ReviewTherapeutic advances in hematology2019
Management of myelodysplastic syndromes after failure of response to hypomethylating agents.
Review in Therapeutic advances in hematology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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.
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Who cites it
21 citing papers in PubMed.
- Role of Toll-Like Receptors in Myeloid Neoplasms: Focuses on the Molecular Mechanisms and Clinical Impact on Myelodysplastic Syndromes, Acute Myeloid Leukemia, and Chronic Myeloid Leukemia.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2025Review
- Implications for metabolic disturbances in myelodysplastic syndromes.Seminars in hematology · 2024Review
- Efficacy of Yisui granule on myelodysplastic syndromes in SKM-1 mouse xenograft model through suppressing Wnt/β-catenin signaling pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- Clinical characteristics and prognostic significance of DNA methylation regulatory gene mutations in acute myeloid leukemia.Clinical epigenetics · 2023Article
- Review
- Toll-like receptor and cytokine expression throughout the bone marrow differs between patients with low- and high-risk myelodysplastic syndromes.Experimental hematology · 2022Article
- Article
- Platelet Doubling After First Decitabine Cycle Predicts Response and Survival of Myelodysplastic Syndrome Patients.Current medical science · 2022Article
- Tumor suppressor CEBPA interacts with and inhibits DNMT3A activity.Science advances · 2022Article
- Dynamics of PD-1 expression are associated with treatment efficacy and prognosis in patients with intermediate/high-risk myelodysplastic syndromes under hypomethylating treatment.Frontiers in immunology · 2022Article
- Hypoplastic myelodysplastic syndrome and acquired aplastic anemia: Immune‑mediated bone marrow failure syndromes (Review).International journal of oncology · 2022Review
- Azacitidine Omega-3 Self-Assemblies: Synthesis, Characterization, and Potent Applications for Myelodysplastic Syndromes.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Molecular Targeted Therapy and Immunotherapy for Myelodysplastic Syndrome.International journal of molecular sciences · 2021Review
- Review
- Azacitidine regulates DNA methylation of GADD45γ in myelodysplastic syndromes.Journal of clinical laboratory analysis · 2021Article
- Dendritic Cells of Leukemic Origin: Specialized Antigen-Presenting Cells as Potential Treatment Tools for Patients with Myeloid Leukemia.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2020Review
- Unravelling the Epigenome of Myelodysplastic Syndrome: Diagnosis, Prognosis, and Response to Therapy.Cancers · 2020Review
- Decitabine/Cedazuridine: First Approval.Drugs · 2020Review
- TLR2/6 signaling promotes the expansion of premalignant hematopoietic stem and progenitor cells in the NUP98-HOXD13 mouse model of MDS.Experimental hematology · 2020Article
- Contribution of Aberrant Toll Like Receptor Signaling to the Pathogenesis of Myelodysplastic Syndromes.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypomethylating agents (HMAs) are the standard of care for patients with myelodysplastic syndrome (MDS). However, only around 50% of patients respond to these agents, and responses tend to be transient, with loss of response frequently happening within 2 years and being associated with very poor prognosis and limited therapeutic options. Identification of patients who will respond to HMAs is challenging. Mechanisms underlying resistance to HMAs are not clear yet. Recently, absence of response has been associated with increased cell-cycle quiescence among the hematopoietic progenitor cells. There are no standard-of-care options for patients after HMA failure. However, the increasing knowledge of MDS pathogenesis has led to the development of new potential therapies, including HMAs with longer half-life and exposure, inhibition of the antiapoptotic BCL2 protein with venetoclax or inhibition of immune-checkpoint regulatory proteins such as PD-1 or CTLA-4, innate immunity and targeting of CD33/CD3 with multiple monoclonal antibodies. In addition, multiple targeted agents are opening opportunities to treat subgroups of patients whose disease harbors mutations in
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