By Farhad Ravandi, Francis Giles (auth.), Judith E. Karp MD (eds.)
Acute Myelogenous Leukemia is a well timed compilation of recent recommendations 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 diversified healing brokers and modalities. Bringing jointly new thoughts and findings within the easy and scientific technology of AML, the booklet emphasizes the molecular foundation for brand spanking new treatments that stand to have the best power impression at the scientific face of those ailments. The textual content offers insights into chosen novel techniques 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 circulate of information among the medical and laboratory arenas, and either uncomplicated and scientific scientists will reap the benefits of this translational textual content.
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However, RA target genes required for myeloid differentiation have not been delineated, and so effects on RA-mediated stem cell differentiation, proliferation, or survival may be more relevant to transformation (145). In addition to inhibiting RARa functions, PML-RARa interferes with the functions of PML and PML nuclear bodies, thereby inhibiting apoptosis in response to a variety of stimuli and contributing to genomic instability (146). The reciprocal translocation product RARa-PML accelerates leukemogenesis induced by PML-RARa in a murine model, suggesting that it may also inhibit PML functions and contribute to transformation (147).
Miyoshi H, Kozu T, Shimizu K, et al. The t(8;21) translocation in acute myeloid leukemia results in production of an AMLl-MTG8 fusion transcript. EMBO J 1993;12:2715-2721. 18. Meyers S, Lenny N, Hiebert Sw. The t(8;21) fusion protein interferes with AML-I B-dependent transcriptional activation. Mol Cell Bioi 1995; 15:1974-1982. 19. Wang J, Hishono T, Redner RL, Kajigaya S, Liu JM. ETO, fusion partner in t(8;21) acute myeloid leukemia, represses transcription by interaction with the human N-CoR/mSin3/HDACI complex.
Castilla LH, Wijmenga C, Stacy T, et al. Failure of embryonic hematopoiesis and lethal hemorrhages in mouse embryos heterozygous for a knocked-in leukemia gene CBFB-MYH11. Cell 1996;87:687-696. 29. Yergeau DA, Hetherington CJ, Wang Q, et al. Embryonic lethality and impairment of haematopoiesis in mice heterozygous for an AMLl-ETO fusion gene. Nat Genet 1997;15:303-306. 30. Okuda T, Cai Z, Yang S, et al. Expression of a knocked-in AMLl-ETO leukemia gene inhibits the establishment of normal definitive hematopoiesis and directly generates dysplastic hematopoietic progenitors.
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