McMaster University

McMaster University

Mark WC Hatton

, PhD

Professor Emeritus
Pathology and Molecular Medicine

3N26G Health Sciences Centre
McMaster University
905-525-9140 ext. 22371

Mark WC Hatton

Faculty Biography

Education and Professional Standing

  • Ph.D. University of London (UK) 1972
  • M.Sc. University of London (UK) 1967
  • B.Sc. University of London (UK) 1964
  • Retired from active research in 2006


Research Focus

Over recent years, my research was directed to comparing the dynamics of hemostasis in (a) an intravascular model of coagulation (the acutely-de-endothelialized aorta wall), and (b) in an extravascular model of coagulation (the procoagulant VX-2 lung tumor) in rabbits. For this purpose, interactions between individual radiolabelled rabbit blood proteins and/or radiolabelled rabbit platelets at the site of arterial injury, or within the VX-2 tumor stroma, were measured in vitro and in vivo. Using the VX-2 tumour model, the effusion of hemostasis proteins (and their metabolic products) from the tumour stroma to the interpleural space in vivo was also measured. In addition, observations of antiangiogenic components (angiostatin, D-dimer) in interpleural effusates were compared to similar components in ascites fluid samples obtained from ovarian cancer patients. Rabbit proteins (and their products of catabolism) of past interest included: fibrinogen; prothrombin (thrombin), antithrombin (α, β), heparin cofactor II; factors VII, IX, X, XIII; plasminogen (types I and II), α2-antiplasmin; fibronectin, vitronectin and von Willebrand factor. The ultimate objective was to construct and compare models of hemostasis that take place after arterial injury/healing, and during tumor growth in vivo.

Team Members

I thank all who have worked with me during my research career in the department of Pathology at McMaster. Particular thanks go to Marnie DeReske Timleck, Dr. Mary Richardson, Bonnie Ross, Arlene Scopaz and Suzanne Southward. Without help from these and many other colleagues in the past, much of what I have done would not be conceivable let alone possible.

Selected Publications

  • Hatton MWC, Ross B, Timleck M, Southward SMR, Richardson M. Turnover and fate of fibrinogen and platelets at the surface of the aorta wall immediately after an acute balloon de-endothelializing injury in vivo. Thromb Haemostas  2006; 96: 60-7.
  • Jandu N, Richardson M, Singh G, Hirte HW, Hatton MWC. Human ovarian cancer ascites fluid contains a mixture of completely and incompletely degraded soluble products of fibrin that collectively possess an anti-angiogenic property. Int Gynecol Canc 2006; 16: 1536-1545
  • Hatton MWC, Southward SMR, Ross BL, Clarke BJ, Singh G, Richardson M.  Relationships between tumor burden, tumor size, and the changing concentrations of fibrin degradation products and fibrinolytic factors in the pleural effusions of rabbits with VX2 lung tumors. J Lab Clin Med, 2006; 147: 27-35.
  • Hatton MWC, Southward SMR, Legault K, Ross BL, Clarke BJ, Blajchman MA, Singh G, Richardson M. Fibrinogen catabolism within the procoagulant VX-2 tumor of rabbit lungs in vivo: Effluxing fibrin(ogen) fragments contain an antiangiogenic activity. J Lab Clin Med 2004; 143: 241-254.
  • Richardson M, Gunawan J, Hatton MWC, Seidlitz E, Hirte H, Singh G. Malignant ascites fluid (MAF), including ovarian cancer-associated MAF, contains angiostatin and other factor(s) that inhibit angiogenesis. Gynecol Oncol 2002; 86: 279-287.
  • Hatton MWC, Ross B, Southward SMR. Timleck-DeReske M, Richardson M. Platelet and fibrinogen turnover at the exposed subendothelium measured over 1 year after a balloon catheter injury to the rabbit aorta: Thrombotic eruption at the late re-endothelialization stage. Atherosclerosis 2002; 165: 57-67.
  • Hatton MWC, Southward SMR, Ross B, Legault K, Marien L, Korbie D, Richardson M, Singh G, Clarke BJ, Blajchman MA. Angiostatin-II is the predominant glycoform in pleural effusates of rabbit VX-2 lung tumors. J Lab Clin Med 2002; 139: 316-323.
  • Hatton MWC, Blajchman MA, Sridhara S, Southward SMR, Ross B, Kulzcycky M, Clarke BJ. Metabolism of rabbit plasma-derived factor VII in relation to prothrombin in rabbits. Am J Physiol [Endoc. Metab.] 2001; 281: E507-E515.
  • Hatton MWC, Day S, Southward SMR, DeReske M, Ross B, Seidlitz E, Singh G, Richardson, M. Metabolism of rabbit angiostatin glycoforms I and II in rabbits: Angiostatin-I leaves the intravascular space faster and appears to have greater anti-angiogenic activity than angiostatin-II. J Lab Clin Med 2001; 138: 83-93.
  • Hatton MWC, Ross B, Southward SMR, DeReske M, Blajchman MA. The procoagulant state of the VX-2 tumor in rabbit lung in vivo: relative accumulation of fibrinogen, prothrombin, plasminogen, antithrombin and heparin cofactor II within the tumor. Thrombosis & Haemostasis 1999; 82: 1694-1702.
  • Hatton MWC, Day S, Ross B, Southward SMR, DeReske M, Richardson M. Plasminogen-II accumulates five times faster than plasminogen-I at the site of a balloon de-endothelializing injury in vivo to the rabbit aorta. J Lab Clin Med 1999; 134 : 260-266.
  • Hatton MWC, Ross B, Southward SMR, DeReske M, Richardson M: Pretreatment with Hirudin or Ancrod or Warfarin decreases the adsorption of fibrinogen and platelets by the de-endothelialized rabbit aorta wall immediately after balloon catheter injury in vivo. Arterioscler Thromb Vasc Biol 1998; 18: 816-824.
  • Hatton MWC, Hoogendoorn H, Southward SMR, Ross B, Blajchman MA. Comparative metabolism and distribution of rabbit heparin cofactor-II and rabbit antithrombin in rabbits. Am J Physiol [Endocrin Metab 35] 1997; 272: E824-E831.
  • Hatton MWC, Southward SMR, Ross-Ouellet B, DeReske M, Blajchman MA, Richardson M. An increased uptake of prothrombin, antithrombin and fibrinogen by the rabbit balloon-deendothelialized aorta surface in vivo is maintained until reendothelialization is complete. Arterioscler Thromb Vasc Biol 1996; 16: 1147-1155.
  • Witmer M, Hatton MWC: Antithrombin III-ß associates more readily than -a with the uninjured and de-endothelialized rabbit aorta wall in vitro and in vivo. Arterioscler Thrombos 1991; 11: 530-539
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