ArticleCancer discovery2013
Mechanism-based epigenetic chemosensitization therapy of diffuse large B-cell lymphoma.
Article in Cancer discovery, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers.
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Who cites it
119 citing papers in PubMed.
- Multicenter phase 2 study of oral azacitidine (CC-486) plus CHOP as initial treatment for PTCL.Blood · 2023Trial
- Decitabine combined with RDHAP regimen in relapsed/refractory diffuse large B cell lymphoma.Cancer medicine · 2023Trial
- SWOG 1918: A phase II/III randomized study of R-miniCHOP with or without oral azacitidine (CC-486) in participants age 75 years or older with newly diagnosed aggressive non-Hodgkin lymphomas - Aiming to improve therapy, outcomes, and validate a prospective frailty tool.Journal of geriatric oncology · 2022Trial
- A pilot clinical trial of oral tetrahydrouridine/decitabine for noncytotoxic epigenetic therapy of chemoresistant lymphoid malignancies.Seminars in hematology · 2021Trial
- Epigenetic priming with azacitidine-BEAM versus decitabine-BEAM conditioning for autologous transplantation in non-Hodgkin's lymphoma.Bone marrow transplantation · 2026Article
- Phase I study of oral azacitidine plus salvage chemotherapy in relapsed/refractory diffuse large B-cell lymphoma.Annals of hematology · 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
- DNA methyltransferase inhibitors in oncology: clinical progress, limitations and future directions.Epigenomics · 2026Review
- Mechanisms of chemoresistance in diffuse large B‑cell lymphoma and novel therapeutic strategies (Review).International journal of oncology · 2026Review
- miR-155 aberrant expression impairs tumor rejection because of its targeting of ICOSL and multiple pathways implicated in the antitumor response.Pharmacological reviews · 2026Review
- Ferroptosis-related gene analysis revealing novel biomarkers and therapeutic targets in diffuse large B-cell lymphoma.Scientific reports · 2025Article
- Orally available decitabine prodrug OR-2100 induces mitotic perturbation for the treatment of double-hit lymphoma.Blood neoplasia · 2025Article
- Unraveling the Epigenetic Landscape of Mature B Cell Neoplasia: Mechanisms, Biomarkers, and Therapeutic Opportunities.International journal of molecular sciences · 2025Review
- Review
- Targeting EP300 in diffuse large b-cell lymphoma: efficacy of A485 and synergistic effects with XPO1 inhibition.BMC cancer · 2025Article
- Polycomb repressive complex 2 (PRC2) pathway's role in cancer cell plasticity and drug resistance.Functional & integrative genomics · 2025Review
- Prognostic genes related to mitochondrial dynamics and mitophagy in diffuse large B-cell lymphoma are identified and validated using an integrated analysis of bulk and single-cell RNA sequencing.Frontiers in immunology · 2025Article
- Influence of the gut microbiome on lymphoma treatment: current evidence and future therapeutic directions.Therapeutic advances in medical oncology · 2025Review
- Cancer epigenetic therapy: recent advances, challenges, and emerging opportunities.Epigenomics · 2025Review
59 more citing papers are in PubMed but not listed here.
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22 authors.
Funding
Abstract
unlabelledAlthough aberrant DNA methylation patterning is a hallmark of cancer, the relevance of targeting DNA methyltransferases (DNMT) remains unclear for most tumors. In diffuse large B-cell lymphoma (DLBCL) we observed that chemoresistance is associated with aberrant DNA methylation programming. Prolonged exposure to low-dose DNMT inhibitors (DNMTI) reprogrammed chemoresistant cells to become doxorubicin sensitive without major toxicity in vivo. Nine genes were recurrently hypermethylated in chemoresistant DLBCL. Of these, SMAD1 was a critical contributor, and reactivation was required for chemosensitization. A phase I clinical study was conducted evaluating azacitidine priming followed by standard chemoimmunotherapy in high-risk patients newly diagnosed with DLBCL. The combination was well tolerated and yielded a high rate of complete remission. Pre- and post-azacitidine treatment biopsies confirmed SMAD1 demethylation and chemosensitization, delineating a personalized strategy for the clinical use of DNMTIs. SIGNIFICANCE: The problem of chemoresistant DLBCL remains the most urgent challenge in the clinical management of patients with this disease. We describe a mechanism-based approach toward the rational translation of DNMTIs for the treatment of high-risk DLBCL.
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