MAML2 rearrangement as a useful diagnostic marker discriminating between Warthin tumour and Warthin-like mucoepidermoid
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ORIGINAL ARTICLE
MAML2 rearrangement as a useful diagnostic marker discriminating between Warthin tumour and Warthin-like mucoepidermoid carcinoma Michał Bieńkowski 1 Wojciech Biernat 1
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Michał Kunc 1
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Mariola Iliszko 2
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Alina Kuźniacka 2
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Michał Studniarek 3
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Received: 26 November 2019 / Revised: 11 March 2020 / Accepted: 17 March 2020 # The Author(s) 2020
Abstract Warthin tumour is the second most common benign neoplasm of salivary glands. Despite its relatively characteristic histology, it may sometimes mimic other lesions. Here, we report two female non-smoker patients diagnosed with low-grade mucoepidermoid carcinoma with oncocytic epithelium and prominent lymphoid (Warthin-like) stroma and with molecularly confirmed MAML2 rearrangement. In addition, we screened a consecutive series of 114 Warthin tumour cases by means of MAML2 break apart fluorescence in situ hybridization to assess its value in differential diagnosis. MAML2 rearrangement was detected in both mucoepidermoid carcinoma cases, while all Warthin tumours were negative. Taking into account the literature data, Warthin-like mucoepidermoid carcinomas are more frequently observed in women, while a slight male predominance and smoking history are typical for Warthin tumour. In addition, the patients with Warthin-like mucoepidermoid carcinoma were significantly younger than those with Warthin tumour. To conclude, Warthin-like mucoepidermoid carcinoma may usually be suspected based on histology, while the diagnosis can be confirmed by means of molecular assays such as FISH. The investigation of MAML2 status is particularly advised when Warthin tumour is considered in a young, non-smoking, female patient. Keywords Warthin tumour . Warthin-like mucoepidermoid carcinoma . T(11;19) translocation . MAML2 rearrangement
Introduction Warthin tumour (WT) is the second most common benign neoplasm of salivary glands. It usually arises as a slow-growing, painless mass in the parotid of male smokers [1]. The mechanism of WT development has not been clearly defined;
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00428-020-02798-5) contains supplementary material, which is available to authorized users. * Michał Bieńkowski [email protected] 1
Department of Pathomorphology, Faculty of Medicine, Medical University of Gdańsk, Mariana Smoluchowskiego 17, Gdańsk 80-214, Poland
2
Department of Biology and Medical Genetics, Faculty of Medicine, Medical University of Gdańsk, Gdańsk, Poland
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Department of Radiology, Faculty of Medicine, Medical University of Gdańsk, Gdańsk, Poland
however, smoking-induced oncocytic metaplasia and salivary gland heterotopia in peri- and intraparotideal lymph nodes are most probably involved [2]. Conventional WT is characterized by a dense lymphoid stroma and cystic spaces lined by bilayer oncocytic epithelium forming papillary projections. Its metaplastic or infarcted variants display coagulative necrosis, fibrosis, and inflammation along with squamous or mucinou
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