ArticleCancers2022
Epigenetic Alteration of the Cancer-Related Gene TGFBI in B Cells Infected with Epstein-Barr Virus and Exposed to Aflatoxin B1: Potential Role in Burkitt Lymphoma Development.
Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Mechanistic interactions between Plasmodium falciparum and Epstein-Barr virus in endemic Burkitt Lymphoma pathogenesis: a narrative review (2010-2026).Infectious agents and cancer · 2026Review
- TGFBI in tumors and the tumor immune microenvironment: functional roles, mechanisms, and therapeutic targeting.Frontiers in immunology · 2026Review
- Aflatoxin B1 induces subtle but coordinated histone modifications in Epstein-Barr virus infected and non-infected Burkitt lymphoma cells.Environment international · 2025Article
- DNA Methylation Epitypes of Burkitt Lymphoma with Distinct Molecular and Clinical Features.Blood cancer discovery · 2025Article
- S100P is a core gene for diagnosing and predicting the prognosis of sepsis.Scientific reports · 2025Article
- TGFBI regulates the TGF-β pathway to affect the malignant progression and cisplatin sensitivity in diffuse large B-cell lymphoma.Annals of hematology · 2025Article
- Global, regional, and national epidemiology of childhood Burkitt Lymphoma from 1990 to 2021: statistical analysis of incidence, mortality, and DALYs.Frontiers in public health · 2025Article
- The Functional Interaction Between Epstein-Barr Virus and MYC in the Pathogenesis of Burkitt Lymphoma.Cancers · 2024Review
- Aflatoxin B1 and Epstein-Barr virus-induced CCL22 expression stimulates B cell infection.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Comparison of genomic alterations in Epstein-Barr virus-positive and Epstein-Barr virus-negative diffuse large B-cell lymphoma.Cancer medicine · 2024Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 3 countries.
Funding
Abstract
Burkitt lymphoma (BL) is a malignant B cell neoplasm that accounts for almost half of pediatric cancers in sub-Saharan African countries. Although the BL endemic prevalence is attributable to the combination of Epstein-Barr virus (EBV) infection with malaria and environmental carcinogens exposure, such as the food contaminant aflatoxin B1 (AFB1), the molecular determinants underlying the pathogenesis are not fully understood. Consistent with the role of epigenetic mechanisms at the interface between the genome and environment, AFB1 and EBV impact the methylome of respectively leukocytes and B cells specifically. Here, we conducted a thorough investigation of common epigenomic changes following EBV or AFB1 exposure in B cells. Genome-wide DNA methylation profiling identified an EBV-AFB1 common signature within the TGFBI locus, which encodes for a putative tumor suppressor often altered in cancer. Subsequent mechanistic analyses confirmed a DNA-methylation-dependent transcriptional silencing of TGFBI involving the recruitment of DNMT1 methyltransferase that is associated with an activation of the NF-κB pathway. Our results reveal a potential common mechanism of B cell transformation shared by the main risk factors of endemic BL (EBV and AFB1), suggesting a key determinant of disease that could allow the development of more efficient targeted therapeutic strategies.
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