ReviewBritish journal of cancer2012
The DNA damage response in viral-induced cellular transformation.
Review in British journal of cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 43 citations in OpenAlex.
- Respiratory Models Reveal DNA Damage Response Modulation by Merkel Cell Polyomavirus.International journal of molecular sciences · 2026Article
- How human papillomavirus (HPV) targets DNA repair pathways for viral replication: from guardian to accomplice.Microbiology and molecular biology reviews : MMBR · 2025Review
- Kaposi's sarcoma herpesvirus exploits the DNA damage response to circularize its genome.Nucleic acids research · 2024Article
- Insights into the multifunctional roles of geminivirus-encoded proteins in pathogenesis.Archives of virology · 2022Review
- C4, the Pathogenic Determinant ofFrontiers in microbiology · 2020Article
- Marek's Disease Virus Disables the ATR-Chk1 Pathway by Activating STAT3.Journal of virology · 2019Article
- miR-18a reactivates the Epstein-Barr virus through defective DNA damage response and promotes genomic instability in EBV-associated lymphomas.BMC cancer · 2018Article
- Human papillomavirus type 16 E6 and E7 oncoproteins interact with the nuclear p53-binding protein 1 in an in vitro reconstructed 3D epithelium: new insights for the virus-induced DNA damage response.Virology journal · 2018Article
- Review
- Induction of DNA Damages upon Marek's Disease Virus Infection: Implication in Viral Replication and Pathogenesis.Journal of virology · 2017Article
- Core binding factor (CBF) is required for Epstein-Barr virus EBNA3 proteins to regulate target gene expression.Nucleic acids research · 2017Article
- Activation of DNA Damage Response Induced by the Kaposi's Sarcoma-Associated Herpes Virus.International journal of molecular sciences · 2016Review
- Simian virus 40 large T antigen induces IFN-stimulated genes through ATR kinase.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Epstein-Barr virus essential antigen EBNA3C attenuates H2AX expression.Journal of virology · 2014Article
- What's the damage? The impact of pathogens on pathways that maintain host genome integrity.Cell host & microbe · 2014Review
- Commentary on the regulation of viral proteins in autophagy process.BioMed research international · 2014Review
- Genomic Instability and Cancer.Journal of carcinogenesis & mutagenesis · 2014Article
- Dual expression of Epstein-Barr virus, latent membrane protein-1 and human papillomavirus-16 E6 transform primary mouse embryonic fibroblasts through NF-κB signaling.International journal of clinical and experimental pathology · 2014Article
- Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The DNA damage response (DDR) has emerged as a critical tumour suppressor pathway responding to cellular DNA replicative stress downstream of aberrant oncogene over-expression. Recent studies have now implicated the DDR as a sensor of oncogenic virus infection. In this review, we discuss the mechanisms by which tumour viruses activate and also suppress the host DDR. The mechanism of tumour virus induction of the DDR is intrinsically linked to the need for these viruses to promote an S-phase environment to replicate their nucleic acid during infection. However, inappropriate expression of viral oncoproteins can also activate the DDR through various mechanisms including replicative stress, direct interaction with DDR components and induction of reactive oxygen species. Given the growth-suppressive consequences of activating the DDR, tumour viruses have also evolved mechanisms to attenuate these pathways. Aberrant expression of viral oncoproteins may therefore promote tumourigenesis through increased somatic mutation and aneuploidy due to DDR inactivation. This review will focus on the interplay between oncogenic viruses and the DDR with respect to cellular checkpoint control and transformation.
Indexed as
Identifiers
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.