Acquired Coagulation Abnormalities and Thrombosis in Multiple Myeloma
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).
|Publisher||Erasmus MC: University Medical Center Rotterdam|
|Promotor||Sonneveld, P. (Pieter)|
|Sponsor||Orthobiotech, Janssen-Cilag, Celgene, Shire|
|Keywords||cell disorder, coagulation abnormalities, multiple myeloma, thrombosis|
Auwerda, J.J.A.. (2008, December 18). Acquired Coagulation Abnormalities and Thrombosis in Multiple Myeloma. Erasmus MC: University Medical Center Rotterdam. Retrieved from http://hdl.handle.net/1765/14217