Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/58975
Type: Artigo de periódico
Title: p63 and CD10: Reliable markers in discriminating benign sclerosing lesions from tubular carcinoma of the breast?
Author: Schenka, NGD
Schenka, AA
Queiroz, LD
Matsura, MD
Alvarenga, M
Vassallo, J
Abstract: The immunohistochemical detection of myoepithelial cells in benign sclerosing lesions of the breast is useful in distinguishing them from tubular carcinoma. So far, this detection has been carried out using antibodies against cytoskeletal proteins, such as alpha-smooth muscle actin (1A4) and calponin. However, the specificity of these markers has been questioned since they may be expressed in stromal myofibroblasts and vascular smooth muscle. Recently, two novel myoepithelial markets have been described: the nuclear protein p63, a member of the p53 family, and the surface antigen CID 10, also known as common acute lymphoblastic leukemia antigen (CALLA). The authors assessed the use of p63 and CD10 in the differential diagnosis between benign sclerosing lesions, such as sclerosing adenosis and radial scar, and tubular carcinoma, in comparison to the traditional myoepithelial markers 1A4 and calponin. p63, CD10: 1A4, and calponin were expressed in myoepithelial cells of all benign lesions and were consistently negative in all cases of tubular carcinoma. In contrast to cytoskeletal proteins, p63 and CD10 were mostly confined to myoepithelial cells and thus were more specific than the traditional counterparts. However, 1A4 was more intensely expressed and more reproducible than the novel markers. In conclusion, p63 and CD10 may be used as a complement to 1A4 in distinguishing benign sclerosing lesions from tubular carcinoma of the breast.
Subject: p63
CD10
myoepithelial cells
benign sclerosing lesions of the breast
tubular carcinoma
Country: EUA
Editor: Lippincott Williams & Wilkins
Rights: fechado
Date Issue: 2006
Appears in Collections:Unicamp - Artigos e Outros Documentos

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