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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

C-Met overexpression in node-positive breast cancer identifies patients with poor clinical outcome independent of Her2/neu.

Receptor tyrosine kinases play an important role in malignant transformation of epithelial cells by activating signal transduction pathways important for proliferation, invasion and metastasis. In a pilot study (n = 40), we evaluated expression of the c-Met and Her2/neu receptor tyrosine kinases and the c-Met ligand hepatocyte growth factor/scatter factor ( HGF/ SF) in primary breast cancers and their lymph node metastases using both conventional immunohistochemistry and confocal immunofluorescence. Neither c-Met and HGF/ SF nor Her2/neu expression correlated with established prognostic factors such as age, lymph node involvement, estrogen receptor (ER), progesterone receptor (PR), tumor size, or grade. Both staining methods confirmed a significant correlation between c-Met overexpression and a high risk of disease progression. Furthermore, among tumors with c-Met overexpression, only 50% also overexpress Her2/neu, thus identifying a subset of patients with aggressive disease in addition to Her2/neu. Median disease-free survival in patients with c-Met overexpressing tumors was 8 months compared to 53 months when c-Met expression was low (p = 0.037; RR = 3.0). This significant impact of c-Met on tumor aggressiveness independent of Her2/neu was also confirmed by multivariate analysis. In conclusion, the role of c-Met expression as a prognostic variable and consequently as an interesting target for novel therapeutic approaches deserves further analysis in a larger cohort of patients.[1]

References

  1. C-Met overexpression in node-positive breast cancer identifies patients with poor clinical outcome independent of Her2/neu. Lengyel, E., Prechtel, D., Resau, J.H., Gauger, K., Welk, A., Lindemann, K., Salanti, G., Richter, T., Knudsen, B., Vande Woude, G.F., Harbeck, N. Int. J. Cancer (2005) [Pubmed]
 
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