Abstract
Objectives: Plasmacytoid cells (PLCs) in salivary pleomorphic adenoma (SPA) are regarded as modified neoplastic myoepithelia and define plasmacytoid myoepithelioma (pMYO). However, histochemically, immunohistochemically and ultrastructurally, PLCs fail to demonstrate frank myogenous properties. Epithelial–mesenchymal transition (EMT) may explain the phenotypes in SPA. Our aim was to evaluate (1) PLCs with accepted or purported myoepithelial and EMT-related markers; and (2) pMYOs for PLAG1 aberrations by using fluorescence in situ hybridization. Study Design: Eight SPAs with or without PLC-predominance and 3 pMYOs were immunohistochemically studied. Results: PLCs in SPA and pMYO exhibited strong, scattered to diffuse positivity for K7, rare K14 positivity and were mostly negative for α-smooth muscle actin, h-caldesmon, and p63/p40. S100 staining was strong and diffuse, whereas calponin was variable. DOG1 was negative. PLCs in pMYO and PLC-rich SPA exhibited selective or diffuse WT1 and D2-40 immunoreactivity. EMT markers SNAIL/SLUG exhibited strong and variable immunoreactivity in PLCs in contrast to weak or absent E-cadherin expression. SOX10 was diffusely and strongly positive. PLAG1 rearrangement was present in 1 pMYO. Conclusions: PLCs mostly fail to express myoepithelial markers; PLCs are neoplastic cells adapting to microenvironmental changes and capable of EMT; and tumors composed solely of PLCs are apparently SPAs depleted of a ductal component.
Original language | English (US) |
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Pages (from-to) | 515-529 |
Number of pages | 15 |
Journal | Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology |
Volume | 128 |
Issue number | 5 |
DOIs | |
State | Published - Nov 2019 |
Bibliographical note
Funding Information:We would like to thank Dr. Elizabeth A. Bilodeau, School of Dental Medicine, University of Pittsburgh, Pittsburg, PA, for her valuable assistance in this project; and Mr. Brian Dunnette, University of Minnesota, Minneapolis, MN, for his assistance with the preparation of the illustrations.
Publisher Copyright:
© 2019 Elsevier Inc.