کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3026933 | 1182933 | 2016 | 6 صفحه PDF | دانلود رایگان |
• How the coagulation system relates to cancer etiology at the genetic level is largely unknown
• Factor V Leiden or prothrombin gene G20210A heterozygosity is unlikely to be major contributors to the risk of solid cancers
• Common SNPs in the F5, F7, F10, and EPCR genes are associated with risk of breast cancer, but data are lacking for other solid cancers
• Common SNPs in the TFPI, but not the TF, genes are associated with clinicopathological tumor characteristics and molecular subtypes in breast cancer
ABSTRACTHypercoagulability is a frequently finding in patients with cancer, and is associated with an increased risk of venous thrombosis (VT). Cancer-associated VT is associated with poor prognosis and represents the leading non-cancer cause of death among these patients. Conversely, patients experiencing VT are at increased risk of subsequent cancer, suggesting an epidemiological bidirectional link between cancer and hemostasis, and indicating a role of the hemostatic system in cancer development. How the coagulation system relates to cancer etiology at the genetic level is largely unexplored. Data on the association of polymorphisms in genes involved in coagulation with cancer development is important to clarify the role of the coagulation system in cancer pathogenesis. Effects of coagulation-related gene polymorphisms on cancer risk may possibly be translated into novel treatment- and prevention strategies of cancer-associated thrombosis and the cancer itself. This article reviews the current knowledge of the relation between polymorphisms in genes involved in coagulation and cancer risk in solid tumors.
Journal: Thrombosis Research - Volume 140, Supplement 1, April 2016, Pages S49-S54