ArticleCancer cell2024
IRF4 requires ARID1A to establish plasma cell identity in multiple myeloma.
Article in Cancer cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Integrated Genomic and Epigenomic Analysis Reveals Epigenetic Plasticity in Disease Progression and Multidrug Resistance in Multiple Myeloma.Cancer research · 2026Article
- CRISPR application in hematological disorders: from bench to bedside.Blood advances · 2026Review
- Decoding immunotherapy resistance in multiple myeloma: genetic insights and approaches to counter resistance.Science China. Life sciences · 2026Review
- Multiple myeloma: A tale of deregulated transcription factors.HemaSphere · 2026Review
- IRF2 is an essential transcription factor with pathogenic and prognostic impact in multiple myeloma.Blood · 2026Article
- Targeting PRKCN, an Essential Driver Orchestrating mTOR-IRF4 Axis Independently of Kinase Activity, in Multiple Myeloma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Spatial proteomics in precision medicine: technologies, bioinformatics, and translational applications.Precision clinical medicine · 2026Review
- Catalytic Inhibition of p300 Preferentially Targets IRF4 Oncogenic Activity and Tumor Growth in Multiple Myeloma.Cancer research · 2026Article
- Synergistic targeting of the ARID2-MYC axis by pomalidomide and panobinostat overcomes intrinsic IMiD resistance in multiple myeloma.Scientific reports · 2026Article
- Epigenetic reprogramming in multiple myeloma-Challenges and opportunities.International journal of cancer · 2026Review
- ID2 Suppresses Multiple Myeloma Cell Proliferation by Repressing the Activity of the Transcription Factor TCF3.Blood cancer discovery · 2026Article
- Phosphorylation Protects Oncogenic RAS from LZTR1-Mediated Degradation.bioRxiv : the preprint server for biology · 2026Article
- A bortezomib resistance-related gene signature predicts prognosis, with ARID5B downregulation associated with poor overall survival in multiple myeloma.Discover oncology · 2026Article
- Co-condensation between transcription factor and cBAF selectively modulates chromatin remodeling and gene expression.Nature communications · 2025Article
- Spatially-resolved Photoproximity Profiling of MYC Identifies a MYC-BAF Liability in Cancer Cells.bioRxiv : the preprint server for biology · 2025Article
- Targeting ARID1A: the key to dominating the differentiation fate of germinal center B cells.Science China. Life sciences · 2025Article
- Targeting of IRAK4 and GSPT1 enhances therapeutic efficacy in AML via c-Myc destabilization.Leukemia · 2025Article
- Extramedullary myeloma is genomically complex and characterized by near-universal MAPK pathway alterations.Blood advances · 2025Article
- Loss of BCL7A permits IRF4 transcriptional activity and cellular growth in multiple myeloma.Blood · 2025Article
- Enhancer Extrachromosomal Circular DNA ANKRD28 Elicits Drug Resistance via POU2F2-Mediated Transcriptional Network in Multiple Myeloma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
21 authors.
Funding
Abstract
Multiple myeloma (MM) is an incurable plasma cell malignancy that exploits transcriptional networks driven by IRF4. We employ a multi-omics approach to discover IRF4 vulnerabilities, integrating functional genomics screening, spatial proteomics, and global chromatin mapping. ARID1A, a member of the SWI/SNF chromatin remodeling complex, is required for IRF4 expression and functionally associates with IRF4 protein on chromatin. Deleting Arid1a in activated murine B cells disrupts IRF4-dependent transcriptional networks and blocks plasma cell differentiation. Targeting SWI/SNF activity leads to rapid loss of IRF4-target gene expression and quenches global amplification of oncogenic gene expression by MYC, resulting in profound toxicity to MM cells. Notably, MM patients with aggressive disease bear the signature of SWI/SNF activity, and SMARCA2/4 inhibitors remain effective in immunomodulatory drug (IMiD)-resistant MM cells. Moreover, combinations of SWI/SNF and MEK inhibitors demonstrate synergistic toxicity to MM cells, providing a promising strategy for relapsed/refractory disease.
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