ArticleOncogene2004
Telomere erosion and chromosomal instability in cells expressing the HPV oncogene 16E6.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 64 citations in OpenAlex.
- Advances in understanding the mechanisms of the human papillomavirus oncoproteins.Biochemical Society transactions · 2025Review
- Viral oncogenesis in cancer: from mechanisms to therapeutics.Signal transduction and targeted therapy · 2025Review
- Review
- The Causes and Consequences of DNA Damage and Chromosomal Instability Induced by Human Papillomavirus.Cancers · 2024Review
- Human Papillomavirus-Induced Chromosomal Instability and Aneuploidy in Squamous Cell Cancers.Viruses · 2024Review
- HPV16 E6 induces chromosomal instability due to polar chromosomes caused by E6AP-dependent degradation of the mitotic kinesin CENP-E.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Beta Human Papillomavirus 8 E6 Induces Micronucleus Formation and Promotes Chromothripsis.Journal of virology · 2022Article
- The Drivers, Mechanisms, and Consequences of Genome Instability in HPV-Driven Cancers.Cancers · 2022Review
- Association of Relative Telomere Length and Risk of High Human Papillomavirus Load in Cervical Epithelial Cells.Balkan journal of medical genetics : BJMG · 2021Article
- NFX1-123 is highly expressed in cervical cancer and increases growth and telomerase activity in HPV 16E6 expressing cells.Cancer letters · 2019Article
- Generation of Immortalised But Unstable Cells after hTERT Introduction in Telomere-Compromised and p53-Deficient vHMECs.International journal of molecular sciences · 2018Article
- Mechanisms of Oncogene-Induced Replication Stress: Jigsaw Falling into Place.Cancer discovery · 2018Review
- Telomeres: Implications for Cancer Development.International journal of molecular sciences · 2018Review
- Telomere Dynamics in Immune Senescence and Exhaustion Triggered by Chronic Viral Infection.Viruses · 2017Review
- Telomerase Induction in HPV Infection and Oncogenesis.Viruses · 2017Review
- Evolution of genetic instability in heterogeneous tumors.Journal of theoretical biology · 2016Article
- Human viruses and cancer.Viruses · 2014Review
- The Asian-American E6 variant protein of human papillomavirus 16 alone is sufficient to promote immortalization, transformation, and migration of primary human foreskin keratinocytes.Journal of virology · 2012Article
- Article
- Nucleotide deficiency promotes genomic instability in early stages of cancer development.Cell · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Progression to advanced-stage cervical carcinomas is characterized by a recurrent pattern of chromosomal rearrangements. Structural chromosome rearrangements are generated through the fusion of broken chromosome ends. These chromosome breaks may be induced by mutagenic agents such as ionizing radiation, or chromosome ends may be exposed through extensive telomere shortening. The human papilloma virus oncogene 16E6 induces telomerase activity in human keratinocytes, a model system for cervical tumor formation. The present study explores the relationship between 16E6 expression, telomerase activity, and chromosomal instability. We show that the frequency of anaphase bridges is dependent on the level of telomerase activity in 16E6/E7-expressing clones, and is the result of telomere shortening. High frequencies of anaphase bridges, associated with low telomerase activity, correlate with increased chromosome instability. Anaphase bridge formation is also associated with the presence of micronuclei, which are shown to contain unstable chromosomes frequently involved in rearrangements. As anaphase bridges are observed in both high and low telomerase 16E6/E7 clones, but not in hTERT-expressing control clones, expression of 16E6 in these immortalized clones is not sufficient to stabilize shortened telomeres completely. We suggest a model in which HPV-induced tumorigenesis may be dependent on persistent bridge-breakage-fusion cycles that allow for continued genomic rearrangements.
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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.