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Inflammatory myofibroblastic tumor is a neoplasm of intermediate biological potential, a marked inflammatory component, and characteristic genetic changes. Once it was identified as an independent nosological entity from a rather heterogeneous group of inflammatory pseudotumors. This paper describes a case of inflammatory myofibroblastic tumor of the chest in a child, by discussing the criteria for differential diagnosis in the use of up-to-date radiology techniques. When thoracic neoplasms are detected, it is necessary to determine their site and the most likely origin organ as exactly as possible and to assess the X-ray pattern of the pathological process. By applying the state-of-the-art radiodiagnostic techniques, the clarification of the pattern of the disease makes it possible to choose an optimal treatment policy and a surgical procedure and scope, to avoid anesthesia overload, and to decrease the probability of resurgery. Our observation is to demonstrate possible problems in the diagnosis of inflammatory myofibroblastic tumor of the lung in childhood and to recall again the algorithm of radiological approaches to detecting mediastinal and lung masses.

To verify the pathologic features, anaplastic lymphoma kinase (ALK) expression and biologic behavior of inflammatory myofibroblastic tumors (IMTs) of the central nervous system (CNS), we analyzed 10 cases of IMTs-CNS (8 cranial, 1 spinal, and 1 orbital). Our series of IMTs of the CNS showed a male predominance (male:female = 6:4) and a wide age range (10-60 years; mean age, 46.7 years). Lesion location also varied, but they were basically dura-based. Radiologically, they showed two patterns: isolated mass forming (n = 6) and an en plaque-like pattern (n = 4). Histopathologically, plasma cell granuloma (PCG)-like (n = 5) or fibrohistiocytic (FHC) variant (n = 5) was present. No correlation was found between the radiologic and histopathologic patterns. Spindle-shaped mesenchymal cells of IMTs expressed smooth muscle actin (SMA) in all cases. ALK expression was not found in our IMTs of the CNS. Late recurrence was found in 2 cases in different sites (20%). Pathologically, IMT-CNS could be subclassified into PCG-like and FHC. Immunostaining for SMA was found to helpfully discriminate myofibroblastic cells and to make a differential diagnosis. Although our cases did not show ALK immunoreactivity, some IMTs-CNS can recur, which suggests the neoplastic potential of these tumors. The rearrangement of the ALK gene in IMTs-CNS should be verified by an examination of more cases.