Results 221 to 230 of about 125,674 (260)
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CRKL Binding to BCR-ABL and BCR-ABL Transformation

Leukemia & Lymphoma, 1999
The 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
K S, Kolibaba   +4 more
openaire   +2 more sources

Discovery of SIAIS178 as an effective BCR-ABL degrader by recruiting von Hippel-Lindau (VHL) E3 Ubiquitin Ligase.

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 ...
Quanju Zhao   +14 more
semanticscholar   +1 more source

Biology of BCR-ABL

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).
R, Chopra, Q Q, Pu, A G, Elefanty
openaire   +2 more sources

BCR/ABL and leukemia

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
A, Butturini, R B, Arlinghaus, R P, Gale
openaire   +2 more sources

The BCR/ABL hybrid gene

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.
J, Groffen, N, Heisterkamp
openaire   +2 more sources

Essential thrombocythemia with BCR/ABL rearrangement

Cancer Genetics and Cytogenetics, 1996
Essential 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
openaire   +4 more sources

Osteopontin is upregulated by BCR-ABL

Biochemical and Biophysical Research Communications, 2005
Chronic 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
openaire   +2 more sources

Targeting of BCR-ABL: Lessons learned from BCR-ABL inhibition.

Cellular and molecular biology (Noisy-le-Grand, France), 2017
In 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
openaire   +1 more source

BCR-ABL-negative chronic myeloid leukemia

Current Hematologic Malignancy Reports, 2007
Constitutive activation of protein tyrosine kinases plays a central role in the pathogenesis of myeloproliferative disorders, including BCR-ABL-negative chronic myeloid leukemia. Current research is focused on elucidating the full spectrum of causative mutations in this rare, heterogeneous disease.
Sonja, Burgstaller   +2 more
openaire   +2 more sources

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