By Farhad Ravandi, Francis Giles (auth.), Judith E. Karp MD (eds.)
Acute Myelogenous Leukemia is a well timed compilation of latest innovations within the molecular pathogenesis and molecular remedy of acute myelogenous leukemia (AML). the point of interest is on chosen severe molecular determinants of AML pathogenesis and pathophysiology and the exploitation of those elements via varied healing brokers and modalities. Bringing jointly new suggestions and findings within the simple and medical technological know-how of AML, the publication emphasizes the molecular foundation for brand spanking new remedies that stand to have the best power effect at the medical face of those ailments. The textual content presents insights into chosen novel options at present 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 move of data among the medical and laboratory arenas, and either simple and medical scientists will take advantage of this translational textual content.
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Extra info for Acute Myelogenous Leukemia
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.
Preferential alkylation by 1,3-bis 2-chloroethyl)-I-nitrosourea (BCND) of guanines with guanines as neighboring bases in DNA. Biochem PharmacoI1988;37:1061-1066. 68. Lown JW, McLaughlin LW. Nitrosourea-induced DNA single-strand breaks. Biochem Pharmacol 1979;28: 1631-1638. 69. Giles F, Thomas D, Garcia-Manero G, et al. A Phase I and pharmacokinetic study of VNP4010 1M, a novel sulfonylhydrazine alkylating agent, in patients with refractory leukemia. Clin Cancer Res 2004;10(9): 2908-2917. 70. Tanimoto M, Scheinberg DA, Cordon-Cardo C, Huie D, Clarkson BD, Old LJ.
N-terminal C/EBPa mutation s often produce frameshifts and premature stop codons, leading to a ribosome-scanning-mediated increase in translation from an internal ATG and expression of the C/EBPap30 oncoprotein. Mutations in the BR-LZ are usually inframe and generall y occur in the "hinge" region, between the LZ and the BR, or between the first and second leucines of the LZ, generating CIEBPaLZ oncoproteins that cannot bind DNA. (B) ClEBPa. oncoprotein s are expected to contribute to myeloid transformation by inhibiting myeloid differentiation.