ReviewBlood cancer journal2021
Differentiation therapy for myeloid malignancies: beyond cytotoxicity.
Review in Blood cancer journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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
47 citing papers in PubMed, 64 citations in OpenAlex.
- Ziftomenib in Relapsed or RefractoryJournal of clinical oncology : official journal of the American Society of Clinical Oncology · 2025Trial
- Article
- Dynamic genetic and nongenetic RAS-pathway activation drives resistance to FLT3 and BCL2 inhibitor therapy.Blood · 2026Article
- Novel noscapine derivative induces AML differentiation by dual-engaging DHODH and mitochondrial lipids to trigger a metabolic-epigenetic-transcriptional cascade.Acta pharmaceutica Sinica. B · 2026Article
- TCEA1 Suppresses Acute Promyelocytic Leukemia by Upregulating C/EBPε and IRF8.International journal of molecular sciences · 2026Article
- Article
- Enhanced efficacy of a specific HDAC3 inhibitor in combination with 5-azacitidine against diffuse large B-cell lymphoma.Blood neoplasia · 2026Article
- Targeting WNK1 Releases Differentiation Block in Acute Myeloid Leukemia.bioRxiv : the preprint server for biology · 2026Article
- Targeting aberrant DNA methylation across subtypes of pediatric high-grade glioma inhibits tumor growth and RUNX3 represents a targetable methylated tumor suppressor.Cell communication and signaling : CCS · 2026Article
- Differentiation Syndrome in Acute Myeloid Leukemia: Molecular Mechanisms, Clinical Spectrum, and Emerging Therapeutic Paradigms.International journal of molecular sciences · 2026Review
- Review
- The complex journey of targeting RAS in oncology.BMC cancer · 2025Review
- Microvesicle inhibition enhances the therapeutic effects of ATRA in acute promyelocytic leukemia cells via changes in miRNAs: the promising antileukemic potential of imipramine.Clinical and experimental medicine · 2025Article
- A dual chemodrug-loaded hyaluronan nanogel for differentiation induction therapy of refractory AML via disrupting lysosomal homeostasis.Science advances · 2025Article
- Unleashing the TLR9-driven multilineage differentiation of myeloid leukemia cellsMolecular therapy. Nucleic acids · 2025Article
- Norchelerythrine fromInternational journal of oncology · 2025Article
- Single cell RNA sequencing improves the next generation of approaches to AML treatment: challenges and perspectives.Molecular medicine (Cambridge, Mass.) · 2025Review
- A LANA peptide inhibits tumor growth by inducing CHD4 protein cleavage and triggers cell death.Cell chemical biology · 2024Article
- Spermidine metabolism regulates leukemia stem and progenitor cell function through KAT7 expression in patient-derived mouse models.Science translational medicine · 2024Article
- Human papillomavirus-associated head and neck squamous cell carcinoma cells lose viability during triggered myocyte lineage differentiation.Cell death & disease · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Blocked cellular differentiation is a central pathologic feature of the myeloid malignancies, myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). Treatment regimens promoting differentiation have resulted in incredible cure rates in certain AML subtypes, such as acute promyelocytic leukemia. Over the past several years, we have seen many new therapies for MDS/AML enter clinical practice, including epigenetic therapies (e.g., 5-azacitidine), isocitrate dehydrogenase (IDH) inhibitors, fms-like kinase 3 (FLT3) inhibitors, and lenalidomide for deletion 5q (del5q) MDS. Despite not being developed with the intent of manipulating differentiation, induction of differentiation is a major mechanism by which several of these novel agents function. In this review, we examine the new therapeutic landscape for these diseases, focusing on the role of hematopoietic differentiation and the impact of inflammation and aging. We review how current therapies in MDS/AML promote differentiation as a part of their therapeutic effect, and the cellular mechanisms by which this occurs. We then outline potential novel avenues to achieve differentiation in the myeloid malignancies for therapeutic purposes. This emerging body of knowledge about the importance of relieving differentiation blockade with anti-neoplastic therapies is important to understand how current novel agents function and may open avenues to developing new treatments that explicitly target cellular differentiation. Moving beyond cytotoxic agents has the potential to open new and unexpected avenues in the treatment of myeloid malignancies, hopefully providing more efficacy with reduced toxicity.
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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.