Download e-book for kindle: Acute Myelogenous Leukemia (Contemporary Hematology) by Judith E. Karp

By Judith E. Karp

ISBN-10: 1588296210

ISBN-13: 9781588296214

This is a well timed compilation of latest suggestions 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 components by means of different healing brokers and modalities. there's an emphasis all through at the bidirectional movement of information among the medical and laboratory arenas.

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Huang S, Houghton Pl. Targeting mTOR signaling for cancer therapy. Curr Opin PharmacoI2003;3:371-377. II MOLECULAR FOUNDATIONS OF AML PATHOGENESIS AND PHYSIOLOGY 2 Aberrant Transcription Factors in AML Alan D. Friedman CONTENTS INTRODUCTION ABERRANT TRANSCRIPTION FACfORS ASSOCIATED WITH AML FUTURE DlRECTIONSITHERAPEUTIC TARGETING REFERENCES Summary Several transcription factors both playa central role in normal hematopoiesis and are altered in subset s of acute myeloid leukemia (AML ). I , and RARa control myeloid development, and GATA-I is required for erythroid and megakaryocytic development.

Anti-sense inhibition of c-Myb reduces the proliferation of normal hematopoietic progenitors and of AML blasts (46). v-Myb induces an avian myeloproliferative disease and is activated, unlike c-Myb, by deletion ofthe C-terminal negative regulatory domain and by additional point mutations (47). 't-A G1 to S transition \)" c~c\\«I. c Sp/? Myeloid differentiation Fig. 2. Model for transformation by CBF oncoproteins and AMLl mutations. These alterations are expected to contribute to myeloid transformation by inhibiting differentiation, via inhibition of target genes such as MPO , NE, and MCSFR, and by inhibiting apoptosis in response to stress conditions such as DNA damage, hypoxia, or excessive cytokine signaling via inhibition of p14ARF-dependent and independent p53 induction.

In addition, EVI-1 prevents granulocytic differentiation in response to G-CSF (94). The AML1-EVIl fusion protein expressed from t(3;21) in a small proportion of therapy related MDSIAML or CML blast crisis cases shares many of the activities of EVI-1, including inhibition ofTGF-~ signaling and blockade of granulocytic maturation (92,93). 7. CIEBPa CCAAT/Enhancer binding protein a (C/EBPa) binds DNA via its C-terminal basic region leucine zipper (bZIP) motif and activates transcription via N-terminal transactivation domains (TADs) (95,96).

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Acute Myelogenous Leukemia (Contemporary Hematology) by Judith E. Karp

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