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Vimentin, smooth muscle actin, desmin, S-100 protein, p53, and estrogen receptor expression in elastofibroma and nodular fasciitis.

Elastofibroma and nodular fasciitis are two rare, benign soft tissue tumors. Elastofibroma is suggested to develop as a result of abnormal degeneration of elastic fibers after local trauma. Similarly, fibroblastic proliferation, which is triggered by local trauma or nonspecific inflammatory event, is suggested to play an important role in the origin of nodular fasciitis. In this immunohistochemical study, vimentin, smooth muscle actin (SMA), desmin, S-100 protein, p53, and estrogen receptors were applied to paraffin sections of 10 elastofibroma and four nodular fasciitis specimens to learn more about their histogenesis and biological behavior. All cases with nodular fibrosis were strongly SMA and vimentin positive, while only three weakly stained with estrogen receptor antibody. There was no immunreactivity for S-100, desmin, and p53 in nodular fasciitis. However, all elastofibroma cases were stained positively with vimentin. No staining was observed with SMA, S-100, desmin, and p53 in elastofibroma. The staining pattern of nodular fasciitis supported a myofibroblastic origin, whereas the SMA negativity in elastofibroma was correlated with fibroblastic origin.

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