Proceedings of the National Academy of Sciences of the United States of America

About the PNAS Member Editor
Name Coller, Barry S.
Location The Rockefeller University
Primary Field Medical Genetics, Hematology and Oncology
Secondary Field Medical Physiology and Metabolism
 Election Citation
Coller is a leader in investigating platelet physiology, vascular biology and adhesion phenomena in sickle cell disease. He produced monoclonal antibodies that inhibit platelet aggregation and adhesion of sickle red blood cells to the blood vessel walls. One of these antibodies has been developed into a drug routinely used after angioplasty in humans. He has also identified mutations in genes that cause a human bleeding disorder.
 Research Interests
Blood platelets help to arrest bleeding at sites of vascular injury by adhering to damaged blood vessels, aggregating one with another, and facilitating thrombin generation and fibrin clot formation. Platelet abnormalities, therefore, result in excessive bleeding. Platelets also contribute to thrombotic vascular disease since platelet aggregation can close off a blood vessel that is narrowed by atherosclerosis, resulting in a myocardial infarction or stroke. By studying human genetic disorders of platelet surface receptors, I and others identified the GPIIb/IIIa (IIb 3) integrin receptor as important in platelet aggregation. I then produced monoclonal antibodies that block the binding of ligands to the receptor, and thus prevent platelet aggregation. I helped to develop one of these antibodies into a drug (abciximab; Centocor) that prevents thrombotic complications of coronary angioplasty and stent placement. It is now being evaluated as treatment for stroke. Recently, I began collaborative studies to understand better the vascular complications of sickle cell disease, including stroke and episodes of severe bone pain. We have identified the V 3 integrin receptor and adherent leukocytes as important in producing blood vessel obstruction by sickle cells. We are now testing new therapeutic interventions to inhibit the interactions between leukocytes, sickle red blood cells, and the blood vessel wall.

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