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Tajima S.,Shizuoka Saiseikai General Hospital | Koda K.,Fujieda Municipal General Hospital
International Journal of Clinical and Experimental Pathology | Year: 2015

Some neoplasms are associated with granulomatous inflammation. Granuloma formation in tumor tissue is caused by the cytokines derived from either the main tumor or other cells surrounding the tumor. In other instances, granulomatous inflammation is observed in the lymph nodes draining a tumor. This has been recognized as a sarcoid-like reaction. Herein, we report of a 75-year-old man with pulmonary squamous cell carcinoma (SCC), where granulomatous inflammation was observed extensively at the primary site. The carcinoma seemed to partly regress. In the regressing area, tumor cell debris was surrounded by granuloma. In contrast, no granuloma was identified in the dissected regional lymph nodes. To the best of our knowledge, such a case of SCC had not been described thus far. More case studies are required to determine whether tumor-related granuloma is the main cause of regression or whether it is just a secondary phenomenon caused by the attack and destruction of the tumor by lymphocytes.


Tajima S.,Shizuoka Saiseikai General Hospital | Koda K.,Fujieda Municipal General Hospital
International Journal of Clinical and Experimental Pathology | Year: 2015

Development of malignant peripheral nerve sheath tumors (MPNSTs) is a stepwise process that involves the alteration of many cell cycle regulators and the double inactivation of the NF1 gene. Inactivation of the TP53 gene and deletion of the CDKN2A/p16 gene are known to play an important role in the process. Herein, we present a 19-year-old man with a familial history of neurofibromatosis type 1, in whom the tumor arose from the intercostal nerve and showed 3 components: a neurofibroma, a low-grade MPNST, and a high-grade MPNST. Loss of p16 expression and homozygous deletion of the CDKN2A/p16 gene were observed in both the low-grade and the high-grade MPNST. In contrast to low-grade MPNSTs, high-grade MPNSTs generally tend to lose expression of p16 and harbor homozygous deletion of the CDKN2A/p16 gene. Loss of p16 expression and homozygous deletion of the CDKN2A/p16 gene in low-grade MPNST in our case might be related to its progression to high-grade MPNST. To the best of our knowledge, this is the first study correlating the p16 expression status and CDKN2A/p16 gene alteration in low-grade MPNSTs.


Tajima S.,Shizuoka Saiseikai General Hospital | Koda K.,Fujieda Municipal General Hospital
International Journal of Clinical and Experimental Pathology | Year: 2015

Ectomesenchymal chondromyxoid tumors (ECTs) are rare. Only approximately 55 cases have been reported in the English literature. Distinguishing ECTs from soft tissue myoepithelioma (STM) is often difficult owing to morphological and immunohistochemical similarities. Here, we present a case of an ECT arising from the anterior dorsum of the tongue in a 24-year-old woman. Grossly, the tumor was soft, had a myxoid appearance, and measured 8 × 7 × 7 mm. Microscopically, it was well-demarcated, lacked a fibrous capsule, and predominantly consisted of short, spindle to ovoid cells in a myxoid background. Vimentin, glial fibrillary acidic protein (GFAP), and S-100 protein were strongly positive on immunohistochemical analysis. While CD56 was moderately immunopositive, cytokeratin (AE1/AE3) and alpha-smooth muscle actin (αSMA) showed focal weak positivity. Thus, the immunohistochemical findings suggested a diverse immunophenotype, indicating mesenchymal (vimentin and αSMA positive), neurogenic (S100, GFAP, and CD56 positive), and epithelial differentiation (cytokeratin positive). This reflected the fact that ECTs probably arise from uncommitted ectomesenchymal cells that have the potential for multilineage differentiation. The immunohistochemical staining pattern observed for ECTs slightly differs from that of STMs. Strongly positive staining for GFAP and weakly positive staining for cytokeratin are observed in ECTs, whereas the opposite is typically observed for STMs. These findings indicated that the patterns of expression on immunohistochemistry differ between ECTs and STMs, although inevitably, there was some overlap. Thus, CD56 expression in the case presented here is noteworthy, and it could potentially become an adjunct diagnostic marker for ECT instead of previously used CD57.


Tajima S.,Shizuoka Saiseikai General Hospital | Koda K.,Fujieda Municipal General Hospital
International Journal of Clinical and Experimental Pathology | Year: 2015

Complete dissection of tracheobronchial adenoid cystic carcinoma (TACC) by surgery alone is sometimes difficult and has a greater propensity than tracheobronchial mucoepidermoid carcinoma (TMEC) for its surgical margin to become positive. In addition, TACC is more likely to present distant metastases than TMEC. Considering these facts, TACC and TMEC should be differentiated based on histopathological examination of biopsy specimens. Herein, we present a case of 54-year-old woman with a tumor in the right main bronchus, whose biopsy specimen was difficult to diagnose as TACC or TMEC. The specimen from the rounded protrusion of the tumor showed squamous differentiation, along with the presence of glandular and basaloid cells, making morphological examination alone ineffective in rendering a definite diagnosis. Thus, the addition of immunohistochemical analysis, aSMA and CD43 expression in basaloid cells and c-kit expression in glandular cells, was useful for accurately diagnosing TACC in this case. The squamous component was considered to be neoplastic because of its increased expression of cyclin D1 and overexpression of p16. The surgically resected specimen contained typical morphology of ACC, and the diagnosis of TACC was definitely confirmed.


Tajima S.,Shizuoka Saiseikai General Hospital | Koda K.,Fujieda Municipal General Hospital
International Journal of Clinical and Experimental Pathology | Year: 2015

Certain genetic events that occur at various stages of carcinogenesis can result in phenotypic changes. In breast carcinoma, these changes may occur either in situ, at the primary invasive site, or at a distant metastatic site. This report presents a case of dedifferentiation-like progression of breast carcinoma showing transition from luminal-type carcinoma to triple-negative carcinoma (i.e. negative for estrogen receptor, progesterone receptor, and HER2) with myoepithelial features. An 87-year-old woman was referred to us from another hospital for surgery. Preoperative ultrasonography revealed a mass measuring 16 × 12 × 8 mm. Following partial mastectomy, gross examination revealed a whitish tumor on the cut surface measuring 15 × 10 × 8 mm. Histopathological investigation revealed a predominant high-grade carcinoma containing some short spindle-shaped cells and expressing p63, muscle-specific actin, and alpha smooth muscle actin. The tumor also showed decreased expression of pan-cytokeratin and increased expression of vimentin on immunohistochemistry. Estrogen receptor was not detected by immunostaining. A high Ki-67 labeling index and diffuse nuclear accumulation of p53 were observed in the high-grade carcinoma. In the peripheral area, low-grade carcinoma with estrogen receptor expression was observed, but appeared displaced by the high-grade carcinoma. The high-grade carcinoma exhibiting myoepithelial carcinoma-like morphology and molecular phenotype was deemed to be carcinoma showing dedifferentiation-like changes arising from the peripherally situated pre-existing low-grade carcinoma. Thus, follow-up ought to be mandatory, considering the presumably aggressive nature of the predominant carcinoma showing dedifferentiation-like changes in this case.

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