Prothrombin is a carbohydrate-protein compound in plasma essential to coagulation. In response to bleeding, a complex series of clotting-factor interactions leads to its conversion by thromboplastin to thrombin, which transforms fibrinogen in plasma into fibrin. Fibrin and platelets combine to form a clot. Hemophilia is caused by a hereditary lack of one of the clotting factors. Vitamin K is needed to synthesize prothrombin, so conditions that impair the vitamin's absorption result in prothrombin deficiency and a tendency to prolonged bleeding.
Prothrombin and prothrombin fragment F1+2 (F1+2) were demonstrated in the tumor stroma on cancer cells and on small blood vessels in areas of neoangiogenesis at the host-tumor interface (gastric and pancreatic cancer tissues). F1+2 is an indicator of local activation of blood coagulation in cancer tissue.
Thrombin itself is impossible to quantitate and so the use of surrogate markers is necessary. The measurement of F1+2 would be an excellent marker of thrombin generation. This is helped by the fact that F1+2 is not generated in vivo by any other mechanism. Fragment 1+2 has a half life of about 1 hour and is cleared from the bloodstream by the liver.