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2002
Vahid Afshar-Kharghan
MD Baylor College of Medicine
"Genetic factors that influence platelet function in PV and ET, and their
effect on the frequency of thrombotic complications."
One of the most important complications of myeloproliferative disorders is the organ damage caused by occlusion of blood vessels such as stroke or heart attack. Bleeding is also a common problem among patients with myeloproliferative disorders. Currently, we cannot predict which patient will develop a thrombotic (occlusion of blood flow) or hemorrhagic complication. The number and function of blood cells (including platelets) are abnormal in patients with myeloproliferative disorders. Platelets play an important role in the formation of blood clots and cessation of bleeding in normal individuals. In patients with myeloproliferative disorders, in addition to having an abnormal platelet count, platelet function is frequently altered. The change in platelet function is not similar among all patients with myeloproliferative disorders. Some of these patients have platelets that have less activity compared to normal platelets (hypoactive), while others have platelets that are hyperactive. We propose that the level of platelet activity determines which patients are at a higher risk of thrombosis and which ones are at risk of bleeding complication. We will identify the inherited and acquired factors that modulate platelet function in patients with myeloproliferative disorders, and will try to determine new risk factors that can be used to predict the risk of developing thrombotic or bleeding problems.
Dr. Josef Prchal
Baylor College of Medicine
"Continuation of 2001 Grant"
The principal goal of the Research Proposal is to find the cause of Essential Thrombocythemia (ET) by identifying the gene(s) and its (their) mutation(s) that cause Essential Thrombocythemia (ET.) Additionally, we will attempt to identify the mutations of genes causing congenital thrombocythemia. We believe that successful fulfillment of this goal is an essential prerequisite for a) accurate and rapid diagnosis of ET, b) design of rational specific therapeutic strategies, and c) eventual cure of ET.
Dr. Josef Prchal
Baylor College of Medicine
"Continuation of 2000 Grant"
Polycythemia Vera (PV) is an acquired clonal myeloproliferative disorder. Our ultimate aim in identification of the gene or genes that lead to the development of PV phenotype - an essential requirement for the development of specific PV therapy and ultilmate PV cure. Based on our on-going evaluation of the accumulating data, it appears that the first acquired mutation is a loss of inhibitory function by another genetic event(s) necessary for full PV (and ET) phenotype. There is frequent overlap of PV and ET. Some PV Patients first present with thrombocytosis without elevation of red cell mass that may preceed by even several years the development of full PV phenotype; yet these subjects already have a PV specific defect, i.e. the presence of EPO independent crythroid progenitors when tested in vitro in the presence of scrum. We believe that the delineation of ET lesion will help to clarify the clinical complexity of PV phenotype.
