ArticleCommunications biology2024
Targeting heterochromatin eliminates chronic myelomonocytic leukemia malignant stem cells through reactivation of retroelements and immune pathways.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Viral mimicry escape as a necessary feature of malignant transformation.Nature reviews. Cancer · 2026Review
- Article
- Transposable elements in hematopoietic stem cells upon aging and myeloid malignancies.Mobile DNA · 2026Review
- MORC2 promotes acute myeloid leukemia by silencing LINE-1 retrotransposon.Functional & integrative genomics · 2026Article
- Targeting RhoA nuclear mechanoactivity rejuvenates aged hematopoietic stem cells.Nature aging · 2026Article
- Overcoming immunotherapy barriers in pediatric brain tumors: epigenetic strategies.Frontiers in oncology · 2026Review
- Revisiting Clonal Evolution Through the Light of Retrotransposons.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Chronic Myelomonocytic Leukemia Microenvironment in Disease Progression and Therapy: Focus on Stepwise Reconfiguring of Myeloid-Immune Cell Interactions Driving Immune Tolerance.Current hematologic malignancy reports · 2025Review
- Endogenous retroelements in hematological malignancies: From epigenetic dysregulation to therapeutic targeting.American journal of hematology · 2025Review
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Authors and funding
19 authors.
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Abstract
Chronic myelomonocytic leukemia (CMML) is a severe myeloid malignancy affecting the elderly, for which therapeutic options are limited. DNA hypomethylating agents (HMAs) provide transient responses, failing to eradicate the malignant clone. Hematopoietic stem cell (HSC) aging involves heterochromatin reorganization, evidenced by alterations in histone marks H3K9me2 and H3K9me3. These repressive marks together with DNA methylation are essential for suppressing transposable elements (TEs). In solid cancers, the antitumor efficacy of HMAs involves the derepression of TEs, mimicking a state of viral infection. In this study, we demonstrate a significant disorganization of heterochromatin in CMML HSCs and progenitors (HSPCs) characterized by an increase in the repressive mark H3K9me2, mainly at the level of TEs, and a repression of immune and age-associated transcripts. Combining HMAs with G9A/GLP H3K9me2 methyltransferase inhibitors reactivates these pathways, selectively targeting mutated cells while preserving wild-type HSCs, thus offering new therapeutic avenues for this severe myeloid malignancy.
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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.