ArticleCell2017
HPV16 E7 Genetic Conservation Is Critical to Carcinogenesis.
Article in Cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 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
165 citing papers in PubMed.
- Human papillomavirus and the landscape of secondary genetic alterations in oral cancers.Genome research · 2019Trial
- Article
- Improving cervical screening risk stratification through extended human papillomavirus genotyping and age-specific data.European journal of public health · 2026Article
- Longitudinal analysis of high-risk HPV infections reveals within-host viral genome changes over time.PLoS pathogens · 2026Article
- Genetic Variation of HPV53 and the Identification of T-Cell Epitopes.Microorganisms · 2026Article
- Covalent inhibitors of human papillomavirus type 16 E6 protein restore p53 function and suppress growth of HPV-driven tumors in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- HPV16 genetic variation provides evidence of positive natural selection driven by HLA class I.Nature communications · 2026Article
- Genetic Variability and Conserved T-Cell Epitope Prediction of the HPV16 E1 Protein in Cervix Samples from Peru.Pathogens (Basel, Switzerland) · 2026Article
- Characterization of patient-derived HPV16 E6 and E7 variant alleles.Journal of virology · 2026Article
- Human papillomavirus16 E7 enhances cell stemness by regulating the APC2/SPIN4/β-catenin axis in cervical cancer.Oncogenesis · 2026Article
- Long-term human papillomavirus genotype-specific risk of cervical high-grade intraepithelial lesion and cancer-By age group and triage cytology.International journal of cancer · 2026Article
- A phase 1 trial of HPV16 E7 T-cell receptor-engineered T cells in patients with relapsed/refractory HPV16-positive cancers (KITE-439 trial).Frontiers in oncology · 2026Article
- AI-driven radiogenomics in gynecologic oncology: from radiological digital biopsy to a new paradigm in precision therapy.Frontiers in oncology · 2026Review
- Phenotypic effect of the mutations H78Y and L83V in the E6 protein of human papillomavirus.Archives of virology · 2025Article
- HPV16 E6 and E7 Genetic Variability in Oral and Anal Samples from HIV-Positive MSM.Pathogens (Basel, Switzerland) · 2025Article
- Albumin-recruiting lipid nanoparticle potentiates the safety and efficacy of mRNA vaccines by avoiding liver accumulation.Nature materials · 2025Article
- The actin nucleation promoting factor WASH facilitates clathrin-independent endocytosis of human papillomaviruses.EMBO reports · 2025Article
- Whole-genome sequencing of 1,083 HPV45 cases and controls identifies genetic variants associated with glandular cervical lesions.International journal of cancer · 2025Article
- HPV-driven cancers: a looming threat and the potential of CRISPR/Cas9 for targeted therapy.Virology journal · 2025Review
105 more citing papers are in PubMed but not listed here.
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Authors and funding
32 authors.
Funding
Abstract
Although most cervical human papillomavirus type 16 (HPV16) infections become undetectable within 1-2 years, persistent HPV16 causes half of all cervical cancers. We used a novel HPV whole-genome sequencing technique to evaluate an exceptionally large collection of 5,570 HPV16-infected case-control samples to determine whether viral genetic variation influences risk of cervical precancer and cancer. We observed thousands of unique HPV16 genomes; very few women shared the identical HPV16 sequence, which should stimulate a careful re-evaluation of the clinical implications of HPV mutation rates, transmission, clearance, and persistence. In case-control analyses, HPV16 in the controls had significantly more amino acid changing variants throughout the genome. Strikingly, E7 was devoid of variants in precancers/cancers compared to higher levels in the controls; we confirmed this in cancers from around the world. Strict conservation of the 98 amino acids of E7, which disrupts Rb function, is critical for HPV16 carcinogenesis, presenting a highly specific target for etiologic and therapeutic research.
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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.