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Cytology of fine‐needle aspiration of inflammatory myofibroblastic tumor
Author(s) -
Stoll Lisa Marie,
Li Qing Kay
Publication year - 2011
Publication title -
diagnostic cytopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.417
H-Index - 65
eISSN - 1097-0339
pISSN - 8755-1039
DOI - 10.1002/dc.21444
Subject(s) - medicine , pathology , cytokeratin , nuclear atypia , atypia , fine needle aspiration , cytology , biopsy , immunohistochemistry
Inflammatory Myofibroblastic Tumor (IMT) is a rare spindle cell neoplasm with a relatively indolent course. Its morphology may be confused with both reactive processes and/or malignant neoplasms on FNA specimens. Herein we discuss the cytologic features and IHC studies of IMT. The archives of the Department of Pathology at the Johns Hopkins Hospital were searched for IMT. A total of 257 cases were identified over a period of 11 years. Among them, 20 cases had cytology material. The patients' ages ranged from 7 to 81 years old with a median age of 54 years. The locations of the tumor in descending order were: liver (9/20, 45%), lung (8/20, 40%), abdomen (1/20, 5%), pelvis (1/20, 5%), and kidney (1/20, 5%). On FNA, the majority of tumors consisted of bland spindle cells with oval nuclei and small prominent nucleoli in a background of lymphocytes and plasma cells. Focal cytological atypia and “ganglion‐like” cells were identified in 7 cases, likely related to the risk of metastases and malignant transformation. The lesional cells expressed ALK (8/17, 47.1%) and actin (10/10, 100%), but with variable expression of cytokeratin. Ki‐67 showed low proliferative indices. ALK gene rearrangement was detected by FISH in three out of three cases and correlated with ALK protein expression by IHC. The cytologic diagnosis of IMT is challenging. When encountering a spindle cell lesion with prominent inflammatory component, a high index of suspicion in combination with the use of ancillary studies increases the diagnostic yield of IMT. Diagn. Cytopathol. 2010. © 2010 Wiley‐Liss, Inc.