scholarly journals The preferential occurrence ofFLT3-TKD mutations in inv(16) AML and impact on survival outcome: a combined analysis of 1053 core-binding factor AML patients

2012 ◽  
Vol 160 (4) ◽  
pp. 557-559 ◽  
Author(s):  
Chung H. Kok ◽  
Anna L. Brown ◽  
Michelle Perugini ◽  
Diana G. Iarossi ◽  
Ian D. Lewis ◽  
...  
Keyword(s):  
Survival Outcome ◽  
Core Binding Factor ◽  
Combined Analysis ◽  
Binding Factor ◽  
Impact On Survival

Identification of common and distinct epigenetic re-programming properties of Core-Binding Factor (CBF) Fusion Proteins

2016 ◽  
Vol 228 (03) ◽  
Author(s):  
J Loke ◽  
A Ptasinska ◽  
MR Imperato ◽  
SA Assi ◽  
P Cauchy ◽  
...  
Keyword(s):  
Fusion Proteins ◽  
Core Binding Factor ◽  
Binding Factor

Predictive value of molecular remissions postconsolidation chemotherapy in patients with Core Binding Factor Acute Myeloid Leukemia (CBF-AML) - a single center analysis

2016 ◽  
Vol 35 (4) ◽  
pp. 810-813 ◽  
Author(s):  
Uday Deotare ◽  
Marwan Shaheen ◽  
Joseph M. Brandwein ◽  
Bethany Pitcher ◽  
Suzanne Kamel-Reid ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Predictive Value ◽  
Myeloid Leukemia ◽  
Single Center ◽  
Core Binding Factor ◽  
Binding Factor ◽  
Acute Myeloid

scholarly journals Minimal residual disease eradication with epigenetic therapy in core binding factor acute myeloid leukemia

2017 ◽  
Vol 92 (9) ◽  
pp. 845-850 ◽  
Author(s):  
Brittany Knick Ragon ◽  
Naval Daver ◽  
Guillermo Garcia-Manero ◽  
Farhad Ravandi ◽  
Jorge Cortes ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Minimal Residual Disease ◽  
Myeloid Leukemia ◽  
Residual Disease ◽  
Epigenetic Therapy ◽  
Core Binding Factor ◽  
Disease Eradication ◽  
Binding Factor ◽  
Minimal Residual ◽  
Acute Myeloid

scholarly journals Population-based disparities in survival among patients with core-binding factor acute myeloid leukemia: A SEER database analysis

2014 ◽  
Vol 38 (7) ◽  
pp. 773-780 ◽  
Author(s):  
Andrew M. Brunner ◽  
Traci M. Blonquist ◽  
Hossein Sadrzadeh ◽  
Ashley M. Perry ◽  
Eyal C. Attar ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Population Based ◽  
Seer Database ◽  
Database Analysis ◽  
Core Binding Factor ◽  
Binding Factor ◽  
Acute Myeloid

Extracellular KIT receptor mutants, commonly found in core binding factor AML, are constitutively active and respond to imatinib mesylate

Blood ◽  
2005 ◽  
Vol 106 (12) ◽  
pp. 3958-3961 ◽  
Author(s):  
Jörg Cammenga ◽  
Stefan Horn ◽  
Ulla Bergholz ◽  
Gunhild Sommer ◽  
Peter Besmer ◽  
...  
Keyword(s):  
Imatinib Mesylate ◽  
Kinase Inhibitors ◽  
Kinase Inhibitor ◽  
Therapeutic Option ◽  
Extracellular Domain ◽  
Genetic Alterations ◽  
Myelogenous Leukemia ◽  
Core Binding Factor ◽  
Kit Receptor ◽  
Binding Factor

Multiple genetic alterations are required to induce acute myelogenous leukemia (AML). Mutations in the extracellular domain of the KIT receptor are almost exclusively found in patients with AML carrying translocations or inversions affecting members of the core binding factor (CBF) gene family and correlate with a high risk of relapse. We demonstrate that these complex insertion and deletion mutations lead to constitutive activation of the KIT receptor, which induces factor-independent growth of interleukin-3 (IL-3)–dependent cells. Mutation of the evolutionary conserved amino acid D419 within the extracellular domain was sufficient to constitutively activate the KIT receptor, although high expression levels were required. Dose-dependent growth inhibition and apoptosis were observed using either the protein tyrosine kinase inhibitor imatinib mesylate (STI571, Gleevec) or by blocking the phosphoinositide-3-kinase (PI3K)–AKT pathway. Our data show that the addition of kinase inhibitors to conventional chemotherapy might be a new therapeutic option for CBF-AML expressing mutant KIT.

scholarly journals Core-Binding Factor Subunit Beta Is Not Required for Non-Primate Lentiviral Vif-Mediated APOBEC3 Degradation

2014 ◽  
Vol 88 (20) ◽  
pp. 12112-12122 ◽  
Author(s):  
Y. Ai ◽  
D. Zhu ◽  
C. Wang ◽  
C. Su ◽  
J. Ma ◽  
...  
Keyword(s):  
Core Binding Factor ◽  
Binding Factor

scholarly journals Cytoplasmic Sequestration of the Polyomavirus Enhancer Binding Protein 2 (PEBP2)/Core Binding Factor α (CBFα) Subunit by the Leukemia-Related PEBP2/CBFβ-SMMHC Fusion Protein Inhibits PEBP2/CBF-Mediated Transactivation

1998 ◽  
Vol 18 (7) ◽  
pp. 4252-4261 ◽  
Author(s):  
Yuka Kanno ◽  
Tomohiko Kanno ◽  
Chohei Sakakura ◽  
Suk-Chul Bae ◽  
Yoshiaki Ito
Keyword(s):  
Nuclear Translocation ◽  
Binding Protein ◽  
Myelogenous Leukemia ◽  
Luciferase Assay ◽  
Β Subunit ◽  
Core Binding Factor ◽  
Α Subunit ◽  
Enhancer Binding Protein ◽  
Binding Factor ◽  
Minimal Region

ABSTRACT The polyomavirus enhancer binding protein 2 (PEBP2)/core binding factor (CBF) is a transcription factor composed of two subunits, α and β. The gene encoding the β subunit is disrupted by inv(16), resulting in the formation of a chimeric protein, β-SMMHC, which is associated with acute myelogenous leukemia. To understand the effect of β-SMMHC on PEBP2-mediated transactivation, we used a luciferase assay system in which contribution of both the α and β subunits was absolutely required to activate transcription. Using this system, we found that the minimal region of the β subunit required for transactivation resides between amino acid 1 and 135, which is known to dimerize with the α subunit. In contrast, β-SMMHC, despite having this minimal region for dimerization and transactivation, failed to support transcription with the α subunit. Furthermore β-SMMHC blocked the synergistic transcription achieved by PEBP2 and CCAAT/enhancer binding protein α. By using a construct in which the PEBP2 α subunit was fused to the glucocorticoid receptor ligand binding domain, we demonstrated that coexpressed β-SMMHC tightly sequestered the α subunit in the cytoplasm and blocked dexamethasone-dependent nuclear translocation of the α subunit. Thus, the result suggess that β-SMMHC inhibits PEBP2-mediated transcription via cytoplasmic sequestration of the α subunit. Lastly proliferation of ME-1 cells that harbor inv(16) was blocked by an antisense oligonucleotide complementary to the junction of the chimeric mRNA, suggesting that β-SMMHC contributes to leukemogenesis by blocking the differentiation of myeloid cells.

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