Absence of chromosomal translocations and protein expression of ALK in sinonasal adenocarcinomas
Acta Otorrinolaringol Esp. 2017 Jan-Feb;68(1):9-14.
doi: 10.1016/j.otorri.2016.02.003.
Epub 2016 May 13.
[Article in
English,
Spanish]
Affiliations
- 1 Departamento de Otorrinolaringología, Instituto Universitario de Oncología del Principado de Asturias, Hospital Universitario Central de Asturias, Oviedo, Asturias, España.
- 2 Departamento de Otorrinolaringología, Instituto Universitario de Oncología del Principado de Asturias, Hospital Universitario Central de Asturias, Oviedo, Asturias, España. Electronic address: llorentependas@telefonica.net.
- 3 Departamento de Anatomía Patológica, Hospital Universitario Central de Asturias, Oviedo, Asturias, España.
Abstract
Introduction:
Chromosomal translocations at 2p23 cause overexpression of anaplastic lymphoma kinase (ALK), a receptor tyrosine kinase involved in signalling pathways that regulate cell proliferation. This translocation occurs in 5% of lung adenocarcinoma and has been demonstrated to be useful as a therapeutic target for crizotinib. sinonasal adenocarcinomas (SNAC) are histologically similar to lung adenocarcinomas; the aim of this study was to evaluate the presence of ALK alterations in SNAC.
Method:
Break-apart fluorescent in-situ hybridization was used to analyse the presence of ALK translocations in 96 tumour samples. In addition, ALK protein expression was studied by immunohistochemistry.
Results:
The samples of SNAC did not show ALK translocation. Moreover, ALK protein expression was absent in all cases.
Conclusions:
These results suggest that ALK is not involved in SNAC.
Keywords:
ALK; Adenocarcinoma nasosinusal; Carcinoma nasosinusal; FISH; Sinonasal adenocarcinoma; Sinonasal carcinoma.
Copyright © 2016 Elsevier España, S.L.U. and Sociedad Española de Otorrinolaringología y Cirugía de Cabeza y Cuello. All rights reserved.
MeSH terms
-
Adenocarcinoma / genetics*
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Adenocarcinoma / metabolism
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Adenocarcinoma / pathology
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Aged
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Aged, 80 and over
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Anaplastic Lymphoma Kinase
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Chromosomes, Human, Pair 2 / genetics
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Chromosomes, Human, Pair 2 / ultrastructure*
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Crizotinib
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Female
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Follow-Up Studies
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Gene Expression Regulation, Neoplastic*
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Humans
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In Situ Hybridization, Fluorescence
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Male
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Middle Aged
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Neoplasm Proteins / biosynthesis
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Neoplasm Proteins / genetics*
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Nose Neoplasms / chemistry
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Nose Neoplasms / genetics*
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Nose Neoplasms / metabolism
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Nose Neoplasms / pathology
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Paranasal Sinus Neoplasms / genetics*
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Paranasal Sinus Neoplasms / metabolism
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Paranasal Sinus Neoplasms / pathology
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Pyrazoles
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Pyridines
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Receptor Protein-Tyrosine Kinases / biosynthesis
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Receptor Protein-Tyrosine Kinases / genetics*
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Translocation, Genetic*
Substances
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Neoplasm Proteins
-
Pyrazoles
-
Pyridines
-
Crizotinib
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ALK protein, human
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Anaplastic Lymphoma Kinase
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Receptor Protein-Tyrosine Kinases