Soluble c-Met in serum of patients with multiple myeloma: correlation with clinical parameters

• Published in: European journal of haematology Vol. 87; no. 5; pp. 394 - 399
• Main Authors: Wader, Karin F., Fagerli, Unn-Merete, Holt, Randi U., Børset, Magne, Sundan, Anders, Waage, Anders
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.11.2011
• Subjects: Biomarkers, Tumor - blood; c-Met; Female; hepatocyte growth factor; hepatocyte growth factor receptor; Humans; Male; multiple myeloma; Multiple Myeloma - blood; Proto-Oncogene Proteins c-met - blood; shedding
• ISSN: 0902-4441; 1600-0609
• DOI: 10.1111/j.1600-0609.2011.01622.x

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.