Absence of chromosomal translocations and protein expression of ALK in sinonasal adenocarcinomas.

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.