The functional interplay between the t(9;22)-associated fusion proteins BCR/ABL and ABL/BCR in Philadelphia chromosome-positive acute lymphatic leukemia. [PDF]
PLoS Genetics, 2015 The hallmark of Philadelphia chromosome positive (Ph(+)) leukemia is the BCR/ABL kinase, which is successfully targeted by selective ATP competitors. However, inhibition of BCR/ABL alone is unable to eradicate Ph(+) leukemia.
Anahita Rafiei +8 more
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The diversity of BCR-ABL fusion proteins and their relationship to leukemia phenotype [editorial; comment] [PDF]
Blood, 1996 HE PHILADELPHIA (Ph) chromosome was the first T chromosomal abnormality associated with a specific malignant disease in humans, namely chronic myeloid leukemia (CML).’ Later it was identified as one partner in a reciprocal translocation between ...
J. Melo
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Relationship Between BCR/ABL Fusion Proteins and Leukemia Phenotype [PDF]
Blood, 1997 To the Editor: We read with interest the recent Editorial in Blood by Melo[1][1] concerning the relationship between BCR/ABL variant transcripts and the leukemia phenotype determination. Regarding the chronic myeloid leukemia (CML), a strict correlation was suggested between at least three ...
Emilia G +3 more
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Flow cytometric immunobead assay for the detection of BCR–ABL fusion proteins in leukemia patients [PDF]
Leukemia, 2009 BCR-ABL fusion proteins show increased signaling through their ABL tyrosine kinase domain, which can be blocked by specific inhibitors, thereby providing effective treatment. This makes detection of BCR-ABL aberrations of utmost importance for diagnosis, classification and treatment of leukemia patients.
Nancy Boeckx +28 more
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Cell Communication and Signaling, 2021 Background The fusion oncoprotein Bcr-Abl is mostly located in the cytoplasm, which causes chronic myeloid leukemia (CML). After moving into the nucleus, the fusion protein can induce apoptosis of CML cells.
Yuhang Peng +5 more
doaj +2 more sources
Reciprocal t(9;22) ABL/BCR fusion proteins: leukemogenic potential and effects on B cell commitment. [PDF]
PLoS ONE, 2009 BACKGROUND:t(9;22) is a balanced translocation, and the chromosome 22 breakpoints (Philadelphia chromosome--Ph+) determine formation of different fusion genes that are associated with either Ph+ acute lymphatic leukemia (Ph+ ALL) or chronic myeloid ...
Xiaomin Zheng +4 more
doaj +2 more sources
Influence of BCR/ABL fusion proteins on the course of Ph leukemias.
Acta Biochimica Polonica, 2004 The hallmark of chronic myeloid leukemia (CML) and a subset of acute lymphoblastic leukemia (ALL) is the presence of the Philadelphia chromosome as a result of the t(9;22) translocation. This gene rearrangement results in the production of a novel oncoprotein, BCR/ABL, a constitutively active tyrosine kinase.
S. S. Maliuta +3 more
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Activation of tyrosinase kinase and microfilament-binding functions of c-abl by bcr sequences in bcr/abl fusion proteins. [PDF]
Molecular and Cellular Biology, 1991 Chronic myelogenous leukemia and one type of acute lymphoblastic leukemia are characterized by a 9;22 chronosome translocation in which 5' sequences of the bcr gene become fused to the c-abl proto-oncogene. The resulting chimeric genes encode bcr/abl fusion proteins which have deregulated tyrosine kinase activity and appear to play an important role in
J. R. Mcwhirter, Jean Y. J. Wang
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CGP 57148, a Tyrosine Kinase Inhibitor, Inhibits the Growth of Cells Expressing BCR-ABL, TEL-ABL, and TEL-PDGFR Fusion Proteins [PDF]
Blood, 1997 CGP 57148 is a compound of the 2-phenylaminopyrimidine class that selectively inhibits the tyrosine kinase activity of the ABL and the platelet-derived growth factor receptor (PDGFR) protein tyrosine kinases. We previously showed that CGP 57148 selectively kills p210BCR-ABL–expressing cells. To extend these observations, we evaluated the ability of CGP
Martin Carroll +23 more
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Chronic myeloid leukemia with an e1a3 BCR-ABL fusion protein: transformation to lymphoid blast crisis [PDF]
Biomarker Research, 2014 Chronic myelogenous leukemia (CML) results from the neoplastic transformation of a hematopoietic stem cell. CML is cytogenetically characterized by the presence of the Philadelphia chromosome (Ph’). Most patients with CML express e13a2 or e14a2 mRNAs that result from a rearrangement of the major breakpoint cluster regions (M-BCR) generating the 210-kDa
Martinez-Serra, Jordi +12 more
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