ArticleJournal of virology2004
Clonal selection for transcriptionally active viral oncogenes during progression to cancer.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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.
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Who cites it
56 citing papers in PubMed, 138 citations in OpenAlex.
- Molecular heterogeneity of HPV-associated cancers and strategies to overcome treatment resistance.Cancer heterogeneity and plasticity · 2026Article
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- HPV16 E6/E7-mediated regulation of PiwiL1 expression induces tumorigenesis in cervical cancer cells.Cellular oncology (Dordrecht, Netherlands) · 2024Article
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- The Hallmarks of Cervical Cancer: Molecular Mechanisms Induced by Human Papillomavirus.Biology · 2024Review
- Microbial Communities in Gynecological Cancers and Their Association with Tumor Somatic Variation.Cancers · 2023Article
- Cells with stem-like properties are associated with the development of HPV18-positive cervical cancer.Cancer science · 2023Article
- Viruses in colorectal cancer.Molecular oncology · 2022Review
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- Detection of HPV and Human Chromosome Sites by Dual-Color FluorescenceFrontiers in oncology · 2021Article
- Article
- Risk stratification of HPV 16 DNA methylation combined with E6 oncoprotein in cervical cancer screening: a 10-year prospective cohort study.Clinical epigenetics · 2020Article
- Vorinostat, a pan-HDAC inhibitor, abrogates productive HPV-18 DNA amplification.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- HPV integration hijacks and multimerizes a cellular enhancer to generate a viral-cellular super-enhancer that drives high viral oncogene expression.PLoS genetics · 2018Article
- The role of integration in oncogenic progression of HPV-associated cancers.PLoS pathogens · 2017Review
- Distinguishing potential bacteria-tumor associations from contamination in a secondary data analysis of public cancer genome sequence data.Microbiome · 2017Article
- Article
- Evidence of disrupted high-risk human papillomavirus DNA in morphologically normal cervices of older women.Scientific reports · 2016Article
- Human papillomaviruses: shared and distinct pathways for pathogenesis.Current opinion in virology · 2015Review
- Integration of the full-length HPV16 genome in cervical cancer and Caski and Siha cell lines and the possible ways of HPV integration.Virus genes · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Primary keratinocytes immortalized by human papillomaviruses (HPVs), along with HPV-induced cervical carcinoma cell lines, are excellent models for investigating neoplastic progression to cancer. By simultaneously visualizing viral DNA and nascent viral transcripts in interphase nuclei, we demonstrated for the first time a selection for a single dominant papillomavirus transcription center or domain (PVTD) independent of integrated viral DNA copy numbers or loci. The PVTD did not associate with several known subnuclear addresses but was almost always perinucleolar. Silent copies of the viral genome were activated by growth in the DNA methylation inhibitor 5-azacytidine. HPV-immortalized keratinocytes supertransduced with HPV oncogenes and selected for marker gene coexpression underwent crisis, and the surviving cells transcribed only the newly introduced genes. Thus, transcriptional selection in response to environmental changes is a dynamic process to achieve optimal gene expression for cell survival. This phenomenon may be critical in clonal selection during carcinogenesis. Examination of HPV-associated cancers supports this hypothesis.
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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.