Abstract
e22227 Background: Thromboembolism is frequent in patients with cancer. Although it is known that several acquired factors take place in this process, the role of the genetic factors is controversial. In this study we analysed the most common genetic polymorphisms which have a role in the development of thrombosis. Methods: Study population consists of 292 (158 with thrombosis and 134 without thrombosis) patients treated between 2004 and 2008. Thrombosis was diagnosed by clinically and radiological measures in any time during the course of disease. Factor V Leiden G1691A, Prothrombin G20210A, Methlene Tetra Hydrofolate Reductase (MTHFR) C677T and Plazminogen Activator Inhibitor (PAI-1) 4G/5G were analysed with PCR-RFLP (Polymerase Chain Reaction- Restriction Fragment Length Polymorphism). Results: In the study group 48 and 1 patient had heterozygot and homozygot polymorphism for Factor V Leiden G1691A respectively. In the control group 32 heterozygot and 1 homozygot polymorphism and there was no statistically significant differents between study and control group (p=0,462).For Protrombin G20210A 11 and 4 heterozygot polymorphism were observed in control and study group respectively. While there was 1 homozygot polymorphism in study group there was no in control group and the difference between two groups was not statistically significant (p=0,198). For MTHFR C677T, 48 and 24 heterozygot polymorphism, 15 and 12 homozygot polymorphism were observed in study and control group respectively. The difference between two groups were statistically significant (p=0,04). There was no statistically significant difference between two groups for PAI-1 4G/5G polymorphisms (p=0,362). In subgroup analyses, statistically significant difference was found only in MTHFR C677T polymorphism in patients with GI cancer and with and without thrombosis (p=0,028). Conclusions: The studies investigating the relationship between genetic factors and thrombosis revealed controversial results. However, we found no genetic factor relevant to thrombosis other than MTHFR C677T polymorphism. Further studies investigating genetic and acquired factors in the development of the thrombosis in detail are warranted for documenting clearly the role of genetic polymorphisms. No significant financial relationships to disclose.
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