ArticleHaematologica2024
Hypomethylating agent decitabine sensitizes diffuse large B-cell lymphoma to venetoclax.
Article in Haematologica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Inhibition of PRMT5 sensitizes B-cell non-Hodgkin lymphoma cells to both intrinsic and extrinsic apoptotic cell death.Blood neoplasia · 2026Article
- A53-Adapted Decitabine-Containing R-CHOP in Newly Diagnosed Diffuse Large B-Cell Lymphoma Defined by LymphGen: Preliminary Results of a Prospective Proof-of-Concept Study.Journal of clinical medicine · 2026Article
- Enhanced efficacy of a specific HDAC3 inhibitor in combination with 5-azacitidine against diffuse large B-cell lymphoma.Blood neoplasia · 2026Article
- Targeting signaling pathways in lymphoma: From molecular mechanisms to clinical breakthroughs.Chinese medical journal · 2026Review
- Venetoclax combined with chidamide and decitabine successfully induced remission in relapsed/refractory classical Hodgkin lymphoma: a case report and literature review.Frontiers in immunology · 2026Review
- T Cells Spatially Regulate B Cell Receptor Signaling in Lymphomas through H3K9me3 Modifications.Advanced healthcare materials · 2025Article
- Development of a robust BH3 drug toolkit for precision medicine in hematologic malignancies.Theranostics · 2025Article
- Macrophage Membrane-Coated Liposomes Delivering Vonoprazan Disrupt Mitochondrial Oxidative Phosphorylation in Diffuse Large B-Cell Lymphoma.International journal of nanomedicine · 2025Article
- Review
- Tumor Biology Hides Novel Therapeutic Approaches to Diffuse Large B-Cell Lymphoma: A Narrative Review.International journal of molecular sciences · 2024Review
- Editorial: Genetic/epigenetic mechanisms and related clinical strategy in leukemia.Frontiers in oncology · 2023Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Despite recent advances in the therapy of diffuse large B-cell lymphoma (DLBCL), many patients are still not cured. Therefore, new therapeutic strategies are needed. The anti-apoptotic B-cell lymphoma 2 (BCL2) gene is commonly dysregulated in DLBCL due to various mechanisms such as chromosomal translocation t(14;18)(q32;q21) and copy number alterations; however, targeting BCL-2 with the selective inhibitor, venetoclax, led to response in only a minority of patients. Thus, we sought to identify a rational combination partner of venetoclax to improve its activity against DLBCL cells. Utilizing a functional assay, dynamic BH3 profiling, we found that the DNA hypomethylating agent decitabine increased mitochondrial apoptotic priming and BCL-2 dependence in DLBCL cells. RNA-sequencing analysis revealed that decitabine suppressed the pro-survival PI3K-AKT pathway and altered the mitochondria membrane composition in DLBCL cell lines. Additionally, it induced a DNA damage response and increased BAX and BAK activities. The combination of decitabine and venetoclax synergistically suppressed proliferation of DLBCL cells both in vitro and in vivo in a DLBCL cell line-derived xenograft mouse model. Our study suggests that decitabine plus venetoclax is a promising combination to explore clinically in DLBCL.
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Registered trials
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