There is abundant evidence that t-MDS and AML are clonal disorders. Multiple cytogenetic abnormalities, including deletions (5q, 7q, 20q), numerical abnormalities (trisomy 8, deletion 7) and translocations [11q23, t(3;21), t(15;17) and clonal point mutations of RAS, FLT3 and AML1], have been identified in t-MDS/AML. Population-based analysis of clon-ality using X-inactivation assays in females has convincingly demonstrated that t-MDS/AML is a clonal disease. Thus, t-MDS/AML is a clonal disease that is the consequence of an acquired somatic mutation that confers a proliferative and/or survival advantage on hematopoietic progenitors.
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