.............................................................2005 | .2004 | 2003 | 2002 | 2001 | 2000
 |
||
 |
||
 |
||
 |
||
 |
||
 |
|
|
|
|
|
|
|
Grants Awarded |
|
||
 |
||
 |
||
 |
||
 |
||
 |
||
 |
||
 |
||
2004
Alison Moliterno, MD
John Hopkins
"Proteomic Approach to the Diagnosis of Chronic MPD's."
The long-term goal of this project is to define the protein signature of platelets in patients with Chronic MPD’s. By comparing different profiles we hope to identify characteristics associated with each particular disease, clotting risk, or disease transformation. Platelet proteins are easily obtained from patients in a clinical setting.
Mingjiang Xu, MD, Ph.D.
University of Illinois, at Chicago
"Exploration of a unique phosphatase as a potential therapeudic target
for treatment of PV."
Investigation of abnormal functioning of protein tyrosine phosphatases(PTP) patients which is activated by PTP-MEG2. Investigate the role of PTP-MEG2 and whether it can serve as a good target for drugs which can be used to treat PV. This study would target a potential molecular mechanism underlying the pathobiology of PV.
Ron Hoffman, MD
University of Illinois at Chicago
"Continuation of 2003 grant. "
Organizational grant for International MPD Research Consortium in application for $25 million grant from NCI.
Jose Lopez, MD
Baylor College of Medicine
"Macrophage-derived Prothrombotic Microparticles and Thrombosis in Myeloproliferative
Disorders."
One of the most striking and unexplained features of MPDs are clots at unusual sites, such as in the veins coming out of the liver. Because platelets arise from the abnormla cells causing the MPDs, they have been blamed for the abnormal clotting. However, platelets normally do not participate in the formation of clots in veins. We propose that the clots observed in pstients suffering from MPDs are caused by the production of a clotting factor released from cells in the liver, called Kupffer cells. Because Kupffer cels derive from blood cells, they too are affected by mutations causing the MPDs. We hypothesize that these mutations render Kupffer cells hyper-reactive to compounds present in very high concentrations in the blood arriving from the gut. These compounds stimulate Kupffer cells to produce large amounts of the clotting factor, which may then produce clots in the veins coming out of the liver, as well as in other parts of the body. We expect this work to shed light on the causes of excessive clotting patients with MPDs and to lead to improvements in its therapy.
