Researchers from Harvard Medical School, Boston, have found that most individuals with acute myeloid leukemia (AML) inappropriately express a protein known as CDX2 in their leukemic cells.
CDX2 regulates the expression of a number of genes that encode members of the HOX family of proteins, which might provide a new set of targets for the treatment of individuals with AML.
In the study, which appears in the April print issue of the Journal of Clinical Investigation, Stefan Fröhling and colleagues show that the gene encoding CDX2 is expressed in 90% of the patients with AML that they analyzed. Moreover, reducing the amount of CDX2 in human AML cell lines decreased their ability to proliferate, indicating that CDX2 has a causal role in the pathogenesis of AML.
Further evidence of this was provided by the observation that mouse hematopoietic cells engineered to express CDX2 were induced to proliferate and were able to cause full-blown AML when transplanted into mice. Expression of CDX2 in the mouse hematopoietic cells induced altered expression of a number of genes that encode HOX family of proteins, leading the authors to conclude that aberrant expression of CDX2 drives the dysregulated HOX gene expression observed in most individuals with AML.
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