ArticleNature communications2024
Epigenetic-based differentiation therapy for Acute Myeloid Leukemia.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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.
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Who cites it
11 citing papers in PubMed.
- Exploration of novel hydroxamic acid-based candidates integrating chalcone scaffold cap as multitarget HDAC inhibitors: design, anti-prostatic cancer assessment,Journal of enzyme inhibition and medicinal chemistry · 2026Article
- The interaction between NPMc+ and Orai1 induces abnormal calcium influx to facilitate leukemogenesis.The FEBS journal · 2026Article
- Deacetylase inhibitors CM-444 and CM-1758 enhance chemotherapy response in AML via ALOX5.British journal of haematology · 2026Article
- IRF2 is an essential transcription factor with pathogenic and prognostic impact in multiple myeloma.Blood · 2026Article
- Diagnosis-Driven Targeted Therapy in Acute Myeloid Leukemia: Clinical Integration of Tyrosine Kinase, BCL-2, and CD33-Directed Strategies with Midostaurin, Venetoclax, and Gemtuzumab Ozogamicin.Journal of clinical medicine · 2026Review
- Histone deacetylases: Function in tumor development and therapeutic prospects (Review).Oncology letters · 2026Review
- Deep Learning Identifies Abnormal Promyelocytes in Peripheral Blood Based on Morphological Analysis.Diagnostics (Basel, Switzerland) · 2026Article
- Visomitin as a differentiation-inducing therapeutic agent through SYK inhibition in AML.Frontiers in pharmacology · 2026Article
- Review
- Article
- Acetylation of Histone H3 in Cancer Progression and Prognosis.International journal of molecular sciences · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
30 authors.
Funding
Abstract
Despite the development of novel therapies for acute myeloid leukemia, outcomes remain poor for most patients, and therapeutic improvements are an urgent unmet need. Although treatment regimens promoting differentiation have succeeded in the treatment of acute promyelocytic leukemia, their role in other acute myeloid leukemia subtypes needs to be explored. Here we identify and characterize two lysine deacetylase inhibitors, CM-444 and CM-1758, exhibiting the capacity to promote myeloid differentiation in all acute myeloid leukemia subtypes at low non-cytotoxic doses, unlike other commercial histone deacetylase inhibitors. Analyzing the acetylome after CM-444 and CM-1758 treatment reveals modulation of non-histone proteins involved in the enhancer-promoter chromatin regulatory complex, including bromodomain proteins. This acetylation is essential for enhancing the expression of key transcription factors directly involved in the differentiation therapy induced by CM-444/CM-1758 in acute myeloid leukemia. In summary, these compounds may represent effective differentiation-based therapeutic agents across acute myeloid leukemia subtypes with a potential mechanism for the treatment of acute myeloid leukemia.
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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.