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The expression of Met /hepatocyte growth factor receptor gene in giant cell tumors of bone and other benign musculoskeletal tumors
Author(s) -
Ferracini Riccardo,
Scotlandi Katia,
Cagliero Elga,
Acquarone Francesca,
Olivero Martina,
Wunder Jay,
Baldini Nicola
Publication year - 2000
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/1097-4652(200008)184:2<191::aid-jcp6>3.0.co;2-b
Subject(s) - hepatocyte growth factor , receptor tyrosine kinase , giant cell tumors , oncogene , cancer research , pathology , biology , c met , immunohistochemistry , receptor , hepatocyte growth factor receptor , autocrine signalling , cell , medicine , giant cell , cell cycle , biochemistry , genetics
Overexpression of the hepatocyte growth factor receptor ( Met /HGF receptor), a transmembrane tyrosine kinase encoded by the MET proto‐oncogene, is involved in transformation and invasive behavior of human carcinomas and sarcomas. We have previously found that bone sarcomas express high levels of Met /HGF receptor while in some cases the ligand HGF is co‐expressed with the receptor, activating an autocrine loop. In this study, we analyzed 40 biopsy samples of a collection of giant cell tumors and other rare benign tumors of bone for expression of the MET proto‐oncogene. These included nonossifying fibromas, osteoblastomas, desmoplastic fibromas of bone, chondroblastomas, and giant cell tumors of bone. Snap frozen samples were tested for the MET and HGF gene expression by immuno‐histochemistry and Western blotting with anti‐ MET antibodies and RT‐PCR. Over 50% of all cases scored positive for MET expression being constantly positive in recurrent or locally aggressive lesions. Sporadic co‐expression of the Met /HGF receptor and ligand is also demonstrated. Met /HGF receptor expression in benign bone neoplasms suggests its early involvement in sarcomagenesis. J. Cell. Physiol. 184:191–196, 2000. © 2000 Wiley‐Liss, Inc.