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The interleukin‐6/Janus kinase/ STAT 3 pathway in pleomorphic adenoma and carcinoma ex pleomorphic adenoma of the lacrimal gland
Author(s) -
Andreasen Simon,
Heegaard Steffen,
Grauslund Morten,
Homøe Preben
Publication year - 2016
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/aos.13122
Subject(s) - carcinoma ex pleomorphic adenoma , cancer research , pleomorphic adenoma , janus kinase , myoepithelial cell , lacrimal gland , jak stat signaling pathway , adenoma , medicine , pathology , immunohistochemistry , biology , cytokine , signal transduction , tyrosine kinase , salivary gland , microbiology and biotechnology
Purpose Pleomorphic adenoma ( PA ) is the most common tumour of the lacrimal gland, but very little is known about its biology. It has a tendency to recur and an ability to transform into the high‐grade malignancy carcinoma ex pleomorphic adenoma (ca‐ex‐ PA ), which is also largely unexplored. In this study, we examine the expression of the interleukin‐6/Janus kinase/ STAT 3 ( IL ‐6/ JAK / STAT 3) pathway components in PA and ca‐ex‐ PA . Methods Sixteen PA s and two ca‐ex‐ PA s were examined with immunohistochemistry. Seven PA s were subjected to microdissection and subsequent qPCR . Results The IL ‐6/ JAK / STAT 3 pathway was overexpressed in PA compared to normal lacrimal gland. Overexpression of phosphorylated JAK 1 (p‐ JAK 1) and cyclin D1 was significantly overexpressed in ductal cells compared with myoepithelial cells in PA . A shift from p‐ JAK 1 to p‐ JAK 2 and p‐Tyk2 overexpression was seen between PA and ca‐ex‐ PA , combined with a high p‐ STAT 3 expression in the latter. Conclusion The IL ‐6/ JAK / STAT 3 pathway is overexpressed in PA , and this overexpression was even more pronounced in ca‐ex‐ PA , with a shift in the JAK s mediating STAT 3 phosphorylation. Future studies are needed to clarify whether PA and ca‐ex‐ PA could be treated with targeted therapy directed against components of the IL ‐6/ JAK / STAT 3 pathway.