Evidence map›Paper›PMID 30186959›Full record

ArticleLaryngoscope investigative otolaryngology2018

Comparison of PI3K Pathway in HPV-Associated Oropharyngeal Cancer With and Without Tobacco Exposure.

Si-Young Kiessling, Martina Anja Broglie, Alex Soltermann, Gerhard Frank Huber, Sandro Johannes Stoeckli

Open access · goldAbstract read
In one paragraph

Article in Laryngoscope investigative otolaryngology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.2field-weighted citation impact, top 23% of its field
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

6 citing papers in PubMed, 11 citations in OpenAlex.

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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

5 authors at 3 institutions in 1 country.

Si-Young KiesslingDepartment of Otorhinolaryngology, Head and Neck Surgery Cantonal Hospital of St. Gallen St. Gallen Switzerland.ORCID 0000-0003-1023-1737
Martina Anja BroglieDepartment of Otorhinolaryngology, Head and Neck Surgery Cantonal Hospital of St. Gallen St. Gallen Switzerland.
Alex SoltermannInstitute of Pathology and Molecular Pathology University Hospital of Zurich Zurich Switzerland.
Gerhard Frank HuberDepartment of Otorhinolaryngology, Head and Neck Surgery University Hospital of Zurich Zurich Switzerland.
Sandro Johannes StoeckliDepartment of Otorhinolaryngology, Head and Neck Surgery Cantonal Hospital of St. Gallen St. Gallen Switzerland.
University of St.Gallen · CHUniversity Hospital of Zurich · CHUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThe aim of the study was to evaluate whether HPV associated OPSCC with tobacco exposure follows a different carcinogenic pathway compared to HPV associated OPSCC without tobacco exposure and to investigate its prognostic significance. The question was addressed with focus on components of the PI3K pathway.

methods184 patients with newly diagnosed OPSCC treated with curative intent were consecutively enrolled. The expression level of p16, p53, PI3K, mTOR, and PTEN was assessed by immunohistochemistry and analyzed in relation to the risk factors HPV status and tobacco exposure.

results94 of 184 (51%) patients were p16 positive, p53 overexpression was detected in 48 of 184 (26%) cases. PI3K overexpression with 70 of 184 (38%) cases was significantly higher in p16 positive tumors. mTOR overexpression was present in 90 of 184 (49%) cases and significantly higher in p16 negative tumors. PTEN loss was found in 42 of 184 (23%) cases without association to p16 expression. p16 positive OPSCC showed lower rates of p53 expression and mTOR expression as well as higher rates of PI3K expression irrespective of tobacco exposure. Survival analysis showed a distinct intermediate survival rate of p16 positive smokers. The markers PI3K, mTOR, and PTEN did not have a significant impact on survival.

conclusionHPV associated OPSCC with tobacco exposure follows the same expression level of the PI3K pathway as HPV associated OPSCC without tobacco exposure. The impaired survival rate of the intermediate risk group cannot be explained by different expression patterns of PI3K, mTOR, and PTEN. LEVEL OF EVIDENCE: 2b.

Indexed as

HPVOropharyngeal cancerPI3Ktobacco

Identifiers

PMID30186959
PMCPMC6119789
OpenAlexW2885626345

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.