Evidence map›Paper›PMID 23055340›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2012

EGFR status and KRAS/BRAF mutations in intestinal-type sinonasal adenocarcinomas.

Cristina García-Inclán, Fernando López, Jhudit Pérez-Escuredo, Mari Paz Cuesta-Albalad, Blanca Vivanco, Irene Centeno, Milagros Balbín, Carlos Suárez, José Luis Llorente, Mario A Hermsen

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
  2. Genome-wide somatic mutation analysis of sinonasal adenocarcinoma with and without wood dust exposure.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2024
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  15. Metastatic behaviour of sinonasal adenocarcinomas of the intestinal type (ITAC).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 · 2016
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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

10 authors at 1 institution in 1 country.

Cristina García-InclánDepartment of Otolaryngology, IUOPA, Hospital Universitario Central de Asturias, Oviedo, Spain.
Fernando López
Jhudit Pérez-Escuredo
Mari Paz Cuesta-Albalad
Blanca Vivanco
Irene Centeno
Milagros Balbín
Carlos Suárez
José Luis Llorente
Mario A Hermsen
Hospital Universitario Central de Asturias · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIntestinal-type sinonasal adenocarcinoma (ITAC) is a rare tumour that is etiologically related to professional exposure to wood dust and exhibits a poor prognosis. Treatment alternatives to surgery and radiotherapy are needed and may be found in anti-EGFR agents. EGFR gene copy number gains and KRAS/BRAF mutations have been reported to act as positive and negative predictors, respectively, of therapeutic response to EGFR targeted therapies in colorectal adenocarcinoma, a tumour type claimed to be genetically similar to ITAC. Therefore, the aim of this study was to evaluate the occurrence and consequence of EGFR alterations and KRAS and BRAF mutations in a large series of ITAC.

methodsEGFR protein expression was studied in 98 paraffin embedded tissue samples, organized in a tissue microarray. Gene copy number analysis was performed by FISH using the same tissue microarray, complemented by microarray CGH and MLPA analysis on DNA extracted from 65 fresh frozen tissues. Mutations in EGFR, KRAS and BRAF were analysed by direct sequencing on 65 fresh frozen tissues.

resultsEGFR gene copy number gains were observed in 45 %, and protein over-expression in 21 % of the cases. No mutations were found in EGFR or BRAF, while KRAS mutations were present in 12 % of the cases. Neither protein overexpression nor gene copy number gain correlated to histological subtype, tumour stage or clinical follow-up.

conclusionIn the largest series of ITAC published to date, and using a number of different techniques, EGFR alterations were frequently observed. Although apparently not useful as a prognostic factor, there may be a basis for investigating EGFR targeted therapies in this group of patients, especially because negative response predictors such as KRAS and BRAF mutations are infrequent or absent, respectively.

Indexed as

MutationAdenocarcinomaAdultAgedAged, 80 and overComparative Genomic HybridizationDNA Mutational AnalysisErbB ReceptorsFemaleGene DosageHumansIn Situ Hybridization, FluorescenceMaleMiddle AgedNose NeoplasmsOligonucleotide Array Sequence AnalysisBRAF protein, humanEGFR protein, humanErbB ReceptorsKRAS protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)ras Proteins

Identifiers

PMID23055340
PMCPMC12995005
OpenAlexW1969020720

What OpenQuestion holds

Textmetadata
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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.