ReviewMolecular cancer research : MCR2022
B-cell Lymphoma 6 (BCL6): From Master Regulator of Humoral Immunity to Oncogenic Driver in Pediatric Cancers.
Review in Molecular cancer research : MCR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
32 citing papers in PubMed, 54 citations in OpenAlex.
- Proteolysis Targeting Chimeric-Based Technology in Myeloma and Lymphoma.Molecular cancer therapeutics · 2026Review
- Surveying the Genomic Landscape of Mantle Cell Lymphoma Indicates the Importance of Multimodal Genomic and Transcriptomic Exploration.medRxiv : the preprint server for health sciences · 2026Article
- Beyond TLS Presence: A Functional Framework Integrating Maturity, Location, and Immune Context.Cancers · 2026Review
- Human body single-cell atlas of three-dimensional genome organization and DNA methylation.Science (New York, N.Y.) · 2026Article
- BCL6 regulates skeletal muscle mass and mitochondrial bioenergetics.Molecular metabolism · 2026Article
- Decoding the impact of nsSNP variants on BCL6 function through integrated computational analysis.Current research in structural biology · 2026Article
- A lipid nanoparticle-based peptide-proteolysis-targeting chimera degrades BCL6 for diffuse large B-cell lymphoma treatment.Discover oncology · 2026Article
- Evaluation of immunoglobulin A1/immunoglobulin A2 ratio and B cell lymphoma-6 in relation to apoptosis-associated speck-like protein in diabetic kidney disease patients.BMC immunology · 2026Article
- Splice-site mutations in POU2AF1 are associated with B-cell lymphomagenesis and therapeutic response.Scientific reports · 2026Article
- Conservation and diversity of genes expressed in the spines of the sea urchin.Genes & genomics · 2026Article
- An Update on Clinically Advanced PROTAC Degraders and Their Synthesis.Molecules (Basel, Switzerland) · 2025Review
- Rewiring the Fusion Oncoprotein EWSR1::FLI1 in Ewing Sarcoma with Bivalent Small Molecules.Journal of the American Chemical Society · 2025Article
- Selectively targeting BCL6 using a small-molecule inhibitor is a potential therapeutic strategy for glioblastoma.Genes & diseases · 2025Article
- Article
- Curcumin ameliorates hepatic steatosis and insulin resistance through the JNK2/FOXO1/Bcl6 axis and regulate the intestinal flora structure.Journal of physiology and biochemistry · 2025Article
- Article
- Unveiling vitamin C: A new hope in the treatment of diffuse large B‑cell lymphoma (Review).International journal of oncology · 2025Review
- Clinical characteristics and genetic analysis of a patient with diffuse pulmonary lymphangiomatosis: a case report and literature review.BMC pulmonary medicine · 2025Review
- PROTACs coupled with oligonucleotides to tackle the undruggable.Bioanalysis · 2025Review
- Chemoresistance in Pancreatic Cancer: The Role of Adipose-Derived Mesenchymal Stem Cells and Key Resistance Genes.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B-cell lymphoma 6 (BCL6) is a protooncogene in adult and pediatric cancers, first identified in diffuse large B-cell lymphoma (DLBCL) where it acts as a repressor of the tumor suppressor TP53, conferring survival, protection, and maintenance of lymphoma cells. BCL6 expression in normal B cells is fundamental in the regulation of humoral immunity, via initiation and maintenance of the germinal centers (GC). Its role in B cells during the production of high affinity immunoglobins (that recognize and bind specific antigens) is believed to underpin its function as an oncogene. BCL6 is known to drive the self-renewal capacity of leukemia-initiating cells (LIC), with high BCL6 expression in acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), and glioblastoma (GBM) associated with disease progression and treatment resistance. The mechanisms underpinning BCL6-driven therapy resistance are yet to be uncovered; however, high activity is considered to confer poor prognosis in the clinical setting. BCL6's key binding partner, BCL6 corepressor (BCOR), is frequently mutated in pediatric cancers and appears to act in concert with BCL6. Using publicly available data, here we show that BCL6 is ubiquitously overexpressed in pediatric brain tumors, inversely to BCOR, highlighting the potential for targeting BCL6 in these often lethal and untreatable cancers. In this review, we summarize what is known of BCL6 (role, effect, mechanisms) in pediatric cancers, highlighting the two sides of BCL6 function, humoral immunity, and tumorigenesis, as well as to review BCL6 inhibitors and highlight areas of opportunity to improve the outcomes of patients with pediatric cancer.
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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.