The molecular pathology of acute myeloid leukemia.
The pathogenesis of acute myelogenous leukemia (AML) involves an array of molecular alterations that disrupt almost every facet of cell transformation. These processes include the regulation of cell proliferation, differentiation, self-renewal, survival, cell cycle checkpoint control, DNA repair and chromatin stability, and cell dissemination. Normal regulatory networks are disrupted or usurped by these leukemogenic insults, and the understanding of these alterations is guiding the design of new therapeutic strategies. This overview describes some of the critical molecular alterations and implicates the rogue leukemogenic proteins in the onset and progression of AML.
Licht
Jonathan D
JD
Mt. Sinai School of Medicine, Division of Hematology/Oncology, One Gustave L. Levy Pl., Box 1079, New York, NY 10029-6504, USA. jonathan.licht@mssm.edu
Sternberg
David W
DW
D002453:Cell Cycle; D016923:Cell Death; D002454:Cell Differentiation; D002455:Cell Division; D002470:Cell Survival; D002471:Cell Transformation, Neoplastic; D018450:Disease Progression; D015321:Gene Rearrangement; D042822:Genomic Instability; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000235:genetics* / Q000473:pathology*; D009154:Mutation; D009363:Neoplasm Proteins / Q000502:physiology; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism
D009363:Neoplasm Proteins; D014157:Transcription Factors