Evidence map›Paper›PMID 42095034›Full record

ArticleJournal of neurological surgery. Part B, Skull base2026

Comprehensive Genomic Profiling of Sinonasal Carcinomas: Identification of Common Mutations and Potential Targets for Therapy.

Gabriel Bitar, Beau Hsia, Saif Alshaka, Bastien A Valencia, Jeeho Kim, Mariko Sato, John Crawford, Michael L Levy, Sean Polster, Vijay A Patel

Abstract read
In one paragraph

Article in Journal of neurological surgery. Part B, Skull base, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. Article
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

10 authors.

Gabriel BitarSchool of Medicine, Creighton University, Phoenix, Arizona, United States.
Beau HsiaSchool of Medicine, Creighton University, Phoenix, Arizona, United States.ORCID 0009-0009-6403-502X
Saif AlshakaSchool of Medicine, Creighton University, Phoenix, Arizona, United States.
Bastien A ValenciaDepartment of Otolaryngology-Head and Neck Surgery, Mayo Clinic Florida, Jacksonville, Florida, United States.
Jeeho KimDepartment of Otolaryngology-Head and Neck Surgery, Naval Medical Center San Diego, San Diego, California, United States.
Mariko SatoDepartment of Pediatric Oncology, Children's Hospital of Orange County, Orange, California, United States.
John CrawfordChildren's Hospital Orange County, University of California Irvine, Department of Pediatrics and Neurology, Orange, California, United States.
Michael L LevyDepartment of Neurosurgery, University of California San Diego-Rady Children's Hospital, San Diego, California, United States.
Sean PolsterDepartment of Neurosurgery, University of Chicago, Chicago, Illinois, United States.
Vijay A PatelDivision of Pediatric Otolaryngology, Rady Children's Hospital, San Diego, California, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Sinonasal cancers are malignant neoplasms arising from the nasal cavity and paranasal sinuses, including squamous cell carcinoma (SCC), adenocarcinoma, and undifferentiated carcinoma. Due to their rarity, comprehensive genomic data remain limited. Treatments include surgery, radiation, and chemotherapy, with ongoing trials investigating agents like cetuximab, cisplatin, and Tazemetostat. Materials and Methods: We analyzed sinonasal cancer cases from the American Association for Cancer Research (AACR) Project Genomics Evidence Neoplasia Information Exchange (GENIE) database via cBioPortal (v16.1-public, accessed July 22, 2024). Common gene mutations, correlations, and mutual exclusivities were assessed using statistical analyses with false discovery rate correction. Results: Of 2,595 head and neck cancer samples, 122 (4.7%) were sinonasal carcinoma: 70 (57.4%) SCC, 31 (25.4%) undifferentiated carcinoma, and 21 (17.2%) adenocarcinomas. The most frequent mutations were TP53 (tumor protein 53; 40%), PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha; 14%), KMT2D (lysine methyltransferase 2D; 11%), and CDKN2A (cyclin-dependent kinase inhibitor 2A; 9%). Subtype-specific mutations included IDH2 (isocitrate dehydrogenase; 230%) in undifferentiated carcinoma and FAT1 (15%) in adenocarcinoma. TP53 frequently co-occurred with PRKDC (protein kinase, DNA-activated, catalytic subunit; Conclusion: TP53, PIK3CA, and KMT2D mutations are prevalent in sinonasal carcinoma, highlighting potential targets for therapy. Tazemetostat, targeting KMT2D-related DNA (deoxyribonucleic acid) methylation, and cetuximab, targeting the PIK3CA signaling cascade, may offer therapeutic benefits. Further research on mutation-specific therapies could improve treatment strategies.

Indexed as

epigenetic modulationgenomic profilingPI3K/AKT pathwayPIK3CA mutationprecision oncologysinonasal carcinomatargeted therapiesTP53 mutation

Identifiers

PMID42095034
PMCPMC13143389

What OpenQuestion holds

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Registered trials

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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.