Abnormalities of the CEBP alpha transcription factor: A major target in acute myeloid leukemia

Leukemia

Volumn 15, Issue 4, 2001, Pages 688-689

  Tenen, D G ^a  

^a HARVARD INSTITUTES OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

BCR ABL PROTEIN; CCAAT ENHANCER BINDING PROTEIN ALPHA; GENE PRODUCT; HYBRID PROTEIN; PROTEIN TYROSINE KINASE INHIBITOR; RETINOIC ACID RECEPTOR;

ACUTE GRANULOCYTIC LEUKEMIA; ANIMAL EXPERIMENT; ANIMAL MODEL; BLAST CELL; CHROMOSOME TRANSLOCATION 22; CHROMOSOME TRANSLOCATION 8; GENE EXPRESSION REGULATION; GENE MUTATION; GENE REPRESSION; GENE TARGETING; GENETIC SCREENING; GRANULOCYTE; IMMUNOHISTOCHEMISTRY; KNOCKOUT MOUSE; LEUKEMOGENESIS; MOUSE; NONHUMAN; PATHOGENESIS; PRIORITY JOURNAL; REVIEW; TRANSCRIPTION REGULATION;

EID: 0035071416     PISSN: 08876924     EISSN: None     Source Type: Journal    
DOI: 10.1038/sj.leu.2402088     Document Type: Review

References (6)

1. CCAAT/enhancer binding protein alpha is a regulatory switch sufficient for induction of granulocytic development from bipotential myeloid progenitors
2. Transcription factors, normal myeloid development, and leukemia
3. Dominant negative mutations of the tumor suppressor CCAAT/enhancer binding protein alpha (C/EBP alpha) in acute myeloid leukemia
4. Upregulation of interleukin 6 and granulocyte colony-stimulating factor receptors by transcription factor CCAAT enhancer binding protein alpha (C/EBP alpha) is critical for granulopoiesis
5. PML/RARα induces ATRA-sensitive delocalization of the critical granulocytic differentiation factor C/EBP-α to a microspeckled nuclear pattern in t(15;17) APL
6. The t(8:21) fusion product, AML-1-ETO, associates with C/EBP-alpha, inhibits C/EBP-alpha-dependent transcription, and blocks granulocytic differentiation