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49 2004). By the same approach we will assess the functional consequences of inactivating candidate genes identified in our studies of 9pLOH and familial form of MPD-like disorders. The ultimate goal is to identify the primary molecular defect(s) in MPD and secondary mutations that are associated with disease progression. This information will be used to improve clinical management of disease in these patients and will open possibilities for finding new effective treatments. Figure 4: Hypothetical model for the pathogenesis of myeloproliferative disorders. At least two mutations are needed for phenotypic manifestation of MPD. These mutations convey to cells of the MPD clone hypersensitivity to incoming stimulatory signals and resistance to inhibitory signals. The latter may explain why only blood cells descending from the MPD clone are found in peripheral blood (clonal dominance).