scholarly journals Ponatinib circumvents all types of imatinib resistance in chronic myelogenous leukemia cell lines

Cell Cycle ◽  
2013 ◽  
Vol 12 (11) ◽  
pp. 1645-1646 ◽  
Author(s):  
Ophelie Cassuto ◽  
Arnaud Jacquel ◽  
Guillaume Robert ◽  
Patrick Auberger
Keyword(s):  
Cell Lines ◽  
Chronic Myelogenous Leukemia ◽  
Leukemia Cell ◽  
Myelogenous Leukemia ◽  
Chronic Myelogenous Leukemia Cell ◽  
Imatinib Resistance ◽  
Leukemia Cell Lines

Comparative Proteome Profiling and Functional Analysis of Chronic Myelogenous Leukemia Cell Lines

2007 ◽  
Vol 6 (11) ◽  
pp. 4330-4342 ◽  
Author(s):  
Simona Fontana ◽  
Riccardo Alessandro ◽  
Marilisa Barranca ◽  
Margherita Giordano ◽  
Chiara Corrado ◽  
...  
Keyword(s):  
Functional Analysis ◽  
Cell Lines ◽  
Chronic Myelogenous Leukemia ◽  
Leukemia Cell ◽  
Myelogenous Leukemia ◽  
Chronic Myelogenous Leukemia Cell ◽  
Proteome Profiling ◽  
Leukemia Cell Lines

scholarly journals Tyrosine phosphorylation of rasGAP and associated proteins in chronic myelogenous leukemia cell lines

Blood ◽  
1992 ◽  
Vol 79 (9) ◽  
pp. 2215-2220 ◽  
Author(s):  
B Druker ◽  
K Okuda ◽  
U Matulonis ◽  
R Salgia ◽  
T Roberts ◽  
...  
Keyword(s):  
Cell Lines ◽  
Chronic Myelogenous Leukemia ◽  
Kinase Activity ◽  
Philadelphia Chromosome ◽  
Leukemia Cell ◽  
Myelogenous Leukemia ◽  
Hematopoietic Growth Factors ◽  
Chronic Myelogenous Leukemia Cell ◽  
Exon 2 ◽  
Associated Proteins

The Philadelphia chromosome (Ph1), detected in virtually all cases of chronic myelogenous leukemia, is formed by a reciprocal translocation between chromosomes 9 and 22 that fuses BCR encoded sequences upstream of exon 2 of c-ABL. This oncogene produces a fusion protein (p210BCR/ABL) in which the ABL tyrosine kinase activity is elevated. This elevated kinase activity is essential for transformation, but the mechanisms involved are unknown. We report here that p21ras GTPase activating protein (rasGAP) or rasGAP-associated proteins p190 and p62 are phosphorylated on tyrosine in Ph1 (+) cell lines. Further, rasGAP coimmunoprecipitates with p210BCR/ABL in these cell lines. These results suggest that rasGAP or associated proteins are potential substrates for p210BCR/ABL kinase and thus directly link p210BCR/ABL with a signal transduction pathway known to be activated by hematopoietic growth factors (p21ras).

scholarly journals Tyrosine phosphorylation of rasGAP and associated proteins in chronic myelogenous leukemia cell lines

Blood ◽  
1992 ◽  
Vol 79 (9) ◽  
pp. 2215-2220 ◽  
Author(s):  
B Druker ◽  
K Okuda ◽  
U Matulonis ◽  
R Salgia ◽  
T Roberts ◽  
...  
Keyword(s):  
Cell Lines ◽  
Chronic Myelogenous Leukemia ◽  
Kinase Activity ◽  
Philadelphia Chromosome ◽  
Leukemia Cell ◽  
Myelogenous Leukemia ◽  
Hematopoietic Growth Factors ◽  
Chronic Myelogenous Leukemia Cell ◽  
Exon 2 ◽  
Associated Proteins

Abstract The Philadelphia chromosome (Ph1), detected in virtually all cases of chronic myelogenous leukemia, is formed by a reciprocal translocation between chromosomes 9 and 22 that fuses BCR encoded sequences upstream of exon 2 of c-ABL. This oncogene produces a fusion protein (p210BCR/ABL) in which the ABL tyrosine kinase activity is elevated. This elevated kinase activity is essential for transformation, but the mechanisms involved are unknown. We report here that p21ras GTPase activating protein (rasGAP) or rasGAP-associated proteins p190 and p62 are phosphorylated on tyrosine in Ph1 (+) cell lines. Further, rasGAP coimmunoprecipitates with p210BCR/ABL in these cell lines. These results suggest that rasGAP or associated proteins are potential substrates for p210BCR/ABL kinase and thus directly link p210BCR/ABL with a signal transduction pathway known to be activated by hematopoietic growth factors (p21ras).

scholarly journals Lncrna RP1-68D18.2 Promotes K562 Cell Line Resistance to Imatinib through CD44 and Its Downstream Signal Molecules

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 5149-5149
Author(s):  
Tianyou Yan ◽  
Yuping Gong
Keyword(s):  
Cell Line ◽  
Cell Lines ◽  
Chronic Myelogenous Leukemia ◽  
Conflicts Of Interest ◽  
Leukemia Cell ◽  
Myelogenous Leukemia ◽  
Leukemia Cell Line ◽  
Signal Molecules ◽  
Imatinib Treatment ◽  
Imatinib Resistance

Abstract As the first-generation tyrosine kinase inhibitor specifically targeting the BCR-ABL oncoprotein, imatinib has been successfully used in the therapy for chronic myelogenous leukemia (CML) with a significant response and good compliance. However, imatinib resistance becomes the main reason for failure of the treatment of CML. In addition to the common BCR-ABL dependence of imatinib resistance, e.g. BCR-ABL kinase domain mutations and BCR-ABL gene amplification, BCR-ABL independence also plays important roles, which involves alteration of dynamics of drug import and efflux, persistent or compensatory activation of signaling pathways etc. Recently, several studies have reported the correlation of lncRNA with resistance of chemotherapeutic drugs in many cancers. Here, we report, for the first time, discernible overexpression of lncRNARP1-68D18.2 and CD44 mRNA in the imatinib resistant chronic myelogenous leukemia cell line K562R, using lncRNA and mRNA microarray, and further verify it using qPCR. Knockdown of RP1-68D18.2 in K562R cell lines increased their sensitivity to imatinib, and simultaneously caused a decrease in CD44 and c-Myc protein levels. Correspondingly, overexpression of RP1-68D18.2 in K562, a sensitive cell line, led to a slightly decrease in imatinib sensitivity and partially reverse downregulation of c-Myc, p-ERK and p-MEK caused by imatinib treatment. Analysis of correlations revealed positive correlation between RP1-68D18.2 and CD44 mRNA expression in the primary CML blasts and hematological malignant cell lines. We conclude that overexpression of RP1-68D18.2 could promote imatinib resistance in the K562R cell line through the regulation of CD44 and its downstream signal molecules. Disclosures No relevant conflicts of interest to declare.

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