Evidence map›Paper›PMID 26077310›Full record

ArticleInternational forum of allergy & rhinology2015

Human papillomavirus infection and biomarkers in sinonasal inverted papillomas: clinical significance and molecular mechanisms.

Adam Scheel, Giant C Lin, Jonathan B McHugh, Christine M Komarck, Heather M Walline, Mark E Prince, Mark A Zacharek, Thomas E Carey

Abstract read
In one paragraph

Article in International forum of allergy & rhinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 5 pooled it
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 5 syntheses or guidelines pooled it.

  1. Pooled it
  2. Human Papilloma Virus Infection and Sinonasal Inverted Papilloma Recurrence: A Meta-Analysis.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2025
    Pooled it
  3. Pooled it
  4. Pooled it
  5. Malignant transformation of sinonasal inverted papilloma and related genetic alterations: a systematic review.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2017
    Pooled it
  6. Trial
  7. Review
  8. Article
  9. Article
  10. Etiology of sinonasal inverted papilloma: An update.Laryngoscope investigative otolaryngology · 2022
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Etiology of sinonasal inverted papilloma: A narrative review.World journal of otorhinolaryngology - head and neck surgery · 2017
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Adam ScheelDepartment of Otolaryngology, University of Michigan Health Systems, Ann Arbor, MI.
Giant C LinDepartment of Otolaryngology, University of Michigan Health Systems, Ann Arbor, MI.
Jonathan B McHughDepartment of Pathology, University of Michigan Health Systems, Ann Arbor, MI.
Christine M KomarckDepartment of Otolaryngology, University of Michigan Health Systems, Ann Arbor, MI.
Heather M WallineDepartment of Otolaryngology, University of Michigan Health Systems, Ann Arbor, MI.
Mark E PrinceDepartment of Otolaryngology, University of Michigan Health Systems, Ann Arbor, MI.
Mark A ZacharekDepartment of Otolaryngology, University of Michigan Health Systems, Ann Arbor, MI.
Thomas E CareyDepartment of Otolaryngology, University of Michigan Health Systems, Ann Arbor, MI.

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Scott Michael Schuetze · 1988 to 2026
$178.2M
Therapeutic Potential and Mechanism of Action of Potent Small Molecule InhibitorsP50CA097248 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NOR, JACQUES EDUARDO · 2002 to 2013
$25.3M
Scientific Synergy CoreP30DC005188 · NIDCD · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ALTSCHULER, RICHARD A · 2002 to 2016
$10.3M
Training Program in Tumor MicroenvironmentT32CA009676 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Maria G Castro, Analisa Virginia DiFeo · 1992 to 2026
$7.3M
Advanced Research Training in OtolaryngologyT32DC005356 · NIDCD · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CORFAS, GABRIEL · 2002 to 2021
$3.5M
Biomarkers to Guide Treatment and Improve Survival in Oral/Oropharyngeal CancerR01DE019126 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CAREY, THOMAS E. · 2009 to 2012
$1.4M
NCI NIH HHS CA009676NCI NIH HHS P30 CA046592NCI NIH HHS P30 CA46592NCI NIH HHS P50 CA097248NCI NIH HHS T32 CA009676NIDCD NIH HHS P30 DC005188NIDCD NIH HHS P30 DC05188NIDCD NIH HHS T32 DC005356NIDCR NIH HHS R01 DE019126
6 · The paper itself

Abstract

backgroundThe role of human papillomavirus (HPV) in sinonasal inverted papillomas (IPs) is controversial. Determining the prevalence of HPV infection and its impact on the molecular biology of these tumors is critical to characterizing its role in the pathogenesis of IPs.

methodsA total of 112 paraffin-embedded IPs from 90 patients were studied. A tissue microarray was constructed and stained for p16, p53, epidermal growth factor receptor (EGFR), and cyclin D1. HPV presence and types were determined using PGMY 09/11 primers and integration using HPV 11 detection of integrated papillomavirus sequences by ligation-mediated polymerase chain reaction (DIPS-PCR).

resultsHPV was detected in 11 of 90 (12%) patients. HPV 11 was found in 9 samples. HPV 6 and HPV 27 were found in 1 sample each. EGFR staining proportion was higher in HPV-positive IPs vs HPV-negative specimens (56.2% vs 23.6%; p = 0.009). Differences in p16, p53, and cyclin D1 staining were not significant. HPV-positive lesions tend to progress to malignancy (p = 0.064). Three samples were analyzed for integration. Viral integration was found in both malignant tumors but not in the precursor IP.

conclusionDegradation of p53 and p16/cyclin D1 dysregulation are not important mechanisms in low-risk HPV-related IP. The low prevalence of HPV in this series indicates it is not a main etiological factor for IPs; however, when present, low-risk HPV may contribute to the biology of IPs through an increase of EGFR expression and a predisposition for malignant progression by integration into the cellular genome.

Indexed as

Biomarkers, TumorCarcinoma, Squamous CellCyclin D1Cyclin-Dependent Kinase Inhibitor p16Disease ProgressionDNA, ViralErbB ReceptorsFemaleHuman papillomavirus 11HumansImmunohistochemistryMaleNeoplasm ProteinsNeoplasm Recurrence, LocalPapilloma, InvertedPapillomavirus InfectionsBiomarkers, TumorCCND1 protein, humanCDKN2A protein, humanCyclin D1Cyclin-Dependent Kinase Inhibitor p16DNA, ViralEGFR protein, humanErbB ReceptorsNeoplasm ProteinsTumor Suppressor Protein p53Cyclin D1DIPS-PCREGFRHPVintegrationinverted papillomap16p53

Identifiers

PMID26077310
PMCPMC4526407

What OpenQuestion holds

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Registered trials

None linked

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.