ReviewSeminars in oncology2011
Failure of hypomethylating agent-based therapy in myelodysplastic syndromes.
Review in Seminars in oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Prognostic significance ofThe Journal of international medical research · 2020Pooled it
- Checkpoint immunotherapy is associated with preferential activation of tumor antigen-specific CD4Blood neoplasia · 2025Trial
- Combination of dociparstat sodium (DSTAT), a CXCL12/CXCR4 inhibitor, with azacitidine for the treatment of hypomethylating agent refractory AML and MDS.Leukemia research · 2021Trial
- Phase II clinical study of erlotinib for treatment of myelodysplastic syndromes.American journal of hematology · 2014Trial
- Cancer cell type-specific derepression of transposable elements by inhibition of chromatin modifier enzymes.Communications biology · 2025Article
- A phase II trial of azacitidine with ipilimumab, nivolumab, or ipilimumab and nivolumab in previously untreated myelodysplastic syndrome.Haematologica · 2025Article
- Article
- Secondary Acute Myeloid Leukemia in Myelodysplastic Syndrome Patients Aged Over 60 Years.Cureus · 2023Review
- Inhibition of DNMT3B and PI3K/AKT/mTOR and ERK Pathways as a Novel Mechanism of Volasertib on Hypomethylating Agent-Resistant Cells.Biomolecules & therapeutics · 2023Article
- Abnormal regulation of miR-29b-ID1 signaling is involved in the process of decitabine resistance in leukemia cells.Cell cycle (Georgetown, Tex.) · 2023Article
- Gene Expression Profiles Identify Biomarkers of Resistance to Decitabine in Myelodysplastic Syndromes.Cells · 2021Article
- Higher-risk myelodysplastic syndrome in an elderly patient: Long-term partial remission with low-dose prednisone, G-CSF, and epoetin alfa.Clinical case reports · 2021Article
- Mechanisms of Action of Hypomethylating Agents: Endogenous Retroelements at the Epicenter.Frontiers in oncology · 2021Review
- Deciphering the Therapeutic Resistance in Acute Myeloid Leukemia.International journal of molecular sciences · 2020Review
- The DNA methylation landscape of hematological malignancies: an update.Molecular oncology · 2020Review
- Article
- Co-occurrence of RUNX1 and ASXL1 mutations underlie poor response and outcome for MDS patients treated with HMAs.American journal of translational research · 2019Article
- NY-ESO-1 Vaccination in Combination with Decitabine Induces Antigen-Specific T-lymphocyte Responses in Patients with Myelodysplastic Syndrome.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- Article
- The Synergistic Effects of Decitabine Combined with Arsenic Trioxide (ATO) in the Human Myelodysplastic Syndrome Cell Line SKM-1.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2016Article
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 1 institution in 1 country.
Funding
Abstract
Hypomethylating agents such as 5-azacytidine or decitabine have been a major breakthrough in the treatment of patients with myelodysplastic syndromes (MDS). They have been shown to improve transfusion requirements and to change the natural history of the disease. However, with increasing cumulative clinical experience, it has become apparent that these agents are not curative and have their own shortcomings. There is a subgroup of patients who do not respond to frontline therapy and a large, growing cohort of patients that lose response or progress while on hypomethylating agent-based therapy. There are no standard treatment options in this arena and it is therefore a focus of significant research interest. Since the mechanisms of resistance to hypomethylating agents are not known, selection of therapy is largely empiric but must take into account the age, comorbidities, and performance status of the patient, as well as the characteristics of the disease at the time of treatment failure. Higher intensity approaches and allogeneic stem cell transplant can yield improved response rates and long-term disease control but should be limited to a selected cohort of patients who can tolerate the treatment-related morbidities. For the majority of patients who likely will be better candidates for lower intensity therapy, several novel, investigational approaches are becoming available. Among these are newer nucleoside analogues, inhibitors of protein tyrosine kinases, molecules that interact with redox signaling within the cell, immunotherapy approaches, and others. Patients with MDS whose disease has failed to respond to hypomethylating agent therapy should be referred for clinical trials when available. As we learn more about the patterns and mechanisms of failure, the next challenge will be to determine which therapies are suitable for each individual patient.
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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.