Absence of Chromosomal Translocations and Protein Expression of ALK in Sinonasal Adenocarcinomas

Publication date: January–February 2017
Source:Acta Otorrinolaringologica (English Edition), Volume 68, Issue 1
Author(s): Esteban Pacheco, José Luis Llorente, Alejandro López-Hernández, Cristina García-Inclán, María Costales, Sira Potes Ares, Fernando López, Blanca Vivanco, Mario A. Hermsen
IntroductionChromosomal 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.MethodBreak-apart fluorescent in situ hybridisation was used to analyse the presence of ALK translocations in 96 tumour samples. In addition, ALK protein expression was studied by immunohistochemistry.ResultsThe samples of SNAC did not show ALK translocation. Moreover, ALK protein expression was absent in all cases.ConclusionsThese results suggest that ALK is not involved in SNAC.



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