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Absence of chromosomal translocations and protein expression of ALK in sinonasal adenocarcinomas
Esteban Pacheco1, José Luis Llorente1, Alejandro López-Hernández1
1Departamento de Otorrinolaringología, Instituto Universitario de Oncología del Principado de Asturias, Hospital Universitario Central de Asturias, Oviedo, Asturias, España.
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.
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