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Expression of c‐MET, low‐molecular‐weight cytokeratin, matrix metalloproteinases‐1 and ‐2 in spinal chordoma
Author(s) -
Naka Takahiko,
Boltze Carsten,
Samii Amir,
Samii Madjid,
Herold Christian,
Ostertag Helmut,
Iwamoto Yukihide,
Oda Yoshinao,
Tsuneyoshi Masazumi,
Kuester Doerthe,
Roessner Albert
Publication year - 2009
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.1365-2559.2009.03278.x
Subject(s) - chordoma , c met , cytokeratin , immunohistochemistry , matrix metalloproteinase , pathology , hepatocyte growth factor , medicine , clinical significance , biology , receptor
Aims: In skull base chordoma, c‐MET expression has been reported to correlate with younger patient age and favourable prognosis; however, it also contributes to tumour invasiveness, especially in recurrent lesions, suggesting variable roles for c‐MET according to clinical status. The aim of this study was to investigate the significance of c‐MET expression in spinal chordoma, which affects patients who are 10–20 years older than those with skull base chordoma. Methods and results: Using immunohistochemical techniques, the expression of c‐MET and its ligand, hepatocyte growth factor (HGF) was investigated in 34 primary spinal chordomas and compared with other clinicopathological parameters. Expression of c‐MET and HGF was observed in 85.3 and 21.7% of lesions, respectively. c‐MET expression correlated with the expression of an epithelial marker, low‐molecular‐weight cytokeratin (CAM5.2). Lesions with higher c‐MET expression showed significantly stronger expression of proteinases, including matrix metalloproteinase (MMP)‐1 and MMP‐2. However, c‐MET expression was not associated with patient age, proliferative ability estimated by MIB‐1 labelling index, or prognosis. Conclusions: c‐MET expression was observed in most spinal chordomas and correlated with the expression of CAM5.2, suggesting a relationship to an epithelial phenotype.