Results 101 to 110 of about 1,603 (142)
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Osteopontin is upregulated by BCR-ABL
Biochemical and Biophysical Research Communications, 2005Chronic myelogenous leukemia (CML) is characterized by its hallmark oncogene BCR-ABL and the progression from a chronic phase toward an acute leukemia, with a differentiation arrest of the leukemic clone. In the present study, we conducted a microarray analysis using an inducible model of BCR-ABL expression based on the TET-OFF system, and we found ...
S, Flamant +9 more
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Blood, 2007
In Ph+ chronic myeloid leukemia (CML), the constitutively active Bcr-Abl kinase leads to the up-regulation and activation of multiple genes, which may subsequently result in the expression of leukemia-associated antigens. In this study, we investigated the immunogenicity of Bcr-Abl–regulated antigens by stimulating CD8+ T lymphocytes with autologous ...
Florian, Scheich +3 more
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In Ph+ chronic myeloid leukemia (CML), the constitutively active Bcr-Abl kinase leads to the up-regulation and activation of multiple genes, which may subsequently result in the expression of leukemia-associated antigens. In this study, we investigated the immunogenicity of Bcr-Abl–regulated antigens by stimulating CD8+ T lymphocytes with autologous ...
Florian, Scheich +3 more
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Blood, 2006
Abstract The inhibition of BCR/ABL kinase activity by imatinib mesylate (IM, STI571, Gleevec®) is the standard therapy for patients with Philadelphia chromosome+ (Ph+) chronic myeloid leukemia (CML). However, the long term treatment with IM or other BCR/ABL kinase inhibitors may be limited due to the development of resistant disease and ...
Florian Scheich +2 more
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Abstract The inhibition of BCR/ABL kinase activity by imatinib mesylate (IM, STI571, Gleevec®) is the standard therapy for patients with Philadelphia chromosome+ (Ph+) chronic myeloid leukemia (CML). However, the long term treatment with IM or other BCR/ABL kinase inhibitors may be limited due to the development of resistant disease and ...
Florian Scheich +2 more
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Essential thrombocythemia with BCR/ABL rearrangement
Cancer Genetics and Cytogenetics, 1996Essential thrombocythemia (ET) was diagnosed clinically in three patients Karyotypic analysis and reverse transcription polymerase chain reaction for the bcr-abl chimeric transcript showed that two were Philadelphia chromosome (Ph) positive, bcr-abl positive, whereas the third was Ph negative, bcr-abl positive.
Kwong, YL +4 more
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Wrapping BCR-ABL: it's in the bag
Blood, 2010Abstract Leukemia, with its origin in a specific genetic abnormality, will only arise if the cell properly folds and processes the oncogenic protein encoded by the mutant gene. In this issue of Blood, Tsukahara and Maru describe a set of proteins that control the processing of the nascent BCR-ABL oncoprotein, providing new avenues for ...
Junia V, Melo, Duncan R, Hewett
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Mechanisms of Transformation by the BCR/ABL Oncogene
International Journal of Hematology, 2001The Philadelphia chromosome generates a chimeric oncogene in which the BCR and c-ABL genes are fused. The product of this oncogene, BCR/ABL, has elevated ABL tyrosine kinase activity, relocates to the cytoskeleton, and phosphorylates multiple cellular substrates.
M, Sattler, J D, Griffin
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Response: too much BCR-ABL to live on, but too little BCR-ABL to die on?
Blood, 2012The mechanistic understanding of persistence of leukemic stem cells during tyrosine kinase inhibitor therapy is an important unmet prerequisite for targeting residual CML and eradicating the disease.
Andreas Burchert +2 more
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Targeting of BCR-ABL: Lessons learned from BCR-ABL inhibition.
Cellular and molecular biology (Noisy-le-Grand, France), 2017In 1960 researchers reported that balanced translocation between chromosomes 22 and 9 resulted in the generation of Philadelphia chromosome. This breakthrough revolutionized our knowledge related to leukemia biology and contemporary studies revealed that chromosomal translocation resulted in the fusion between the 5' segment of BCR gene and 3' segment ...
X, Lin +10 more
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The Role of MYC in Transformation by BCR-ABL
Leukemia & Lymphoma, 1993The BCR-ABL gene plays a central role in the pathogenesis of chronic myelogenous leukemia. Despite a detailed understanding of the regions of BCR and ABL required for transformation by BCR-ABL, little is known about the signalling pathway by which BCR-ABL causes transformation. The nuclear oncogene c-myc plays a critical role in BCR-ABL transformation.
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Blood, 2011
Abstract 4417 Chronic myeloid leukemia (CML) is characterized by the presence of t(9;22) leading to the BCR/ABL fusion gene while other myeloproliferative disorders such as polycytemia vera (PV) and primary myelofibrosis (PMF) may have a point mutation at V617 F codon of janus kinase 2 gene.
Abhinav Deol, Charles A. Schiffer
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Abstract 4417 Chronic myeloid leukemia (CML) is characterized by the presence of t(9;22) leading to the BCR/ABL fusion gene while other myeloproliferative disorders such as polycytemia vera (PV) and primary myelofibrosis (PMF) may have a point mutation at V617 F codon of janus kinase 2 gene.
Abhinav Deol, Charles A. Schiffer
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