ArticlePloS one2026
Non-invasive host transcriptome and HPV oncogene expression map the molecular landscape of HPV-driven cervical lesions.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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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
2 citing papers in PubMed.
- Molecular insights and therapeutic innovations in low-risk human papillomavirus-associated cutaneous wart.Molecular biology reports · 2026Review
- Exploring the molecular basis ofBioinformatics advances · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cervical cancer remains a significant global health burden. Current screening methods are not yet capable of detecting molecular alterations preceding cytological abnormalities. In this study, we performed integrative transcriptomic profiling of 132 HPV-positive cervical Pap Smear specimens (NILM, ASCUS, LSIL, HSIL), combining HPV genotyping, and E6/E7 mRNA quantification to map molecular progression. Our analysis revealed stage-specific signatures: NILM displayed a "stealth infection" profile marked by upregulated protein synthesis and growth signaling (EGFR/ERBB2) alongside immune suppression. ASCUS presented a critical tipping point with introduction of early oncogenic drivers (CCND1, SHH), while LSIL prioritized viral productivity with suppressed antimicrobial defenses (MPO, DEFA1). HSIL was distinct from earlier stages and defined by cell cycle hyperactivation (CDK1, PLK1), replication licensing (MCMs), and epithelial dedifferentiation. Pathway crosstalk analysis demonstrated minimal overlap between HSIL and earlier stages (OC < 0.07), highlighting molecular discontinuity during malignant transformation. Additionally, E6/E7 mRNA Ct levels were significantly associated with lesion severity (X2 = 24.407, df = 9, p = 0.003), indicating higher viral mRNA expression are associated with more severe cytological abnormalities. These findings highlight the transformative potential of transcriptomic profiling in cervical cancer prevention, offering stage-specific biomarkers to refine risk stratification. By integrating transcriptomics profiling with current clinical testing, clinicians can distinguish transient infections from high-risks lesions likely to progress. This combined approach addresses the critical limitations of morphology and DNA-based methods, enabling more precise therapeutic interventions and reducing unnecessary overtreatment, and the risk of undertreatment or dismissal of high-risk cases.
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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.