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

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

ISBN-10: 1588296210

ISBN-13: 9781588296214

ISBN-10: 1597453226

ISBN-13: 9781597453226

Acute Myelogenous Leukemia is a well timed compilation of recent options within the molecular pathogenesis and molecular treatment 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 components through different healing brokers and modalities. Bringing jointly new options and findings within the uncomplicated and medical technology of AML, the booklet emphasizes the molecular foundation for brand new cures that stand to have the best strength effect at the scientific face of those illnesses. The textual content offers insights into chosen novel options at the moment and prospectively being built, 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 simple and medical scientists will make the most of this translational textual content.

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Extra resources for Acute Myelogenous Leukemia

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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). In this study of 319 patients, elevated MDS1IEVIl was seen in 5% of cases and did not correlate with outcome.

81. Feldman EJ, Brandwein J, Stone R, et al. Phase III randomized multicenter study of a humanized anti-CD33 monoclonal antibody, lintuzumab, in combination with chemotherapy, vs chemotherapy alone in patients with refractory or first-relapsed acute myeloid leukemia. J Clin Oncol 2005;23(18):4110-4116. 82. Sievers EL, Appelbaum FR, Spielberger RT, et al. Selective ablation of acute myeloid leukemia using antibody-targeted chemotherapy: a phase I study of an anti-CD33 calicheamicin immunoconjugate.

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).

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

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