Hyperhomocysteinemia in cancer patients with thrombosis is independent of methylene tetrahydrofolate reductase gene mutation

Abstract

6152 Background: Methylene Tetrahydrofolate reductase (MTHFR) gene mutations and nutritional factors (folic acid/ B12) are primarily responsible for the observed increase in this surrogate marker. Since, cancer patients exhibit increased prevalence of thrombotic events, we hypothesized that upregulation of homocysteine may play a role in cancer associated thrombosis. However, initial screening of cancer patients in the ONCENOX study showed that the malignancy related thrombotic state was independent of molecular defects in Factor V Leiden, Prothrombin 20210 and MTHFR variants. (Hoppensteadt et al. Pathophysiology of Hemostasis and Thrombosis 2003; 33. S1. 03 A. 56). Methods: In the same group of 102 patients who were enrolled in a randomized open label, multidose, active comparator, parallel design study (ONCENOX) and in another group of cancer free patients with thrombosis enrolled in a treatment study with low molecular weight heparin (CORTES, n=50), blood levels of homocysteine were measured using a hi...