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Based on the microscopical and immunohistochem-ical features it was likely that the tumour originatedfrom myofibroblasts. Canine haemangiopericytomawas considered as a differential diagnosis. The originof canine haemangiopericytoma has not been con-

firmed definitively. There is variable immunolabellingof haemangiopericytomas, but the incidence of expres-sion ofa-SMA and vimentin is relatively high (Perezet al., 1996; Mazzei et al., 2002). The histologicalpattern of haemangiopericytoma is also variable, butit has a characteristic appearance with a typicalfingerprint pattern that consists of whorled spindlecells around a central blood vessel (Goldschmidt andHendrick, 2002). Lack of this characteristic structureand the abundance of collagen matrix suggested thatthe tumour in the present case may have originatedfrom myofibroblasts rather than from pericytes.

Myofibroblasts have characteristics of both fibro-blasts and smooth muscle cells and they have variableimmunoreactivity for some muscle actin markers in-cluding a-SMA, calponin and desmin (Qiu et al.,2008). In the present case, vimentin labelling was uni-formly positive, but the intensity and distribution ofa-SMA and calponin labelling differed between areasof the tumour. a-SMA immunoreactivity was strongerin spindle cells beneath the ulcer than in cells in deeperareas. Activated by mechanical stress andcytokines, many kinds of mesenchymal cells can differ-entiate into myofibroblasts, which have been charac-terized by neo-expression of a-SMA (Tomasek et al.,

2002). Therefore, it is possible that spindle cells be-neath the ulcer were transformed into myofibroblastsby inflammatory cytokines released in response tothe ulceration. However, it was difficult to clarifywhether these fibroblastic cells were neoplastic ornon-neoplastic in nature. Weak cytoplasmic expres-sion of calponin was observed in neoplastic cells inthe central part of the mass. Calponin is a calmodu-lin-, F-actin- and tropomyosin-binding protein andis considered to be important in the regulation ofsmooth muscle contraction (Takeuchi et al., 1991;Frid et al., 1992). Therefore, it is reasonable to

consider that calponin co-localized with a

-SMA inthe neoplastic cells. Some reports of human myofibro-blastic sarcomas revealed consistent expressions of cal-ponin and a-SMA (Meng et al., 2007; Qiu et al., 2008).On the other hand, imbalance of expression ofcalponin and a-SMA was observed in other humancases of low-grade myofibroblastic sarcomas and intwo canine cases of inflammatory myofibroblastic tu-mours (Knight et al., 2009; Niedzielska et al., 2009).In these reports, immunoreactivity for calponin wasobserved in almost all of the neoplastic cells, butexpression of a-SMA was localized. Althoughimmunoreactivity for calponin was not investigated,

immunoreactivity for a-SMA in a portion of thespindle-shaped neoplastic cells was also observed inan equine case of spindle cell sarcoma that was proba-bly derived from myofibroblasts (Newman et al.,1999). Therefore, immunohistochemical labelling ob-

served in this tumour may indicate variation in myofi-broblastic differentiation depending on the area of thetumour.

Among human myofibroblastic sarcomas, low-grade myofibroblastic sarcomas are grossly ill-defined and infiltrative and characterized by cellularfascicles of spindle-shaped tumour cells withoutmarked inflammatory infiltration. In a previous re-port, neoplastic cells had mild atypiaand a low mitoticrate (1e6 per 10 high power fields) (Mentzel etal.,1998). Other cases have been hypocellular witha prominent collagenous matrix. The tumour in the

present case also showed grossly ill-defined bordersand cellular fascicles of spindle-shaped tumour cellswith a prominent collagenous matrix. Neoplastic cellshad atypia, but few mitotic figures were observed. Thefact that the mass showed rapid growth despite the lowproliferative potential of these neoplastic cells mightindicate that the observed mitotic rate did not repre-sent the true proliferative potential. Inflammatorycell infiltration beneath the ulcer might be consideredas a secondary change caused by physical trauma andwas not a component of this tumour. Therefore, thistumour was most likely a low-grade myofibroblasticsarcoma. To the best of our knowledge, there is only

one report of 12 cases of feline restrictive orbitalmyofibroblastic sarcoma with features of low-grademyofibroblastic sarcoma (Bell et al., 2011). This maybe the first dog diagnosed as having low-grade myofi-broblastic sarcoma according to the diagnostic criteriafor human myofibroblastic sarcoma.

Acknowledgments

We thank Mrs. S. Suzuki for technical assistance inpreparing the histological specimens.

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Received, July 25th, 2011Accepted, September 1st, 2011

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