Differential Expression of CD66a (BGP), a Cell Adhesion Molecule of the Carcinoembryonic Antigen Family, in Benign, Premalignant, and Malignant Lesions of the Human Mammary Gland

Abstract

CD66a, also known as biliary glycoprotein (BGP), is a member of the carcinoembryonic 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 expression 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 invasive carcinomas of the mammary gland. In normal tissue and benign lesions, CD66a was consistently expressed at the apical sites of epithelial cells and in myoepithelia, whereas CEA was absent or was restricted only to some apical membranes within the ductal tree. The specific staining of myoepithelia was most evident in pseudoinfiltrative radial scars and sclerosing adenosis. However, the apical expression of CD66a disappeared with the development of the malignant phenotype in noninvasive and invasive carcinomas, and changed gradually from low- to high-grade noninvasive carcinomas into a predominant uniform membrane staining all around the atypical cells. CEA expression was irregular in intensity and distribution. The native apical CD66a staining was partially preserved in some highly differentiated invasive carcinomas with a better prognosis, such as tubular and papillary carcinomas. These findings indicate that loss of CD66a expression rather than a change in staining patterns coincides with the development of the malignant phenotype.

CEACAM1 impedes thyroid cancer growth but promotes invasiveness: a putative mechanism for early metastases

“…The loss of cell-cell binding that closely correlates with differentiation and the invasive potential of malignant tumors is accompanied by alteration in expression of cell adhesion molecules (Pignatelli and Vessey, 1994). Dysregulated CEACAM1 protein expression in particular has been noted in several forms of solid neoplasia including breast (Obrink, 1997;Riethdorf et al, 1997;Plunkett and Ellis, 2002), colorectal Brummer et al, 1995), prostate Luo et al, 1999), bladder (Kleinerman et al, 1996), endometrial (Bamberger et al, 1998) and hepatocellular carcinomas (Takanishi et al, 1997). More frequently, however, downregulation has been observed compared with adjacent non-malignant surrounding structures.…”

CEA-related cell adhesion molecule-1 is involved in angiogenic switch in prostate cancer

“…Downregulation of CEACAM1 at the mRNA expression level during tumorigenesis has been shown in several tumor types including hepatomas (Hixson et al, 1985), carcinoma of colon (Neumaier et al, 1993;Nollau et al, 1997b), endometrium (Bamberger et al, 1998), breast (Riethdorf et al, 1997) and prostate (Nollau et al, 1997a;Lin and Pu 1999). On the basis of such results, a tumor suppressive role for CEACAM1 has been postulated.…”

Loss of carcinoembryonic antigen‐related cell adhesion molecule 1 expression is an adverse prognostic factor in hepatocellular carcinoma

“…1,2 CEACAM1 expression was down-regulated in tumor cells of malignancies arising from the liver, [3][4][5][6] breast, 7,8 colon, 9 endometrium, 10 and prostate. [11][12][13] Recent studies [13][14][15][16][17][18][19] showed that CEACAM1 is a negative regulator of tumor cell growth, suggesting that it may function as a tumor suppressor.…”