ReviewCold Spring Harbor perspectives in medicine2014
Oncogenic mechanisms in Burkitt lymphoma.
Review in Cold Spring Harbor perspectives in medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 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
139 citing papers in PubMed, 243 citations in OpenAlex.
- Article
- Diffuse Large B-Cell Lymphoma: From Molecular Stratification to Precision Immunotherapy.Cells · 2026Review
- Single-cell whole-genome sequencing reveals convergent evolution in Burkitt lymphoma.Nature communications · 2026Article
- Article
- Is liquid biopsy a cost-effective method to diagnose Burkitt Lymphoma in children and young adults? A health economic evaluation in Tanzania.BMC medicine · 2026Article
- Burkitt Lymphoma-A Guide to Biological Features, Diagnosis and Differential Diagnosis.Cancers · 2026Review
- B-cell receptor signaling and microenvironment crosstalk in mantle cell lymphoma.Cell communication and signaling : CCS · 2025Review
- Discriminating activating, deactivating and resistance variants in protein kinases.Genome medicine · 2025Article
- Model Systems of Gammaherpesvirus Infection, Immunity, and Disease.Journal of medical virology · 2025Review
- PARP1 Inhibition Halts EBV+ Lymphoma Progression by Disrupting the EBNA2/MYC Axis.Journal of medical virology · 2025Article
- DNA Methylation Epitypes of Burkitt Lymphoma with Distinct Molecular and Clinical Features.Blood cancer discovery · 2025Article
- Genomic mutation profile and metabolic alterations in diffuse large B-cell lymphoma with abdominal bulky mass.Annals of hematology · 2025Article
- Potential diagnostic and prognostic biomarkers of pediatric Burkitt lymphoma identified through miRNA expression profiling.Pediatric research · 2025Article
- Phosphatidylinositol 3-Kinase Inhibition and Allogeneic Stem Cell Transplantation Can Overcome Chemotherapy Resistance in Refractory Burkitt Lymphoma.Journal of hematology · 2025Article
- Autologous Paracrine Prostasin-Matriptase Serine Protease Interaction in Lymphoid Cancer Cells.Cells · 2025Article
- Phosphoproteomic Analysis of Signaling Pathways in Lymphomas.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Single-cell transcriptomics of pediatric Burkitt lymphoma reveals intra-tumor heterogeneity and markers of therapy resistance.Leukemia · 2025Article
- Quantitative modeling of signaling in aggressive B cell lymphoma unveils conserved core network.PLoS computational biology · 2024Article
- Immune evasion: An imperative and consequence of MYC deregulation.Molecular oncology · 2024Review
- Molecular targets of glucocorticoids that elucidate their therapeutic efficacy in aggressive lymphomas.Cancer cell · 2024Article
79 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Burkitt lymphoma is a germinal center B-cell-derived cancer that was instrumental in the identification of MYC as an important human oncogene more than three decades ago. Recently, new genomics technologies have uncovered several additional oncogenic mechanisms that cooperate with MYC to create this highly aggressive cancer. The transcription factor TCF-3 is central to Burkitt lymphoma pathogenesis. TCF-3 is rendered constitutively active in Burkitt lymphoma by two related mechanisms: (1) somatic mutations that inactivate its negative regulator ID3, and (2) somatic mutations in TCF-3 that block the ability of ID3 to bind and interfere with its activity as a transcription factor. TCF-3 is also a master regulator of normal germinal center B-cell differentiation. Within the germinal center, TCF-3 up-regulates genes that are characteristically expressed in the rapidly dividing centroblasts, the putative cell of origin for Burkitt lymphoma, while repressing genes expressed in the less proliferative centrocytes. TCF-3 promotes antigen-independent (tonic) B-cell-receptor signaling in Burkitt lymphoma by transactivating immunoglobulin heavy- and light-chain genes while repressing PTPN6, which encodes the phosphatase SHP-1, a negative regulator of B-cell-receptor signaling. Tonic B-cell-receptor signaling sustains Burkitt lymphoma survival by engaging the PI3 kinase pathway. In addition, TCF-3 promotes cell-cycle progression by transactivating CCND3, encoding a D-type cyclin that regulates the G1-S phase transition. Additionally, CCND3 accumulates oncogenic mutations that stabilize cyclin D3 protein expression and drive proliferation. These new insights into Burkitt lymphoma pathogenesis suggest new therapeutic strategies, which are sorely needed in developing regions of the world where this cancer is endemic.
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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.