ReviewFrontiers in oncology2026
Integrative molecular diagnostics for HPV-driven cervical carcinogenesis: a translational review of mechanisms and multimodal risk stratification.
Review in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Vaginal Microecological Imbalance, Human Papillomavirus Infection, and Cervical Carcinogenesis: Mechanisms and Clinical Implications.International journal of general medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite effective prophylactic vaccines, high-risk human papillomavirus (HPV) infection remains a leading cause of cervical cancer, particularly in regions with limited screening access. Conventional methods, including cytology and HPV DNA testing, lack specificity for identifying lesions at high risk of progression, resulting in overtreatment. This narrative translational review synthesizes current evidence on integrating complementary molecular modalities to improve risk stratification along the biological continuum from HPV infection to malignancy. Persistent high-risk HPV drives carcinogenesis via viral oncoprotein activity, host DNA damage response (DDR) dysregulation, and epigenetic remodeling, yet no single biomarker captures this complexity. Quantitative PCR sensitively detects viral DNA load but not transforming activity; immunocytochemistry for p16INK4a/Ki-67 reflects oncogenic pathway disruption; gene expression and methylation profiling reveal downstream transcriptional changes; and emerging DDR assays (e.g., γH2AX) indicate upstream genomic stress. Multi-omics studies suggest progression risk is best inferred from co-occurring viral activity, host stress responses, and phenotypic dysregulation. A multimodal approach combining viral detection, protein-level transformation markers, and selected molecular signatures, provides a biologically grounded framework to distinguish transient infection from high-risk precancer. Literature was identified through targeted searches of PubMed, Scopus, and Web of Science, emphasizing peer-reviewed studies, meta-analyses, translational investigations, and clinically validated diagnostic platforms published in English. This review proposes a structured, integrative model for cervical cancer risk assessment, offering a tiered, context-appropriate strategy that correlates diagnostic modalities with stages of HPV-mediated transformation. This framework aims to enhance clinical precision, prioritize high-risk individuals, and reduce overtreatment.
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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.