The predominant mechanism for decreased or absent VWF in malignancy is autoantibodies that are inhibitory to VWF function or shorten VWF survival (Kumar et al., 2002 [3]).
We observed a significant increase in nitrite (p < 0.001) and vWF (p < 0.001) level in chemotherapy treated patients compared to untreated cancer patients and healthy controls.
ADAM28 (a disintegrin and metalloproteinase 28) is overexpressed by carcinoma cells in non-small cell lung carcinomas (NSCLC) and plays an important role in cancer cell proliferation and metastasis by reactivation of insulin-like growth factor-1 (IGF-1) and escaping from von Willebrand factor (VWF)-induced apoptosis through digestion of IGF-binding protein-3 and VWF, respectively.
Platelets are known to assist cancer cells in transmigrating through the endothelium, but ligands for the platelet-mediated cancer metastasis remain poorly defined. von Willebrand factor (vWF) is a major platelet ligand that has been widely used as a biomarker in cancer and associated inflammation.
While von Willebrand disease has long been known to result from qualitative and quantitative deficiencies of VWF, it is recently that contribution of elevated levels of VWF to various pathological conditions including thrombosis, inflammation, angiogenesis, and cancer metastasis has been appreciated.
We hypothesized that the role of VWF in cancer metastasis is influenced by its cellular origin and that cancer cell acquisition of VWF expression may contribute to enhanced metastatic potential.