ArticleEBioMedicine2016
Epstein-Barr Virus Infection of Mammary Epithelial Cells Promotes Malignant Transformation.
Article in EBioMedicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
46 citing papers in PubMed, 80 citations in OpenAlex.
- EBV hijacks the metabolic function of CD73 to resist the antitumor function of NK cells.NPJ precision oncology · 2026Article
- Antitumor Activities of Chimeric Anti-EphA2 Antibodies in Xenograft Models of Breast, Pancreatic, and Colorectal Cancers.International journal of molecular sciences · 2026Article
- Transient adenovirus-Cre infection causes long-lasting remodeling of the mammary gland immune landscape.Scientific reports · 2026Article
- Transient adenovirus-Cre infection causes long-lasting remodeling of the mammary gland immune landscape.Research square · 2026Article
- Differential Expression of Epstein-Barr Virus Sequences in Various Breast Cancer Subtypes.Genes · 2025Article
- Article
- The viral origins of breast cancer.Infectious agents and cancer · 2024Review
- Association of Human Papilloma Virus, Cytomegalovirus, and Epstein-Barr Virus with Breast Cancer in Jordanian Women.Medicina (Kaunas, Lithuania) · 2024Article
- Evodiamine suppresses endometriosis development induced by early EBV exposure through inhibition of ERβ.Frontiers in pharmacology · 2024Article
- Role of Epstein-Barr Virus in Breast Cancer: Correlation with Clinical Outcome and Survival Analysis.Journal of Cancer · 2024Article
- Tumor resident, TRA anti-viral CDR3 chemical sequence motifs are associated with a better breast cancer outcome.Genes and immunity · 2023Article
- Epstein-Barr Viral Infection and the Risk for Breast Cancer: A Systematic Review.International journal of hematology-oncology and stem cell research · 2023Review
- Epstein-Barr Virus (EBV) Epithelial Associated Malignancies: Exploring Pathologies and Current Treatments.International journal of molecular sciences · 2022Review
- Association of PD-1/PD-L1 expression and Epstein--Barr virus infection in patients with invasive breast cancer.Diagnostic pathology · 2022Article
- Review
- High-throughput and multi-phases identification of autoantibodies in diagnosing early-stage breast cancer and subtypes.Cancer science · 2022Article
- The Role of Epstein-Barr Virus in Modulating Key Tumor Suppressor Genes in Associated Malignancies: Epigenetics, Transcriptional, and Post-Translational Modifications.Biomolecules · 2022Review
- Interrelated Oncogenic Viruses and Breast Cancer.Frontiers in molecular biosciences · 2022Review
- Review
- Interplay between Epstein-Barr virus infection and environmental xenobiotic exposure in cancer.Infectious agents and cancer · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 10 institutions in 3 countries.
Funding
Abstract
Whether the human tumor virus, Epstein-Barr Virus (EBV), promotes breast cancer remains controversial and a potential mechanism has remained elusive. Here we show that EBV can infect primary mammary epithelial cells (MECs) that express the receptor CD21. EBV infection leads to the expansion of early MEC progenitor cells with a stem cell phenotype, activates MET signaling and enforces a differentiation block. When MECs were implanted as xenografts, EBV infection cooperated with activated Ras and accelerated the formation of breast cancer. Infection in EBV-related tumors was of a latency type II pattern, similar to nasopharyngeal carcinoma (NPC). A human gene expression signature for MECs infected with EBV, termed EBVness, was associated with high grade, estrogen-receptor-negative status, p53 mutation and poor survival. In 11/33 EBVness-positive tumors, EBV-DNA was detected by fluorescent in situ hybridization for the viral LMP1 and BXLF2 genes. In an analysis of the TCGA breast cancer data EBVness correlated with the presence of the APOBEC mutational signature. We conclude that a contribution of EBV to breast cancer etiology is plausible, through a mechanism in which EBV infection predisposes mammary epithelial cells to malignant transformation, but is no longer required once malignant transformation has occurred.
Indexed as
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What OpenQuestion holds
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.