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Background  The procoagulant state in cancer increases the thrombotic risk, but also supports tumor progression. To investigate the molecular mechanisms controlling cancer and hemostasis, we conducted a case-control study of genotypic and phenotypic variables of the tissue factor (TF) pathway of coagulation in breast cancer.    Methods  366 breast cancer patients and 307 controls were genotyped for SNPs (n = 41) in the  F2, F3  (TF) , F5, F7, F10 ,  TFPI  and  EPCR  genes, and assayed for plasma coagulation markers (thrombin generation, activated protein C (APC) resistance, D-dimer, antithrombin, protein C, protein S, and TF pathway inhibitor (TFPI)). Associations with breast cancer were evaluated using logistic regression to obtain odds ratios (ORs) and 95% confidence intervals (CIs), or the chi-square test.    Results  Four SNPs in  F5  (rs12120605, rs6427202, rs9332542 and rs6427199), one in  F10  (rs3093261) ,  and one in  EPCR  (rs2069948) were associated with breast cancer.  EPCR  rs2069948 was associated with estrogen receptor (ER) and progesterone receptor (PR) positivity, while the SNPs in  F5  appeared to follow hormone receptor negative and triple negative patients. The prothrombotic polymorphisms factor V Leiden (rs6025) and prothrombin G20210A (rs1799963) were not associated with breast cancer. High APC resistance was associated with breast cancer in both factor V Leiden non-carriers (OR 6.5, 95% CI 4.1-10.4) and carriers (OR 38.3, 95% CI 6.2-236.6). The thrombin parameters short lag times (OR 5.8, 95% CI 3.7-9.2), short times to peak thrombin (OR 7.1, 95% CI 4.4-11.3), and high thrombin peak (OR 6.1, 95% CI 3.9-9.5) predicted presence of breast cancer, and high D-dimer also associated with breast cancer (OR 2.0, 95% CI 1.3-3.3). Among the coagulation inhibitors, low levels of antithrombin associated with breast cancer (OR 5.7, 95% CI 3.6-9.0). The increased coagulability was not explained by the breast cancer associated SNPs, and was unaffected by ER, PR and triple negative status.    Conclusions  A procoagulant phenotype was found in the breast cancer patients. Novel associations with SNPs in  F5, F10  and  EPCR  to breast cancer susceptibility were demonstrated, and the SNPs in  F5  were confined to hormone receptor negative and triple negative patients. The study supports the importance of developing new therapeutic strategies targeting coagulation processes in cancer.    Electronic supplementary material  The online version of this article (doi:10.1186/1471-2407-14-845) contains supplementary material, which is available to authorized users.

Increased coagulation activity and genetic polymorphisms in the F5, F10 and EPCRgenes are associated with breast cancer: a case-control study