Results 271 to 280 of about 128,389 (322)
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Journal of Medicinal Chemistry, 2019
The oncogenic fusion protein BCR-ABL is the driving force of leukemogenesis in chronic myeloid leukemia (CML). Despite great progress for CML treatment through application of tyrosine kinase inhibitors (TKIs) against BCR-ABL, long-term drug ...
Bei Yang, Biao Jiang, Qian-qian Yin
exaly +2 more sources
The oncogenic fusion protein BCR-ABL is the driving force of leukemogenesis in chronic myeloid leukemia (CML). Despite great progress for CML treatment through application of tyrosine kinase inhibitors (TKIs) against BCR-ABL, long-term drug ...
Bei Yang, Biao Jiang, Qian-qian Yin
exaly +2 more sources
Targeting of BCR-ABL: Lessons learned from BCR-ABL inhibition.
Cellular and molecular biology (Noisy-le-Grand, France), 2016In 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 ...
Muhammad Ismail +10 more
openaire +4 more sources
A Global PROTAC Toolbox for Degrading BCR-ABL Overcomes Drug-Resistant Mutants and Adverse Effects.
Journal of Medicinal Chemistry, 2020The BCR-ABL fusion oncoprotein causes CML or some ALL in Ph+ patients because the ABL kinase is constitutively activated. However, current clinical treatment with ABL inhibitors is seriously limited by the drug resistance and adverse effects.
Yiqing Yang +6 more
semanticscholar +1 more source
Recent advances in Bcr‐Abl tyrosine kinase inhibitors for overriding T315I mutation
Chemical Biology and Drug Design, 2020BCR‐ABL is a gene produced by the fusion of the bcr gene and the c‐abl proto‐oncogene and is considered to be the main cause of chronic myelogenous leukemia (CML) production.
Juan Liu +6 more
semanticscholar +1 more source
CRKL Binding to BCR-ABL and BCR-ABL Transformation
Leukemia & Lymphoma, 1999The SH2-SH3 domain-containing adaptor protein CRKL is the predominant tyrosine phosphorylated protein in chronic myelogenous leukemia (CML) neutrophils and BCR-ABL-expressing cell lines. The amino terminal CRKL SH3 domain binds directly to a proline-rich region in the C-terminus of BCR-ABL. BCR-ABL mutants with deletions of this region were constructed
Brian J. Druker +4 more
openaire +3 more sources
Blood Reviews, 1999
gene on chromosome 9 is the humanhomologue of a gene originally identified in a murineoncogenic virus, the Abelson murine leukaemia virus(A-MuLV). This retrovirus was isolated from a pred-nisolone treated mouse which developed lymphomafollowing innoculation with Moloney murineleukaemia virus (M-MuLV).
Qingqiu Pu +2 more
openaire +3 more sources
gene on chromosome 9 is the humanhomologue of a gene originally identified in a murineoncogenic virus, the Abelson murine leukaemia virus(A-MuLV). This retrovirus was isolated from a pred-nisolone treated mouse which developed lymphomafollowing innoculation with Moloney murineleukaemia virus (M-MuLV).
Qingqiu Pu +2 more
openaire +3 more sources
Leukemia Research, 1996
This review focuses on the role of the chimeric BCR/ABL gene in leukemia development. First, we discuss and update knowledge regarding the molecular biology of BCR/ABL. We then review data regarding transforming activity of BCR/ABL. Third, we discuss the complex interactions between BCR/ABL and leukemia phenotype. We conclude with a brief discussion of
Anna Butturini +2 more
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This review focuses on the role of the chimeric BCR/ABL gene in leukemia development. First, we discuss and update knowledge regarding the molecular biology of BCR/ABL. We then review data regarding transforming activity of BCR/ABL. Third, we discuss the complex interactions between BCR/ABL and leukemia phenotype. We conclude with a brief discussion of
Anna Butturini +2 more
openaire +3 more sources
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 ...
Stephane Flamant +9 more
openaire +3 more sources
Baillière's Clinical Haematology, 1987
A DNA region on chromosome 22, designated M-BCR, contains the chromosomal breakpoint of the Philadelphia (Ph) translocation in all Ph positive CML patients studied to date. M-BCR is part of a gene, BCR, oriented with its 5' end towards the centromere of chromosome 22. All of the CML DNAs analysed have a breakpoint within introns of the BCR gene.
John Groffen, Nora Heisterkamp
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A DNA region on chromosome 22, designated M-BCR, contains the chromosomal breakpoint of the Philadelphia (Ph) translocation in all Ph positive CML patients studied to date. M-BCR is part of a gene, BCR, oriented with its 5' end towards the centromere of chromosome 22. All of the CML DNAs analysed have a breakpoint within introns of the BCR gene.
John Groffen, Nora Heisterkamp
openaire +3 more sources