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 serious molecular determinants of AML pathogenesis and pathophysiology and the exploitation of those elements through various healing brokers and modalities. there's an emphasis all through at the bidirectional stream of data among the medical and laboratory arenas.
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Extra info for Acute Myelogenous Leukemia (Contemporary Hematology)
Smith BD, Levis M, Beran M, Small D, et al. Single-agent CEP-701, a novel FLT3 inhibitor, shows biological and clinical activity in patients with relapsed or refractory acute myeloid leukemia. Blood 2004;103(10): 3669-3676. 125. O'Farrell AM, Yuen HA, Smolich B, et al. SU5416, a small molecule tyrosine kinase receptor inhibitor, on FLT3 expression and phosphorylation in patients with refractory acute myeloid leukemia. Leuk Res 2004; (7):679-689. 126. Beaupre DM, Kurzrock R. RAS and leukemia: from basic mechanisms to gene-directed therapy.
Inhibition of CIEBPa expression and activity is a common feature of AML and arises through several mechanisms. The human C/EBPa promoter is directly bound and activated by CBF; therefore, reduction of CBF activities due to point mutation of the AMLl gene or to expression of the AMLl-ETO or CBF~-SMMHC from the t(8;21) or inv(16) chromosomes is expected to reduce C/EBPa gene transcription (105). Signaling from the constitutively active flt3 receptor (flt3ITD) present in 30% of AML cases also represses C/EBPa mRNA expression (106).
8. Wang Q, Stacy T, Binder M, Marin-Padilla M, Sharpe AH, Speck NA. Disruption of the Cbfa2 gene causes necrosis and hemorrhaging in the central nervous system and blocks definitive hematopoiesis. Proc Nat! Acad Sci USA 1996;93:3444-3449. 9. Wang Q, Stacy T, Miller JD, et al. The CBF~ subunit is essential for CBFa2(AMLl) function in vivo. Cell 1996;87 :697-708. 10. Sasaki K, Yagi H, Bronson RT, et al. Absence offetalliver hematopoiesis in mice deficient in transcriptional coactivator core binding factor B, Proc Nat!