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).

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Orthobiotech, Janssen-Cilag, Celgene, Shire
P. Sonneveld (Pieter)
Erasmus University Rotterdam
Erasmus MC: University Medical Center Rotterdam

Auwerda, J. (2008, December 18). Acquired Coagulation Abnormalities and Thrombosis in Multiple Myeloma. Retrieved from