ArticleMolecular omics2023
Network modeling suggests HIV infection phenocopies PI3K-AKT pathway mutations to enhance HPV-associated cervical cancer.
Article in Molecular omics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Virus infections and cancers: from mechanisms to therapeutics.Molecular biomedicine · 2026Review
- Paracrine signals from HIV-1-infected immune cells reprogram cervical cancer pathways.iScience · 2026Article
- HIV-driven tumor ecosystem: from chronic immune dysfunction to cancer evolution.Frontiers in microbiology · 2026Review
- Integrative Analysis of Shared Pathogenic Genes and Potential Mechanisms inMediators of inflammation · 2025Article
- Causal associations between sexually transmitted infections, depression, and self-harm: a mendelian randomization and cross-sectional study.BMC infectious diseases · 2024Article
- Role of DDR1 in Regulating MMPs in External Root Resorption.International journal of molecular sciences · 2024Article
- Overexpression of CXCL17 increases migration and invasion of A549 lung adenocarcinoma cells.Frontiers in pharmacology · 2024Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 3 countries.
Funding
Abstract
Women coinfected with human immunodeficiency virus type 1 (HIV-1) and human papillomavirus (HPV) are six times as likely to develop invasive cervical carcinoma compared to those without HIV. Unlike other HIV-associated cancers, the risk of cervical cancer development does not change when HPV/HIV coinfected women begin antiretroviral therapy, suggesting HIV-associated immune suppression is not a key driver of cervical cancer development in coinfected women. Here, we investigated whether the persistent secretion of inflammatory factors in HIV-positive patients on antiretroviral therapy could enhance cancer signaling in HPV-infected cervical cells
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Registered trials
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