ArticleOncotarget2015
c-myc copy number gain is a powerful prognosticator of disease outcome in cervical dysplasia.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 26 citations in OpenAlex.
- Trial
- Whole-Genome Methylation Sequencing Analysis and Functional Verification of LIM-Homeobox Family Genes in Cervical Cancer.International journal of general medicine · 2025Article
- Correlations between C-myc expression, BMI-1 expression, and vaginal microecology with HPV-DNA load in patients with different cervical lesions.American journal of translational research · 2024Article
- Human Papillomavirus 16 E2 Interaction with TopBP1 Is Required for E2 and Viral Genome Stability during the Viral Life Cycle.Journal of virology · 2023Article
- The complexity of human papilloma virus in cancers: a narrative review.Infectious agents and cancer · 2023Review
- Identification of human MHC-I HPV18 E6/E7-specific CD8 + T cell epitopes and generation of an HPV18 E6/E7-expressing adenosquamous carcinoma in HLA-A2 transgenic mice.Journal of biomedical science · 2022Article
- Do or Die: HPV E5, E6 and E7 in Cell Death Evasion.Pathogens (Basel, Switzerland) · 2022Review
- Development of a Novel Mouse Model of Spontaneous High-Risk HPVE6/E7-Expressing Carcinoma in the Cervicovaginal Tract.Cancer research · 2021Article
- Effect ofTranslational cancer research · 2021Article
- Loop-Mediated Isothermal Amplification Assay for Detecting Tumor Markers and Human Papillomavirus: Accuracy and Supplemental Diagnostic Value to Endovaginal MRI in Cervical Cancer.Frontiers in oncology · 2021Article
- Tracing MYC Expression for Small Molecule Discovery.Cell chemical biology · 2019Article
- Genomic amplification of HPV, h-TERC and c-MYC in liquid-based cytological specimens for screening of cervical intraepithelial neoplasia and cancer.Oncology letters · 2019Article
- The transcriptome of human mammary epithelial cells infected with the HCMV-DB strain displays oncogenic traits.Scientific reports · 2018Article
- Article
- Small molecule selectively suppresses MYC transcription in cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Article
- Article
- Genetic association study identifies a functional CNV in the WWOX gene contributes to the risk of intracranial aneurysms.Oncotarget · 2016Article
- Increasing diagnostic accuracy to grade dysplasia in Barrett's esophagus using an immunohistochemical panel for CDX2, p120ctn, c-Myc and Jagged1.Diagnostic pathology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cervical carcinoma develops from preneoplasia by a multistep process. Although most low-grade dysplastic lesions will regress without intervention and even high-grade changes exhibit a substantial rate of regression, a small percentage of dysplasia will progress over time. Thus, indicators are needed to estimate the biological risk and to help avoid overtreatment in women who desire to preserve fertility. In addition to the classical biomarkers, PCR-ELISA-determined HPV genotype and immunohistochemically assessed p16INK4a and Ki-67 expression, cells with integrated HPV and copy number gain of TERC and c-myc were quantified in a panel of 104 benign, intraepithelial neoplastic (CIN I, II, III) and cancerous lesions using fluorescence in situ hybridization. Optimal cut-off values were calculated; Kaplan-Meier curves and a Cox proportional hazard regression model were used to evaluate prognostic signatures. The assay reliably identified HPV integration, TERC and c-myc copy number gain as determined by comparisons with established biomarkers. All biomarker levels increased with the progression of the disease. However, only c-myc copy number gain independently prognosticated a low probability of dysplastic regression. Our results suggest that c-myc plays a key role in the process of dysplastic transformation and might thus be exploited for treatment and follow-up decision-making of cervical dysplasia.
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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.