Expression of Claudin-1 and -4 in Benign Lesions and Invasive Ductal Carcinomas of the Breast.
- Author:
Hyun Joo CHOI
;
Ji Han JUNG
;
Jinyoung YOO
;
Seok Jin KANG
;
Kyo Young LEE
- Publication Type:Original Article
- Keywords:
Breast;
Claudin-1;
Claudin-4;
Immunohistochemistry
- MeSH:
Breast*;
Carcinogenesis;
Carcinoma, Ductal*;
Claudin-1*;
Claudin-4;
Claudins;
Epithelial Cells;
Estrogens;
Humans;
Immunohistochemistry;
Lymph Nodes;
Neoplasm Metastasis;
Receptors, Progesterone;
Tight Junctions
- From:Korean Journal of Pathology
2007;41(4):232-237
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: The claudins are a family of transmembrane proteins associated with tight junctions and they are critical for maintaining cell-to-cell adhesion in sheets of epithelial cells. However, their role in the progression of cancer remains largely unexplored. The aims of this study were to evaluate the expression patterns of claudin-1 and -4 in benign lesions and invasive ductal carcinomas (IDC) of the breast, and relationships between the expression of these markers and the clinicopathological characteristics in IDC patients. METHODS: We examined the claudin-1 and -4 protein expressions by performing immunohistochemical stainings in 54 benign lesions and 120 IDCs via the tissue microarray method. We evaluated the correlation between the expression of these markers and the clinicopathological characteristics of IDC. RESULTS: The expressions of claudin-1 (p=0.099) and -4 (p=0.000) were up-regulated in IDCs as compared with benign lesions. The claudin-1 expression correlated with the loss of estrogen receptor (p=0.036) and progesterone receptor (p=0.011). The claudin-4 expression correlated with lymph node metastasis (p=0.043), the nuclear grade (p=0.030), the histologic grade (p=0.007), and the loss of estrogen receptor (p=0.001) and progesterone receptor (p= 0.029). CONCLUSIONS: These results suggest that claudin-1 and -4 may play a significant role in the carcinogenesis of IDC of the breast and these may represent novel markers for this disease.
