0.008), and two clinical variables (male-gender, P=0.002; IPSS-R H/VH, P=0.026) were independent predicting factors of poor prognosis. For AML-free survival, mutations in DNMT3A (P<0.001), RAS (P=0.001), and TP53 (P=0.047), and two clinical variables (male-gender, P=0.024; IPSS-R H/VH, P=0.005) were independent predicting factors of poor prognosis. By combining these mutations and clinical predictors, we developed a quantitative scoring model for response to azacitidine, overall- and AML-free survival. Response to azacitidine and survival rates became worse significantly with increasing risk-scores. This scoring model can make prognosis prediction more reliable and clinically applicable.
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