Thromb Haemost 1989; 62(04): 1062-1066
DOI: 10.1055/s-0038-1647118
Original Article
Coagulation
Schattauer GmbH Stuttgart

Indirect Activation of Blood Coagulation in Colon Cancer

Marek Z Wojtukiewicz
1   The Department of Medicine, Dartmouth Medical School, Vermont, USA
3   The VA Medical Center, White River Junction, Vermont, USA
,
Leo R Zacharski
1   The Department of Medicine, Dartmouth Medical School, Vermont, USA
3   The VA Medical Center, White River Junction, Vermont, USA
,
Vincent A Memoli
2   The Department of Pathology, Dartmouth Medical School, Vermont, USA
,
Walter Kisiel
4   The Department of Pathology, University of New Mexico School of Medicine, Albuquerque, New Mexico
,
Bohdan J Kudryk
5   The Plasma Protein-Coagulation Laboratory, New York Blood Center, New York, New York
,
Sandra M Rousseau
3   The VA Medical Center, White River Junction, Vermont, USA
,
David C Stump
6   The Departments of Medicine and Biochemistry, University of Vermont Medical School, Burlington, Vermont, USA
› Author Affiliations
Further Information

Publication History

Received 21 April 1989

Accepted after revision 22 August 1989

Publication Date:
24 July 2018 (online)

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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.