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Vocal cord inflammatory myofibroblastic tumor with mucoid deposits harboring TIMP3–ALK fusion: A potential diagnostic pitfall
Author(s) -
Yorita Kenji,
Togashi Yuki,
Nakagawa Hideyuki,
Miyazaki Katsushi,
Sakata Seiji,
Baba Satoko,
Takeuchi Kengo,
Hayashi Yoshihiro,
Murakami Ichiro,
Kuroda Naoto,
Oda Yoshinao,
Kohashi Kenichi,
Yamada Yuichi,
Kiyozawa Daisuke,
Michal Michael,
Michal Michal
Publication year - 2019
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/pin.12796
Subject(s) - pathology , anaplastic lymphoma kinase , vimentin , immunohistochemistry , biology , medicine , malignant pleural effusion , lung cancer
A 35‐year‐old Japanese man who had experienced hoarseness for 10 years presented with a vocal cord lesion. A gross examination revealed a left vocal cord polyp occupying two‐thirds of the vocal space. The endoscopically resected lesion contained scattered atypical fibroblastic, stellate, or ganglion‐like cells with mucoid stroma. Vacuolated cells were also seen. Lymphoplasmacytic infiltrate was largely undetectable. A vocal cord polyp was first suspected, but well‐differentiated liposarcoma and inflammatory myofibroblastic tumor (IMT) were included in the differential diagnoses. The tumor cells were positive for anaplastic lymphoma kinase (ALK), calponin, and vimentin, and negative for other smooth muscle markers by immunohistochemistry. Structures resembling myofibroblasts were not observed by electron microscopy, which confirmed abundant rough endoplasmic reticulum in the tumor cells and accumulated lipid droplets in some tumor cells. ALK gene rearrangement was detected by fluorescence in situ hybridization, and TIMP3–ALK fusion was confirmed by 5′ rapid amplication of cDNA ends. We diagnosed the lesion as an IMT, and an ALK‐ rearranged stellate cell tumor may be postulated. This is the first report of a fusion partner gene of ALK in a case of laryngeal IMT.