Icam1

ICAM-1 (intercellular adhesion molecule-1) is involved in heterotypic adhesion. Rosette et al. (94) studied five breast cancer cell lines and found that ICAM-1 expression on the cell surface positively correlated with metastatic potential. Breast tumors had increased ICAM-1 mRNA levels compared to normal tissue (94). Lynch et al. (95) found that ICAM-1

serum levels were increased in patients with breast carcinoma. ICAM-1 is increased in the tumor cytosol and sera of patients with breast cancer, however, prognostic value could not be established (91). An immuno-histochemical study of 274 patients with invasive breast carcinoma revealed that ICAM-1 was expressed in 50.3% of cases (96). ICAM-1 expression was negatively correlated to tumor size, lymph node metastasis, tumor infiltration, nuclear pleomorphism, and nuclear grade (96). There was improved relapse-free and overall survival in patients with ICAM-1 positive tumors (96). The findings in that study suggested a tumor suppressor role for ICAM-1 (96). Madhavan et al. (93) found that ICAM is downregulated in node positive breast cancer (compared to node negative cases).

3.4 CEACAM1

CEACAM1 (biliary glycoprotein, BGP, CD66a, cell-CAM, C-CAM-1) is a cell adhesion glycoprotein that belongs to the carcinoembryonic antigen (CEA) family and the immunoglobulin superfamily (97). Human BGP has four isoforms (98), but only three of the four isoforms are present in normal and malignant breast (99). BGP is involved in homophilic and heterophilic binding and requires calcium for adhesion (100). BGP is expressed in normal, premalignant, and malignant breast (99, 101), but the subcellular localization is different (99, 101). BGP is expressed on the apical surface of normal ductal and lobular epithelial cells, and is located in the cytoplasm or uniformly over the entire membrane in invasive carcinoma (99, 101). C-CAM-1 has been found to suppress breast cancer tumors (growth suppression) (102). BGP is downregulated at the mRNA and protein levels in 30% of breast cancers (99). Using immuno-histochemistry Riethdorf et al. (101) showed that in a portion of invasive breast carcinomas there was downregulation or loss of BGP expression. Using immunohistochemistry Riethdorf et al. (101) found that 80% of ductal carcinomas and 68% of lobular carcinomas had staining for BGP. There was no relationship between the expression of BGP in the invasive breast carcinomas and grade, age, tumor size, menopausal status, or hormone receptor status (101). Well- differentiated invasive ductal carcinomas (including papillary carcinoma and tubular carcinoma) had strong apical membrane staining for BGP rather than uniform membrane staining as seen in the majority of other carcinomas (101).

3.5 NCAM

NCAM (neural cell adhesion molecule, CD56, Leu19, NKH1) belongs to the immunoglobulin superfamily, is involved in homotypic and hetero-typic adhesion (103, 104), and is expressed by neural, neuroendocrine, and some biphasic tumors including breast phyllodes tumors (105, 106). NCAM is localized to the cell membrane in breast cancer, but can sometimes be cytoplasmic (107). Breast cancer cells (MDA-MB-231) transfected with NCAM produced tumors with slower growth rates (longer latency) than NCAM negative cells (108).

3.6 Mel-CAM

Mel-CAM (CD 146, MUC18, MCAM, A32 antigen, S-Endo-1) is a member of the immunoglobulin superfamily and is involved in Ca2+-independent heterophilic adhesion (109-111). Using a new mouse monoclonal antibody (MN-4) Shih et al. (110) found positive immuno-histochemical staining in normal epithelial and myoepithelial cells of the breast, and in 2 of 11 infiltrating breast carcinomas. In a different study by the same group Mel-CAM was identified in 100% of normal breast and benign proliferating breast epithelium, but only seen (focally) in 17% of breast cancers (109). Transfection of Mel-CAM cDNA into Mel-CAM negative breast cancer cells produced a cohesive cell growth pattern and inhibition of tumor growth (109) (compared to mock trans-fectants). Therefore, Mel-CAM is considered to be a tumor suppressor in breast cancer (111).

3.7 HepaCAM

HepaCAM is a cell adhesion molecule that is a member of the immunoglobulin superfamily (112). It was originally identified in liver. Moh et al. transfected HepaCAM into MCF-7 breast cancer cells (112). In nonconfluent cells hepaCAM was located in cell protrusions; in confluent cells it was located at cell-cell borders; and in polarized cells it was localized to the lateral and basal membranes. HepaCAM is thought to be important in cell-matrix interaction and cell motility (112).

3.8 PECAM

PECAM (platelet endothelial cell adhesion molecule, PECAM-1, CD31, endocam) is an adhesion molecule that is expressed by endothelial cells, leukocytes, and platelets and is involved in homotypic and heterotypic interactions (113). PECAM is expressed in the endothelium of normal breast (100%) and tumor-associated vessels (100%) (114), and antibodies to PECAM have been used to study the vascularization of tumors. CD31 is not seen in normal or hyperplastic breast epithelium (115). A few studies have found that PECAM can be expressed in neoplastic breast epithelium. Fox et al. (114) performed an immuno-histochemical study of 64 invasive breast carcinomas and found one case where the malignant epithelial cells expressed PECAM. Sapino et al. (115) studied 32 cases of high nuclear grade ductal carcinoma in situ (>/= 2 cm) and found CD31 positivity in 11 cases. In that study the associated poorly differentiated invasive ductal carcinomas were CD31 and CD44 positive. The authors suggested that CD31 expression correlates with tumor cell spreading within the ductal system (including Paget's cells at the nipple) (115).

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