Salivary duct carcinoma is a relatively uncommon malignancy of the salivary glands; however, it frequently occurs as a carcinomatous component of carcinoma ex pleomorphic adenoma. We previously reported salivary duct carcinoma with rhabdoid features (SDCRF) as an extremely rare subtype of salivary duct carcinoma, and that it occurred as a salivary counterpart of pleomorphic lobular carcinoma of the breast (PLCB). We collected new cases of SDCRF for this study, in which we examined a total of 17 cases immunohistochemically and genetically. As it is known that PLCB exhibits loss of or aberrant E-cadherin expression and carries nonsense/missense mutations in or deletion of the CDH1 gene, we examined the CDH1 gene status of our SDCRF cases. All of the examined SDCRF cases involved the diffuse proliferation of large ovoid cells with eosinophilic cytoplasm and eccentric nuclei, which displayed reduced cell-cell adhesion. Most cases were positive for pan-cytokeratin, androgen receptor, gross cystic disease fluid protein-15, SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1, and WI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 4, whereas they were negative for vimentin. No and decreased/cytoplasmic E-cadherin expression was ob served in 11 and 4 of 17 cases, respectively, whereas no and decreased/cytoplasmic β-catenin expression were observed in 10 and 5 of 17 cases, respectively. Among the 11 cases that could be genetically analyzed, a nonsense mutation (1 case), missense mutations (6 cases), and insertions (1 case) were detected in the CDH1 gene. In conclusion, we propose that SDCRF is the salivary counterpart of PLCB due to its morphology and immunophenotype, and the genetic status of CDH1. This study was approved by the Institutional Review Board of Shizuoka General Center (SGHIRB#2019007) and Hamamatsu University School of Medicine (20-011). All subjects signed informed consent forms. Written informed consent for the publication of clinical details and/or clinical images was obtained from the patients. A copy of the consent form is available for review by the Editor of this journal. K.K.: designed and drafted the manuscript. K.K. and M.S.: made the histopathologic diagnoses. M.M., K.Y., S.B., T.O., and H.I.: found the cases and collected the clinical data. H. Yamamoto, T.I., and C.T.: performed the immunohistochemistry. H. Yamada and K.I.: performed the genetic analysis. H.S. and M.S.: supervised this manuscript. Conflicts of Interest and Source of Funding: Supported in part by a Grant-in-Aid for the Medical Research Support Project of Shizuoka Prefectural Hospital Organization in 2019 (to K.K.), as well as by AMED (20ck0106554) (to H.S.) and SRF (to H.S.). The authors have disclosed that they have no significant relationships with, or financial interest in, any commercial companies pertaining to this article. Correspondence: Kimihide Kusafuka, DDS, PhD, Department of Pathology, Shizuoka General Hospital, 4-27-1 Kita-Ando, Aoi-ku, Shizuoka City 420-8527, Shizuoka Prefecture, Japan (e-mail: k-kusafuka@i.shizuoka-pho.jp). Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.
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