Premium
Differential expression of c‐Met, its ligand HGF/SF and HER2/neu in DCIS and adjacent normal breast tissue
Author(s) -
Lindemann K,
Resau J,
Nährig J,
Kort E,
Leeser B,
Annecke K,
Welk A,
Schäfer J,
Vande Woude G F,
Lengyel E,
Harbeck N
Publication year - 2007
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/j.1365-2559.2007.02732.x
Subject(s) - hepatocyte growth factor , c met , immunohistochemistry , pathology , ductal carcinoma , receptor tyrosine kinase , breast cancer , stroma , breast carcinoma , her2/neu , in situ hybridization , biology , mammary gland , receptor , medicine , cancer , gene expression , gene , biochemistry
Aims: Tyrosine kinase receptors Her2/neu and c‐Met play an important role in breast cancer development and progression. Our aim was to determine the expression of c‐Met, its ligand hepatocyte growth factor/scatter factor (HGF/SF) and Her2/neu in ductal carcinoma in situ (DCIS) lesions of the breast ( n = 39) by two different immunocytochemical techniques, classical immunohistochemistry and immunofluorescence, and to correlate their expression levels with histopathological and clinical characteristics. Methods and results: Both methods revealed similar c‐Met staining patterns in both the in situ component and the adjacent normal tissue ( P < 0.001). However, an imbalance in c‐Met expression between tumour and surrounding normal tissue was correlated with high‐grade DCIS (Van Nuys Grade 3). No correlation existed between Her2/neu and c‐Met expression. High HGF/SF immunoreactivity was observed in 43.6% of the cases, yet the adjacent cellular stroma revealed only low levels of HGF/SF. No correlation existed between c‐Met, Her2/neu or HGF/SF expression and clinicopathological factors. Conclusion: An imbalance in c‐Met expression between tumour and surrounding normal tissue is associated with an aggressive DCIS phenotype. Moreover, c‐Met and HGF/SF may contribute to tumour development by different means than those controlled by Her2/neu.