Summary
Systemic activation of the coagulation mechanism is known to exist in patients with
colon cancer. The mechanism of such activation was investigated using immunohistochemical
techniques applied to fresh frozen sections of resected primary colon cancer specimens.
Tumor cells stained for tissue factor, factor V, and urokinase-type plasminogen activator.
Perivascular and intercellular areas stained for fibrinogen and the “a” subunit of
factor XIII. Staining was minimal or absent for protein C, protein S, plasminogen
activator inhibitors 1-3, factor VII, factor X, and fibrin (the antigenic site on
the amino-terminal portion of Bβ chain that is exposed following thrombin cleavage
of fibrinopeptide B was not detected). The lack of an intact thrombin- generating
pathway in situ associated with viable colon cancer cells is consistent with the findings
of others that coagulation activation in colon cancer may be triggered by a soluble
tumor product that exerts its effect at sites distant from the tumor. These results
may explain the absence of clinical responsiveness of colon cancer to antithrombotic
drug therapy and may clarify therapeutic strategies for this common tumor.
Keywords
Blood coagulation - Colon cancer