Intraepidermal cells of paget’s carcinoma of the breast can be genetically different from those of the underlying carcinoma
Luca Morandi, BScia,
Annalisa Pession, BScia,
Gian Luca Marucci, MDa,
Maria Pia Foschini, MDa,
Giancarlo Pruneri, MDb,
Giuseppe Viale, MDb,
Vincenzo Eusebi, MD,
aDepartment of Oncology, Section of Pathology, University of Bologna, at Ospedale Bellaria, Bologna, Italy
bDepartment of Pathology, European Institute of Oncology and University of Milan, Milan, Italy
Supported by a grant ex 60% from the University of Bologna and 40% from MURST.
*Address correspondence and reprint requests to Vincenzo Eusebi, MD, FRCPATH, Anatomia Patologica, Ospedale Bellaria, Via Altura 3, 40139, Bologna, Italy
Paget’s carcinoma (PC) of the breast is characterized by neoplastic cells of “glandular” type located within the epidermis of the nipple-areolar complex, often associated with an underlying ductal carcinoma, either in situ or invasive.
At present the origin of PC cells is controversial, although there is a widespread opinion that PC cells are “foreign” elements to the epidermis resulting from an epidermotropic migration of neoplastic elements from an underlying ductal carcinoma.
An alternative view is that some cases result from neoplastic transformation of preexisting, innocent intraepidermal clear cells of the nipple-areolar complex (Toker cells) that migrate from nonneoplastic ducts.
Consequently, 10 cases were studied using methods for clonality (ie, loss of heterozygosity and mitochondrial DNA displacement loop sequence analysis). Microdissection of intraepidermal neoplastic cells and of cells from underlying duct carcinomas and metastases was performed.
In no fewer than 2 cases, PC cells were genetically different from underlying lesions, which showed consistent homology among themselves.
Therefore, it is suggested that the rule of epidermotropism by neoplastic cells from an underlying carcinoma is not applicable to all cases, and that in some cases PC cells might be the result of neoplastic transformation of preexisting intraepidermal nonneoplastic cells.
Consequently, the underlying tumors are coincidental neoplastic lesions (collision tumors.
J Human Pathology
December, 2003 Vol 34, No 12
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