ArticleHaematologica2023
CCRL2 affects the sensitivity of myelodysplastic syndrome and secondary acute myeloid leukemia cells to azacitidine.
Article in Haematologica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 15 citations in OpenAlex.
- A PBD dimer-containing antibody-drug conjugate targeting CCRL2 for high-risk MDS/AML including TP53-mutated disease.Blood advances · 2026Article
- C-C motif chemokine receptor-like 2 promotes the interferon-γ signaling response in myeloid neoplasms with erythroid differentiation and mutatedHaematologica · 2026Article
- CCRL2 and who? An important driver inHaematologica · 2026Article
- Cell Lines in Myelodysplastic Syndromes/Neoplasms (MDS) Research: A Review of Existing Models and Their Applications.International journal of molecular sciences · 2026Review
- A PBD-dimer containing antibody drug conjugate targeting CCRL2 for high-risk MDS/AML.Research square · 2025Article
- Genetic determinants and genomic consequences of non-leukemogenic somatic point mutations.Nature communications · 2025Article
- CD79B in myelodysplastic syndromes and acute myeloid leukemia: an integrative computational andFrontiers in medicine · 2025Article
- Targeting CCRL2 enhances therapeutic outcomes in a tuberculosis mouse model.Frontiers in immunology · 2025Article
- Review
- Review
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- Epigenetic modification of CD4Cell death & disease · 2024Article
- The Genetic Determinants and Genomic Consequences of Non-Leukemogenic Somatic Point Mutations.medRxiv : the preprint server for health sciences · 2024Article
- From cell surface to nucleus: CCRL2 regulates response to hypomethylating agents in myelodysplastic syndromes.Haematologica · 2023Article
- Understanding the Continuum between High-Risk Myelodysplastic Syndrome and Acute Myeloid Leukemia.International journal of molecular sciences · 2023Review
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Authors and funding
18 authors at 2 institutions in 1 country.
Funding
Abstract
Better understanding of the biology of resistance to DNA methyltransferase (DNMT) inhibitors is required to identify therapies that can improve their efficacy for patients with high-risk myelodysplastic syndrome (MDS). CCRL2 is an atypical chemokine receptor that is upregulated in CD34+ cells from MDS patients and induces proliferation of MDS and secondary acute myeloid leukemia (sAML) cells. In this study, we evaluated any role that CCRL2 may have in the regulation of pathways associated with poor response or resistance to DNMT inhibitors. We found that CCRL2 knockdown in TF-1 cells downregulated DNA methylation and PRC2 activity pathways and increased DNMT suppression by azacitidine in MDS/sAML cell lines (MDS92, MDS-L and TF-1). Consistently, CCRL2 deletion increased the sensitivity of these cells to azacitidine in vitro and the efficacy of azacitidine in an MDS-L xenograft model. Furthermore, CCRL2 overexpression in MDS-L and TF-1 cells decreased their sensitivity to azacitidine. Finally, CCRL2 levels were higher in CD34+ cells from MDS and MDS/myeloproliferative neoplasm patients with poor response to DNMT inhibitors. In conclusion, we demonstrated that CCRL2 modulates epigenetic regulatory pathways, particularly DNMT levels, and affects the sensitivity of MDS/sAML cells to azacitidine. These results support CCRL2 targeting as having therapeutic potential in MDS/sAML.
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