ArticleCancer research2009
E2F1 expression is deregulated and plays an oncogenic role in sporadic Burkitt's lymphoma.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- HNRNPU mutations redirect cell cycle control to E2F in MYC-driven lymphomas.Blood advances · 2026Article
- Glutathione overproduction mediates lymphoma initiating cells survival and has a sex-dependent effect on lymphomagenesis.Cell death & disease · 2024Article
- Aberrant Nuclear Translocation of E2F1 and Its Association in Cushing's Disease.Endocrinology · 2022Article
- Virus-Mediated Inhibition of Apoptosis in the Context of EBV-Associated Diseases: Molecular Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2022Review
- Quantifying the Landscape and Transition Paths for Proliferation-Quiescence Fate Decisions.Journal of clinical medicine · 2020Article
- CDCA7 finely tunes cytoskeleton dynamics to promote lymphoma migration and invasion.Haematologica · 2020Article
- Germinal Centre B Cell Functions and Lymphomagenesis: Circuits Involving MYC and MicroRNAs.Cells · 2019Review
- Phosphofructokinases Axis Controls Glucose-Dependent mTORC1 Activation Driven by E2F1.iScience · 2019Article
- Integrated analysis of 10 lymphoma datasets identifies E2F8 as a key regulator in Burkitt's lymphoma and mantle cell lymphoma.American journal of translational research · 2019Article
- CDCA7 is a critical mediator of lymphomagenesis that selectively regulates anchorage-independent growth.Haematologica · 2018Article
- MAZ induces MYB expression during the exit from quiescence via the E2F site in the MYB promoter.Nucleic acids research · 2017Article
- TGF-β induces growth suppression in multiple myeloma MM.1S cells via E2F1.Oncology letters · 2017Article
- Hepatitis B Virus X Protein Upregulates hELG1/ ATAD5 Expression through E2F1 in Hepatocellular Carcinoma.International journal of biological sciences · 2016Article
- V-ATPase: a master effector of E2F1-mediated lysosomal trafficking, mTORC1 activation and autophagy.Oncotarget · 2015Article
- E2F-1 overexpression inhibits human gastric cancer MGC-803 cell growth in vivo.World journal of gastroenterology · 2015Article
- Small compound bigelovin exerts inhibitory effects and triggers proteolysis of E2F1 in multiple myeloma cells.Cancer science · 2013Article
- E2F1-mediated DNA damage is implicated in 8-Cl-adenosine-induced chromosome missegregation and apoptosis in human lung cancer H1299 cells.Molecular and cellular biochemistry · 2013Article
- Largazole Arrests Cell Cycle at G1 Phase and Triggers Proteasomal Degradation of E2F1 in Lung Cancer Cells.ACS medicinal chemistry letters · 2013Article
- Impact of EBV essential nuclear protein EBNA-3C on B-cell proliferation and apoptosis.Future microbiology · 2013Review
- Functional variants at the miRNA binding sites of the E2F1 gene and its mRNA expression.Oncology letters · 2013Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Current treatments of sporadic Burkitt's lymphoma (sBL) are associated with severe toxicities. A better understanding of sBL formation would facilitate development of less toxic therapies. The etiology of sBL remains, however, largely unknown, C-MYC up-regulation being the only lesion known to occur in all sBL cases. Several studies examining the role of C-MYC in the pathogenesis of BL have concluded that C-MYC translocation is not the only critical event and that additional unidentified factors are expected to be involved in the formation of this tumor. We herein report that a gene distinct from C-MYC, E2F1, is involved in the formation of all or most sBL tumors. We found that E2F1 is highly expressed in Burkitt's lymphoma cell lines and sBL lymphoma specimens. Our data indicate that its elevated expression is not merely the consequence of the presence of more cycling cells in this tumor relative to other cell lines or to other neoplasias. In fact, we show that reduction of its expression in sBL cells inhibits tumor formation and decreases their proliferation rate. We also provide data suggesting that E2F1 collaborates with C-MYC in sBL formation. E2F1 expression down-regulation did not affect, however, the proliferation of human primary diploid fibroblasts. Because E2F1 is not needed for cell proliferation of normal cells, our results reveal E2F1 as a promising therapeutic target for sBL.
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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.