Acute Promyelocytic Leukemia: A view from a mouse

Blood Cells, Molecules, and Diseases

Volumn 26, Issue 6, 2000, Pages 620-625

  Kogan, Scott C ^a  

^a UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ARSENIC; CALCIUM BINDING PROTEIN; HYBRID PROTEIN; RETINOIC ACID;

ACUTE GRANULOCYTIC LEUKEMIA; ACUTE MYELOBLASTIC LEUKEMIA; ANIMAL CELL; ANIMAL MODEL; CANCER CHEMOTHERAPY; CANCER SURVIVAL; CANCER THERAPY; GENE TARGETING; GENE TRANSLOCATION; MOUSE; NONHUMAN; PATHOGENESIS; PRIORITY JOURNAL; REVIEW; SUPPRESSOR GENE; TRANSGENE;

MURINAE; MUS MUSCULUS;

EID: 0034474545     PISSN: 10799796     EISSN: None     Source Type: Journal    
DOI: 10.1006/bcmd.2000.0345     Document Type: Article

References (9)

1. 15/17 translocation, a consistent chromosomal change in acute promyelocytic leukaemia
2. Deconstructing a disease: RARalpha, its fusion partners, and their roles in the pathogenesis of acute promyelocytic leukemia
3. bcl-2 inhibits apoptosis of neutrophils but not their engulfment by macrophages
4. A PMLRAR alpha transgene initiates murine acute promyelocytic leukemia
5. Leukemia initiated by PMLRARalpha: The PML domain plays a critical role while retinoic acid-mediated transactivation is dispensable
6. The incidence of acute promyelocytic leukemia appears constant over most of a human lifespan, implying only one rate limiting mutation
7. Retinoic acid and arsenic synergize to eradicate leukemic cells in a mouse model of acute promyelocytic leukemia
8. PMLRARalpha induces ATRAsensitive delocalization of the critical granulocytic differentiation factor C/EBPalpha to a microspeckled nuclear pattern in t(15;17) APL
9. CCAAT/enhancer binding protein epsilon is a potential retinoid target gene in acute promyelocytic leukemia treatment