ArticleHead & neck2014
Molecular profiling of sinonasal undifferentiated carcinoma.
Article in Head & neck, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed, 40 citations in OpenAlex.
- Molecular Basis and Rationale for the Use of Targeted Agents and Immunotherapy in Sinonasal Cancers.Journal of clinical medicine · 2022Review
- Genetic analysis of sinonasal undifferentiated carcinoma discovers recurrent SWI/SNF alterations and a novel PGAP3-SRPK1 fusion gene.BMC cancer · 2021Article
- High-Grade Sinonasal Carcinoma: Classification Through Molecular Profiling.Archives of pathology & laboratory medicine · 2019Review
- Annotating gene sets by mining large literature collections with protein networks.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2018Article
- Recurrent IDH2 R172X mutations in sinonasal undifferentiated carcinoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2017Article
- Human epidermal growth factor receptor 2/neu as a novel therapeutic target in sinonasal undifferentiated carcinoma.Head & neck · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundSinonasal undifferentiated carcinoma (SNUC) remains a poorly characterized malignancy at both the clinical and molecular level, and, consequently, the optimal treatment strategy remains undefined.
methodsWe used a mass spectroscopy-based approach (Sequenom) to evaluate 95 hallmark single nucleotide variations (SNVs) within 12 oncogenes or tumor suppressor genes (AKT, BRAF, CDK4, Beta-catenin, epidermal growth factor receptor [EGFR], FBXW7, JAK2, c-KIT, KRAS, PDGFR, PI3K, and vascular endothelial growth factor [VEGF]) in 13 histologically confirmed SNUC cases.
resultsNone of the samples demonstrated activating mutations in any of the 95 SNVs.
conclusionSelect clinically relevant activating genomic mutations were not identified in the 13 patient samples. However, polymorphisms were noted within the promoter region of VEGF. These may merit future studies as predictive biomarkers for treatment response or overall survival. Additionally, future studies focusing on larger tumor sets and utilizing whole genome or exome sequencing may help define genetic aberrations in SNUC that can be clinically targeted with available or emerging biological agents.
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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.