Case Reports in Medicine Figure 5: (ALK-1, 200x): Positive stain for ALK protein at immunnohistochemistry. However, recently the authors veriﬁed that the IMT can occur in any organ of the body and in all ages [6]. The histological appearance of a gastric IMTs is similar to that of soft tissue IMTs. It has been debated whether IMT is a tumor or inﬂammation, and also whether it is benign or malignant. However, studies on cytogenetic abnormalities, such as rearrangements of the ALK gene on chromosome 2p23, clonal chromosome abnormalities, and DNA aneu- ploidy, and the role of oncogenic viruses in the pathogenesis of IMT suggest that it is a real neoplasm [6, 7, 15, 16]. This entity is characterized by a myoﬁbroblastic prolif- eration, a lymphoplasmacytic inﬁltrate distributed among the tumor cells and a myxoid background stroma. Three architectural patterns have been described in IMT: myxoid hypocellular pattern, a cellular fascicular or nested pattern with variable amounts of myxoid stroma, and a sclerotic, hyalinized pattern with minimal myxoid stroma [3, 4, 13, 17– 21]. These patterns are often mixed in a single tumor. The myoﬁbroblastic cells in IMTs are spindled and/or epithelioid. In our case, the volume of the tumor, the presence of cellular atypia, and the high Ki-67 labeling index suggest aggressive neoplasm. As far as the diﬀerential diagnosis is concerned, there are a few tumors or lesions in the stomach that must be dis- tinguished from IMT. They include gastrointestinal stromal tumor (GIST), inﬂammatory ﬁbroid polyp, smooth muscle neoplasm, peripheral nerve sheath tumor, solitary ﬁbrous tumor, ﬁbromatosis, and, rarely, the follicular dendritic cell sarcoma [12]. GIST may show cyst formation, hemorrhage, or necrosis, which were only occasionally seen in some IMTs. GIST typically does not have the inﬂammatory back- ground seen in the IMT [22, 23]. In addition, some GIST cells have cytoplasmic vacuoles, a feature not seen in the IMT. Immunohistochemically, GIST is typically positive for CD117 but negative for ALK, whereas IMT shows an oppo- site proﬁle. Clinically, IMT presents with an abdominal mass or cystic lesion with related compressive symptoms, such as abdominal pain and vomiting. It was described a case that 3 bled spontaneously into the peritoneal cavity and developed a hemoperitoneum [12]. Kim et al. reported a case with peritoneal dissemination [24] and Leon et al. described an IMT of the gastric remnant in woman with a prior gastrectomy [25]. Most IMTs require surgery to obtain deﬁnite diagnosis and treatment. Nevertheless, local excision is an option in selected cases [26]. Complete resection is the preferred sur- gical treatment, because incomplete excision has been shown to be a risk factor for recurrence [1, 10, 11]. Recently, ALK reactivity was found to be associated with local recurrence, but not distant metastasis, which was con- ﬁned to ALK-negative lesions, suggesting that reactivity may be a favorable prognostic indicator in IMTs [6]. However, other studies did not conﬁrm such an association [8]. Dif- ferentiation between aggressive and nonaggressive forms of IMT remains to be further clariﬁed. After complete resection, the prognosis of IMT is generally good with a low risk of distant metastasis [10, 11, 13]. Concluding, the main diﬃculty in the management of IMT lies in the unpredictable postoperative course. There are no deﬁnitive clinical, histopathological, or genetic features to predict recurrence or metastasis. References [1] H. Shi, L. Wei, L. Sun, and A. Guo, “Primary gastric inﬂamma- tory myoﬁbroblastic tumor: a clinicopathologic and immuno- histochemical study of 5 cases,” Pathology Research and Practice, vol. 206, no. 5, pp. 287–291, 2010. [2] S. B. Goldin, D. Osborne, C. Paidas et al., “Inﬂammatory myoﬁbroblastic tumor of the midesophagus,” Fetal and Pedi- atric Pathology, vol. 26, no. 5-6, pp. 243–254, 2007. [3] W. A. Lee, M. K. Lee, Y. M. Jeen, J. H. Kle, J. J. Chung, and S. H. Yun, “Solitary ﬁbrous tumor arising in gastric serosa,” Pathology International, vol. 54, no. 6, pp. 436–439, 2004. [4] H. R. Makhlouf and L. H. Sobin, “Inﬂammatory myoﬁbrob- lastic tumors (inﬂammatory pseudotumors) of the gastroin- testinal tract: how closely are they related to inﬂammatory ﬁbroid polyps?” Human Pathology, vol. 33, no. 3, pp. 307–315, 2002. [5] B. D. Riedel, R. C. Wong, and E. H. Ey, “Gastric inﬂamma- tory myoﬁbroblastic tumor (inﬂammatory pseudotumor) in infancy: case report and review of the literature,” Journal of Pediatric Gastroenterology and Nutrition, vol. 19, no. 4, pp. 437–443, 1994. [6] C. M. Coﬃn, J. L. Hornick, and C. D. M. Fletcher, “Inﬂamma- tory myoﬁbroblastic tumor: comparison of clinicopathologic, histologic, and immunohistochemical features including ALK expression in atypical and aggressive cases,” American Journal of Surgical Pathology, vol. 31, no. 4, pp. 509–520, 2007. [7] J. R. Cook, L. P. Dehner, M. H. Collins et al., “Anaplastic lymphoma kinase (ALK) expression in the inﬂammatory my- oﬁbroblastic tumor: a comparative immunohistochemical study,” American Journal of Surgical Pathology, vol. 25, no. 11, pp. 1364–1371, 2001. [8] E. A. Montgomery, D. D. Shuster, A. L. Burkart et al., “Inﬂam- matory myoﬁbroblastic tumors of the urinary tract: a clini- copathologic study of 46 cases, including a malignant example