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Transcriptional dysregulation during myeloid transformation in AML
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Journal Article
Transcriptional dysregulation during myeloid transformation in AML
2007
Overview
The current paradigm on leukemogenesis indicates that leukemias are propagated by leukemic stem cells. The genomic events and pathways involved in the transformation of hematopoietic precursors into leukemic stem cells are increasingly understood. This concept is based on genomic mutations or functional dysregulation of transcription factors in malignant cells of patients with acute myeloid leukemia (AML). Loss of the CCAAT/enhancer binding protein-α (
CEBPA
) function in myeloid cells
in vitro
and
in vivo
leads to a differentiation block, similar to that observed in blasts from AML patients.
CEBPA
alterations in specific subgroups of AML comprise genomic mutations leading to dominant-negative mutant proteins, transcriptional suppression by leukemic fusion proteins, translational inhibition by activated RNA-binding proteins, and functional inhibition by phosphorylation or increased proteasomal-dependent degradation. The
PU.1
gene can be mutated or its expression or function can be blocked by leukemogenic fusion proteins in AML. Point mutations in the
RUNX1/AML1
gene are also observed in specific subtypes of AML, in addition to
RUNX1
being the most frequent target for chromosomal translocation in AML. These data are persuasive evidence that impaired function of particular transcription factors contributes directly to the development of human AML, and restoring their function represents a promising target for novel therapeutic strategies in AML.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Animals
/ CCAAT/enhancer-binding protein
/ Cell Transformation, Neoplastic - genetics
/ Cell Transformation, Neoplastic - metabolism
/ Cell Transformation, Neoplastic - pathology
/ Control
/ Genes
/ Genomics
/ Humans
/ Leukemia
/ Leukemia, Myeloid - genetics
/ Leukemia, Myeloid - metabolism
/ Leukemia, Myeloid - pathology
/ Medicine
/ Mutation
/ Oncology
/ Proteins
/ review
