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Soluble c‐Met in serum of patients with multiple myeloma: correlation with clinical parameters
Author(s) -
Wader Karin F.,
Fagerli UnnMerete,
Holt Randi U.,
Børset Magne,
Sundan Anders,
Waage Anders
Publication year - 2011
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.2011.01622.x
Subject(s) - multiple myeloma , hepatocyte growth factor , ectodomain , medicine , bone marrow , c met , pathogenesis , endocrinology , receptor , immunology
Objectives: The receptor tyrosine kinase c‐Met and its ligand, hepatocyte growth factor (HGF), play key roles in tumour genesis and metastasis and contribute in multiple myeloma pathogenesis. Substantial data support that a soluble extracellular fragment of c‐Met may function as a decoy receptor that downregulates the biological effects of HGF and c‐Met. We examined serum levels of soluble c‐Met in patients with myeloma and healthy individuals and investigated a possible relationship with clinical disease parameters and survival. Methods: The concentration of c‐Met and HGF was measured by enzyme‐linked immunosorbent assay in serum ( n = 49) and bone marrow plasma ( n = 16) from patients with multiple myeloma and in serum from healthy controls ( n = 26). Results: The median serum concentration of soluble c‐Met was 186 ng/mL (range 22–562) in patients with multiple myeloma and 189 ng/mL (range 124–397) in healthy individuals. There was a significant negative correlation between serum c‐Met levels and disease stage, bone marrow plasma cell percentage and serum concentration of M‐protein. Conclusion: We have for the first time examined the concentration of soluble c‐Met in serum from patients with myeloma and found equal median levels in patients with myeloma as a group and healthy individuals. Still, serum levels of soluble c‐Met correlated negatively with parameters of disease burden in patients with myeloma. We suggest that a possible role for the c‐Met ectodomain as a negative regulator of HGF/c‐Met activity should be examined in multiple myeloma.