Results 1 to 10 of about 64,154 (248)

The functional interplay between the t(9;22)-associated fusion proteins BCR/ABL and ABL/BCR in Philadelphia chromosome-positive acute lymphatic leukemia. [PDF]

open access: yesPLoS 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
doaj   +9 more sources

Reciprocal t(9;22) ABL/BCR fusion proteins: leukemogenic potential and effects on B cell commitment. [PDF]

open access: yesPLoS 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   +9 more sources

The diversity of BCR-ABL fusion proteins and their relationship to leukemia phenotype. [PDF]

open access: yesBlood, 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
semanticscholar   +3 more sources

Relationship between BCR/ABL fusion proteins and leukemia phenotype. [PDF]

open access: yesBlood, 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
G. Emilia   +3 more
semanticscholar   +5 more sources

Flow cytometric immunobead assay for the detection of BCR–ABL fusion proteins in leukemia patients [PDF]

open access: yesLeukemia, 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.
F. Weerkamp   +28 more
semanticscholar   +5 more sources

Effect of HSP90AB1 and CC domain interaction on Bcr-Abl protein cytoplasm localization and function in chronic myeloid leukemia cells

open access: yesCell 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

Influence of BCR/ABL fusion proteins on the course of Ph leukemias.

open access: yesActa 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.
G. Telegeev   +3 more
semanticscholar   +5 more sources

Activation of tyrosinase kinase and microfilament-binding functions of c-abl by bcr sequences in bcr/abl fusion proteins [PDF]

open access: yesMolecular 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.
John R. McWHIRTER, Jean Y. J. Wang
semanticscholar   +4 more sources

CGP 57148, a tyrosine kinase inhibitor, inhibits the growth of cells expressing BCR-ABL, TEL-ABL, and TEL-PDGFR fusion proteins. [PDF]

open access: yesBlood, 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.
M. Carroll   +23 more
semanticscholar   +5 more sources

Chronic myeloid leukemia with an e1a3 BCR-ABL fusion protein: transformation to lymphoid blast crisis [PDF]

open access: yesBiomarker 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
J. Martinez-serra   +12 more
semanticscholar   +5 more sources

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