Acute Myelogenous Leukemia by Farhad Ravandi, Francis Giles (auth.), Judith E. Karp MD

By Farhad Ravandi, Francis Giles (auth.), Judith E. Karp MD (eds.)

Acute Myelogenous Leukemia is a well timed compilation of recent techniques within the molecular pathogenesis and molecular treatment of acute myelogenous leukemia (AML). the point of interest is on chosen serious molecular determinants of AML pathogenesis and pathophysiology and the exploitation of those elements by means of various healing brokers and modalities. Bringing jointly new recommendations and findings within the easy and medical technological know-how of AML, the booklet emphasizes the molecular foundation for brand new treatments that stand to have the best strength influence at the scientific face of those ailments. The textual content presents insights into chosen novel suggestions at the moment and prospectively being constructed, together with interruption of particular sign transduction pathways, modulation of gene expression, makes an attempt to reinstate differentiation, and immunomodulation. there's an emphasis all through at the bidirectional circulation of information among the medical and laboratory arenas, and either uncomplicated and medical scientists will take advantage of this translational textual content.

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Mechanism of constitutive activation of FLT3 with internal tandem duplication in the juxtamembrane domain. Oncogene 2002;21:2555-2563. 119. Kelly LM, Liu Q, Kutok JL, Williams IR, Boulton CL, Gilliland DG. FLT3 internal tandem duplication mutations associated with human acute myeloid leukemias induce myeloproliferative disease in a murine bone marrow transplant model. Blood 2002;99:310-318. 120. Yamamoto Y, Kiyoi H, Nakano Y, et al. Activating mutation of D835 within the activation loop of FLT3 in human hematological malignancies.

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These fusion proteins retain the N-terminal MLL DNA binding but lack the histone methyltransferase domain. Nevertheless, MLL oncoproteins apparently have increased transcriptional activation potency compared with MLL (55-57). The ENL domain of MLL-ENL directly activates transcription, whereas the ELL domain of MLL-ELL interacts with the transcriptionally active EAFI or EAF2 cofactors (58). In an additional set of fusion proteins, such as MLL-GAS7 or MLL-AFlp, the fusion partner appears to primarily mediate formation of MLL domain homodimers, which themselves have increased trans activating potency (59).

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