ArticleNature2012
Burkitt lymphoma pathogenesis and therapeutic targets from structural and functional genomics.
Article in Nature, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 488 papers, 3 of them syntheses that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
488 citing papers in PubMed, 3 syntheses or guidelines pooled it, 909 citations in OpenAlex.
- A genetic profiling guideline to support diagnosis and clinical management of lymphomas.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Guideline
- RNA-seq research landscape in Africa: systematic review reveals disparities and opportunities.European journal of medical research · 2023Pooled it
- Adverse events in lymphoma patients treated with phosphoinositide 3 kinase Inhibitor in clinical trials: a meta-analysis.Annals of hematology · 2022Pooled it
- Combination Targeted Therapy in Relapsed Diffuse Large B-Cell Lymphoma.The New England journal of medicine · 2024Trial
- Genomic architecture of IRF4 rearrangements in childhood and adult large B-cell lymphomas.Blood advances · 2026Article
- Burkitt lymphoma: current understanding, unmet needs, and research directions.Blood advances · 2026Review
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- Stage-Specific Degradation of Cyclin D3 Orchestrates Myelopoiesis and Restrains Myeloproliferative Neoplasm Development.Cancer research · 2026Article
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- The B-cell Receptor Blueprint in Lymphoma: Mechanisms and Therapeutic Opportunities.Blood cancer discovery · 2026Review
- Aberrant glycosylation in hematologic malignancies: mechanisms, immune evasion, and therapeutic targeting.Blood cancer journal · 2026Review
- Targeted panel sequencing for refining B-cell lymphoma diagnosis: a real-life, reference center experience.Virchows Archiv : an international journal of pathology · 2026Article
- Stabilization of cyclin D3 protein by CDKN1A (p21Cell communication and signaling : CCS · 2026Article
- Burkitt Lymphoma-A Guide to Biological Features, Diagnosis and Differential Diagnosis.Cancers · 2026Review
- miRNA profiling in pediatric and young adult Burkitt leukemia and lymphoma.Virchows Archiv : an international journal of pathology · 2026Article
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- Routine Histopreparations After Tonsillectomy, Tonsillotomy, Adenotomy or Conchotomy: A Necessary Diagnosis in Times of Dwindling Resources?Journal of clinical medicine · 2026Article
- ID2 Suppresses Multiple Myeloma Cell Proliferation by Repressing the Activity of the Transcription Factor TCF3.Blood cancer discovery · 2026Article
428 more citing papers are in PubMed but not listed here.
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Authors and funding
42 authors at 20 institutions in 8 countries.
Funding
Abstract
Burkitt's lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. The normal germinal centre B cell is the presumed cell of origin for both BL and diffuse large B-cell lymphoma (DLBCL), yet gene expression analysis suggests that these malignancies may use different oncogenic pathways. BL is subdivided into a sporadic subtype that is diagnosed in developed countries, the Epstein-Barr-virus-associated endemic subtype, and an HIV-associated subtype, but it is unclear whether these subtypes use similar or divergent oncogenic mechanisms. Here we used high-throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways in BL that cooperate with MYC, the defining oncogene of this cancer. In 70% of sporadic BL cases, mutations affecting the transcription factor TCF3 (E2A) or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival phosphatidylinositol-3-OH kinase pathway in BL, in part by augmenting tonic B-cell receptor signalling. In 38% of sporadic BL cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. These findings suggest opportunities to improve therapy for patients with BL.
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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.