Multiple Myeloma (MM) is a malignant plasma cell disorder which accounts for approximately 10% of the malignant hematologic neoplasms(1, 2). In the pathophysiology of MM, the interaction between myeloma cells and the bone marrow microenvironment leads to a complex signalling network that sustains survival of the malignant cell and mediates tumour progression and drug resistance. Major signalling pathways involved are the IL-6R/ STAT3, Ras/MAPK, PI3K/Akt, notch, WNT- and NF-κB pathways(3). The cytokine interleukin-6 is presumed to play a pivotal role in the pathogenesis and malignant growth of MM(4) and IL-6 levels are elevated in case of active disease(5). IL-6 also plays a stimulatory role in the coagulation mechanism(6). It has been shown to promote the transcription of the factor VIII gene(7), decrease protein S levels in canine models(8), induce ultra large and hyperreactive von Willebrand Factor(9), and inhibit the cleavage of ultra large von Willebrand Factor(6).

Additional Metadata
Keywords cell disorder, coagulation abnormalities, multiple myeloma, thrombosis
Promotor P. Sonneveld (Pieter)
Publisher Erasmus University Rotterdam
Sponsor Orthobiotech, Janssen-Cilag, Celgene, Shire
ISBN 978-90-90-23581-3
Persistent URL
Auwerda, J.J.A. (2008, December 18). Acquired Coagulation Abnormalities and Thrombosis in Multiple Myeloma. Erasmus University Rotterdam. Retrieved from