DIFFERENTIAL EXPRESSION OF CD66A (BGP), A CELL-ADHESION MOLECULE OF THE CARCIOEMBRYONIC ANTIGEN FAMILY, IN BENIGN, PREMALIGNANT, AND MALIGNANT LESIONS OF THE HUMAN MAMMARY-GLAND
L. Riethdorf et al., DIFFERENTIAL EXPRESSION OF CD66A (BGP), A CELL-ADHESION MOLECULE OF THE CARCIOEMBRYONIC ANTIGEN FAMILY, IN BENIGN, PREMALIGNANT, AND MALIGNANT LESIONS OF THE HUMAN MAMMARY-GLAND, The Journal of histochemistry and cytochemistry, 45(7), 1997, pp. 957-963
CD66a, also known as biliary glycoprotein (BGP), is a member of the ca
rcinoembryonic antigen (CEA) family and the human homologue of the rat
cell-CAM. There is evidence that aberrant expression or loss of CD66a
in tumor tissue is of biological significance. No data about its expr
ession in breast carcinoma cells and only sparse information about the
expression of CD66a in normal breast are available thus far. In this
study we used monoclonal antibodies to analyze the expression of CD66a
and CEA in normal tissue, benign lesions, and in noninvasive and inva
sive carcinomas of the mammary gland. In normal tissue and benign lesi
ons, CD66a was consistently expressed at the apical sites of epithelia
l cells and in myoepithelia, whereas CEA was absent or was restricted
only to some apical membranes within the ductal tree. The specific sta
ining of myoepithelia was most evident in pseudoinfiltrative radial sc
ars and sclerosing adenosis. However, the apical expression of CD66a d
isappeared with the development of the malignant phenotype in noninvas
ive and invasive carcinomas, and changed gradually from low- to high-g
rade noninvasive carcinomas into a predominant uniform membrane staini
ng all around the atypical cells. CEA expression was irregular in inte
nsity and distribution. The native apical CD66a staining was partially
preserved in some highly differentiated invasive carcinomas with a be
tter prognosis, such as tubular and papillary carcinomas. These findin
gs indicate that loss of CD66a expression rather than a change in stai
ning patterns coincides with the development of the malignant phenotyp
e.