In a previous report we found that Lewis × antigen was highly expressed by normal epithelial tissues of mammary gland and digestive tract [24]. In order to continue the study of blood group related Lewis antigen involvement in breast cancer,

we have focused this research on the difucosylated Lewis y antigen; this carbohydrate specifically belongs to the ABH Lewis blood group family which is overexpressed on the majority of carcinomas including ovary, pancreas, prostate, breast, colon and non small cell lung cancers [25–27]. We performed immunoprecipitation of MUC1 from breast cancer, benign and normal serum samples with HMFG1 MAb, directed against MUC1 peptide core (DTR) and isolated the glycoprotein. SDS-PAGE and Western blot assays were performed with the

samples obtained by IP; nitrocellulose membrane incubation with C14 MAb showed the same MW band as TGFbeta inhibitor incubation with HMFG1 MAb in breast cancer, benign and normal samples. These results indicate that Lewis y could be involved in MUC1 structure. Sikut et al. found that sialyl Lewis a and sialyl Lewis × epitopes were attached to MUC1 in breast cancer patients serum samples [28]. During many years, the functions of Lewis y were mostly unknown Hedgehog antagonist although it was described as a differentiation and onco-developmental antigen [8]. Basu et al. found that in colon and vulval carcinoma cell lines, sialylated Lewis a and Lewis y were present in the EGF receptor glycoprotein NSC23766 order [29]. In the last decades, further information Tangeritin was achieved; in breast cancer cell lines, Hellström et al. probed that MAbs reactive against Lewis y could be internalized and mediated tumor cell killing by antibody-dependent cellular cytotoxicity (ADCC) and complement dependent cytotoxicity (CDC) [30]. Furthermore, sialylated Lewis a and Lewis y were related with apoptosis; in this sense, Rapoport and Le Pendu found in colon carcinoma cell

lines such as HT29 in which apoptosis was induced by UV irradiation, TNFα and anti-Fas, a major decrease of this antigen as well as Lewis x [31]. On the other hand, in Jurkat human T cell line, the expression of Lewis x and Lewis y was enhanced in the cell surface during apoptosis induced by different agents including anti-Fas antibody [32]. Lewis y is attached to components of the CD66 cluster which is a member of the carcinoembryonic antigen (CEA) family and of the immunoglobulin superfamily. The activation-increase in Lewis y attached to CD66 adhesion molecules implicates a role of the Lewis y determinant in cytoadhesive properties of granulocytes on trafficking and inflammatory responses [5, 33]. In cancer cells, Miyake et al have observed that MAbs which bind to Lewis y antigen, although cross-reacted with H and Lewis b, inhibited cell motility and tumor cell metastasis [34].