By Judith E. Karp
This is a well timed compilation of latest innovations 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 various healing brokers and modalities. there's an emphasis all through at the bidirectional movement of information among the medical and laboratory arenas.
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Additional info for Acute Myelogenous Leukemia (Contemporary Hematology)
An alternatively spliced form, MDSlIEVIl, is extended at its N-terminus by 188 residues, the PR domain, and does not bind CtBP (89). Although detected in human CD34+ cells (90), the function of EVI-1 in normal stem/progenitor cells is uncertain. Translocations involving 3q26 elevate EVI-l expression in 1-2% of AML cases, most likely as a result of juxtaposition with a more active promoter (91). In an additional 10% of AML cases, Part II I Friedman 32 EVI-1 is overexpressed in the absence of evident chromosomal abnormalities and predicts a poor prognosis (90).
Each of the RARa fusions retains the RARa DNA-binding and ligand-binding domain. PML provides a coiled-coil domain that allows PML-RARa to bind DNA as a homodimer. The RARa segment of PMLRARa binds the N-CoR histone deacetylase corepressor complex, and this interaction is only relieved by pharmacological doses of retinoic acid (RA) (141-143). Inhibition of RARa target genes by RARa fusion oncoproteins may account for their ability to arrest myeloid differentiation at the promyelocytic stage (144).
A synthetic inhibitor of the mitogen-activated protein kinase cascade. Proc Nat! Acad Sci USA 1995;92:7686-7689. 190. Favata MF, Horiuchi KY, Manos EJ, et al. Identification of a novel inhibitor of mitogen-activated protein kinase kinase. J Bioi Chern 1998;273:18,623-18,632. 191. Sebolt-Leopold JS. Development of anticancer drugs targeting the MAP kinase pathway. Oncogene 2000; 19:6594--6599. 192. Powis G, Bonjouklian R, Berggren MM, et al. Wortmannin, a potent and selective inhibitor of phosphatidylinositol-3- kinase.