By Judith E. Karp
This is a well timed compilation of recent ideas within the molecular pathogenesis and molecular remedy of acute myelogenous leukemia (AML). the focal point is on chosen severe molecular determinants of AML pathogenesis and pathophysiology and the exploitation of those components by way of varied healing brokers and modalities. there's an emphasis all through at the bidirectional move of data among the scientific and laboratory arenas.
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In addition, we find that C/EBPap30 retains the ability to activate the bcl-2 promoter and inhibit apoptosis. CIEBPaLZ oncoproteins, which cannot bind DNA, also activate the bcl-2 promoter. They may do so by interacting with the p50 subunit of nuclear factor (NF)-KB bound to KB promoter sites. The ClEBPa residue s that contact NF-KB p50 lie on the outer surface of the a-helical BR. This finding offers an explanation for why most ClEBPaLZ mutations are inframe and spare the BR (104). Reduced expression or activity of C/EBPa may contribute to myeloid transformation by impeding differentiation and by dimini shing the antiproliferative effect of intact ClEBPa.
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