ReviewJournal of virology2015
Human papillomavirus carcinogenesis: an identity crisis in the retinoblastoma tumor suppressor pathway.
Review in Journal of virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Loss of p53-DREAM-mediated repression of cell cycle genes as a driver of lymph node metastasis in head and neck cancer.Genome medicine · 2023Pooled it
- What If Trojan Horse Nanoparticles Could Change the Game for HPV Gene-Targeted Therapies?Journal of medical virology · 2026Review
- CDK4/6 inhibition mitigates chemotherapy-induced expansion of TP53-mutant clonal hematopoiesis.Nature genetics · 2026Article
- Review
- Review
- The Natural History of Cervical Cancer and the Case for MicroRNAs: Is Human Papillomavirus Infection the Whole Story?International journal of molecular sciences · 2024Review
- Review
- Human Papillomavirus Is Rare and Does Not Correlate with p16Medicina (Kaunas, Lithuania) · 2024Article
- Article
- CDK4/6 inhibition enhances SHP2 inhibitor efficacy and is dependent upon RB function in malignant peripheral nerve sheath tumors.Science advances · 2023Article
- Human papillomaviruses: Knowns, mysteries, and unchartered territories.Journal of medical virology · 2023Review
- For Better or Worse: Modulation of the Host DNA Damage Response by Human Papillomavirus.Annual review of virology · 2023Review
- Inferring early genetic progression in cancers with unobtainable premalignant disease.Nature cancer · 2023Article
- CDK4/6 inhibition enhances SHP2 inhibitor efficacy and is dependent upon restoration of RB function in malignant peripheral nerve sheath tumors.bioRxiv : the preprint server for biology · 2023Article
- Understanding the mechanisms of HPV-related carcinogenesis: Implications for cell cycle dynamics.Journal of theoretical biology · 2022Article
- HPV-associated oropharyngeal cancer: epidemiology, molecular biology and clinical management.Nature reviews. Clinical oncology · 2022Review
- DeepVISP: Deep Learning for Virus Site Integration Prediction and Motif Discovery.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- CDKN2A Deletion in Melanoma Excludes T Cell Infiltration by Repressing Chemokine Expression in a Cell Cycle-Dependent Manner.Frontiers in oncology · 2021Article
- Human papillomavirus, gene mutation and estrogen and progesterone receptors in breast cancer: a cross-sectional study.The Pan African medical journal · 2021Article
- The interesting relationship between APOBEC3 deoxycytidine deaminases and cancer: a long road ahead.Open biology · 2020Article
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 at 2 institutions in 1 country.
Funding
Abstract
Viruses are obligate intracellular parasites and need to reprogram host cells to establish long-term persistent infection and/or to produce viral progeny. Cellular changes initiated by the virus trigger cellular defense responses to cripple viral replication, and viruses have evolved countermeasures to neutralize them. Established models have suggested that human papillomaviruses target the retinoblastoma (RB1) and TP53 tumor suppressor networks to usurp cellular replication, which drives carcinogenesis. More recent studies, however, suggest that modulating the activity of the Polycomb family of transcriptional repressors and the resulting changes in epigenetic regulation are proximal steps in the rewiring of cellular signaling circuits. Consequently, RB1 inactivation evolved to tolerate the resulting cellular alterations. Therefore, epigenetic reprograming results in cellular "addictions" to pathways for survival. Inhibition of such a pathway could cause "synthetic lethality" in adapted cells while not markedly affecting normal cells and could prove to be an effective therapeutic approach.
Indexed as
Identifiers
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.