Abstract
A dissection of the genetic networks and circuitries is described for two form of leukaemia. Integrating transcription factor binding and gene expression profiling, networks are revealed that underly this important human disease.
Highlights
Acute myeloid leukemia (AML) comprises a group of diseases characterized by the abnormal development of malignant myeloid cells
Several chromosomal fusion proteins and myeloid transcription factor (TF) involved in leukemia have been identified and studied independently, how each individual TF interacts with others, and how each regulatory pathway correlates with others, remains unclear
Gene expression profiles were obtained from cultured bone marrow cells that are stimulated with the granulocyte colonystimulating factor (G-CSF) growth factor to simulate the in vivo myeloid differentiation program [30]
Summary
Acute myeloid leukemia (AML) comprises a group of diseases characterized by the abnormal development of malignant myeloid cells. Several transcription factors (TFs) involved in myeloid development and leukemia have been studied extensively and independently, how these TFs coordinate with others and how their dysregulation perturbs the genetic circuitry underlying myeloid differentiation is not yet known. Several chromosomal fusion proteins and myeloid TFs involved in leukemia have been identified and studied independently, how each individual TF interacts with others, and how each regulatory pathway correlates with others, remains unclear. Such comprehensive delineation of the genetic networks underlying both normal myeloid differentiation and leukemia is crucial to better understand AML pathophysiology and to develop improved therapeutic strategies
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