Abstract: The present invention relates to a method for screening an individual for the presence in his/her genome of a genetic marker that is indicative of an increased risk of deep venous thrombosis, wherein the genetic marker is haplotype 2 of the fibrinogen ? gene (FGG-H2) as given in FIG. 5A. The genetic marker comprises a set of one, two, three or four mutations in the nucleic acid material encoding fibrinogen ?, the mutations being selected from the group consisting of 129A/T (rs2066854), 7874G/A (rs20668?1), 9615?C/T (rs2066864) and 10034C/T (rs2066865).

Abstract: The present invention relates to a method for screening an individual for the presence in his/her genome of a genetic marker that is indicative of an increased risk of deep venous thrombosis, wherein the genetic marker is haplotype 2 of the fibrinogen ? gene (FGG-H2) as given in FIG. 5A. The genetic marker comprises a set of one, two, three or four mutations in the nucleic acid material encoding fibrinogen ?, the mutations being selected from the group consisting of 129A/T (rs2066854), 7874G/A (rs20668?1), 9615C/T (rs2066864) and 10034C/T (rs2066865).

Abstract: Method for screening for the presence of a genetic defect associated with thrombosis and/or poor anticoagulant response to activated protein C (APC). The method is directed at detecting one or more mutations at one or more of the cleavage and/or binding sites for APC of Factor V and/or Factor Va or at Factor VIII and/or Factor VIIIa at either nucleic acid or protein level or both.

Abstract: Method for screening for the presence of a genetic defect associated with thrombosis and/or poor anticoagulant response to activated protein C (APC). The method is directed at detecting one or more mutations at one or more of the cleavage and/or binding sites for APC of Factor V and/or Factor Va or at Factor VIII and/or Factor VIIIa at either nucleic acid or protein level or both.

Abstract: A method for determining whether an individual is at increased risk for thrombosis, comprising detecting the presence or absence of a genetic mutation located in the 3' untanslated region of the prothrombin gene (G to A mutation at position 20210) that is correlated with elevated prothrombin levels in individuals with the mutation, wherein the elevated prothrombin levels are associated with increased risk for thrombosis. Also provided are kits and primers that specifically hybridize adjacent to the region of the prothrombin gene that contains the G to A mutation at position 20210.

Abstract: Method for screening for the presence of a genetic defect associated with thrombosis and/or poor anticoagulant response to activated protein C (APC). The method is directed at detecting one or more mutations at one or more of the cleavage and/or binding sites for APC of Factor V and/or Factor Va or at Factor VIII and/or Factor VIIIa at either nucleic acid or protein level or both.

Abstract: Method for screening for the presence of a genetic defect associated with thrombosis and/or poor anticoagulant response to activated protein C (APC). The method is directed at detecting one or more mutations at one or more of the cleavage and/or binding sites for APC of Factor V and/or Factor Va or at Factor VIII and/or Factor VIIIa at either nucleic acid or protein level or both.

Abstract: The present invention relates to various functional variants of recombinant protein S (PS) that do not significantly bind C4b binding protein (C4BP) and uses of the variants as a therapeutic reagent. In particular the invention is directed at deletion mutants of protein S, having cofactor activity toward APC and lacking at least the two postulated C4BP binding domains of the SHBG-like domain of the corresponding mature wild type protein S. Such a deletion mutant in particular lacks at least amino acid residues 401-457 and 583-635 of the corresponding mature wild type human protein S.

Abstract: The present invention relates to various functional variants of recombinant protein S (PS) that do not significantly bind C4b binding protein (C4BP) and uses of the variants as a therapeutic reagent. In particular the invention is directed at deletion mutants of protein S, having cofactor activity toward APC and lacking at least the two postulated C4BP binding domains of the SHBG-like domain of the corresponding mature wild type protein S. Such a deletion mutant in particular lacks at least amino acid residues 401-457 and 583-635 of the corresponding mature wild type human protein S.