scholarly journals Synergistic Cytotoxicity of Sorafenib with Busulfan and Nucleoside Analogs in Human FMS-like Tyrosine Kinase 3 Internal Tandem Duplications–Positive Acute Myeloid Leukemia Cells

2014 ◽  
Vol 20 (11) ◽  
pp. 1687-1695 ◽  
Author(s):  
Guiyun Song ◽  
Benigno C. Valdez ◽  
Yang Li ◽  
Yan Liu ◽  
Richard E. Champlin ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Tyrosine Kinase ◽  
Myeloid Leukemia ◽  
Nucleoside Analogs ◽  
Leukemia Cells ◽  
Synergistic Cytotoxicity ◽  
Acute Myeloid Leukemia Cells ◽  
Tandem Duplications ◽  
Acute Myeloid

scholarly journals Fms-like tyrosine kinase 3-internal tandem duplications epigenetically activates checkpoint kinase 1 in acute myeloid leukemia cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yudong Zhang ◽  
Lingli Yuan
Keyword(s):  
Acute Myeloid Leukemia ◽  
Survival Rate ◽  
Tyrosine Kinase ◽  
Myeloid Leukemia ◽  
Disease Free Survival ◽  
Checkpoint Kinase ◽  
Checkpoint Kinase 1 ◽  
Acute Myeloid Leukemia Cells ◽  
Tandem Duplications ◽  
Acute Myeloid

AbstractIt is not clear how Fms-like tyrosine kinase 3-internal tandem duplications (FLT3-ITD) regulates checkpoint kinase 1 (CHK1) in acute myeloid leukemia (AML). In this study, we investigated the regulatory effect of FLT3-ITD on CHK1. Our results showed that CHK1 was highly expressed in FLT3-ITD positive AML. The overall survival rate and disease-free survival rate of AML patients with high CHK1 level were lower than those of patients with low CHK1 level. Mechanistically, FLT3-ITD recruited p300 to the CHK1 promoter and subsequently acetylated H3K27, thereby enhancing the transcription of CHK1. Interfering with the expression of CHK1 significantly inhibited the cell proliferation and induced cell apoptosis in FLT3-ITD positive MV4-11 cells. In addition, CHK1 knockdown promoted the sensitivity of MV4-11 cells to the epigenetic inhibitors JQ1 and C646. This study discovers a new therapeutic target for FLT3-ITD + AML and provided evidence for the combination of epigenetic inhibitors for AML treatment.

scholarly journals Inhibition of ATR acutely sensitizes acute myeloid leukemia cells to nucleoside analogs that target ribonucleotide reductase

2018 ◽  
Vol 2 (10) ◽  
pp. 1157-1169 ◽  
Author(s):  
Sarah E. Fordham ◽  
Helen J. Blair ◽  
Claire J. Elstob ◽  
Ruth Plummer ◽  
Yvette Drew ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Mouse Model ◽  
Ribonucleotide Reductase ◽  
Myeloid Leukemia ◽  
Nucleoside Analogs ◽  
Leukemia Cells ◽  
Molecule Inhibitor ◽  
Key Points ◽  
Acute Myeloid Leukemia Cells ◽  
Acute Myeloid

Key Points Loss of ATR signaling is cytotoxic to AML cells in combination with gemcitabine and hydroxyurea via the induction of replication stress. A small molecule inhibitor of ATR in combination with gemcitabine completely eradicates AML in an orthotopic xenograft mouse model.

scholarly journals A tyrosine kinase-STAT5-miR21-PDCD4 regulatory axis in chronic and acute myeloid leukemia cells

Oncotarget ◽  
2017 ◽  
Vol 8 (44) ◽  
pp. 76174-76188 ◽  
Author(s):  
Anne-Sophie Espadinha ◽  
Valérie Prouzet-Mauléon ◽  
Stéphane Claverol ◽  
Valérie Lagarde ◽  
Marc Bonneu ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Tyrosine Kinase ◽  
Myeloid Leukemia ◽  
Leukemia Cells ◽  
Acute Myeloid Leukemia Cells ◽  
Acute Myeloid
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