Results 231 to 240 of about 97,973 (270)
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Tyrosine kinase activity and transformation potency of bcr-abl oncogene products.

Science, 1990
Oncogenic activation of the proto-oncogene c-abl in human leukemias occurs as a result of the addition of exons from the gene bcr and truncation of the first abl exon.
T. Lugo   +3 more
semanticscholar   +1 more source

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   +5 more sources

Wrapping BCR-ABL: it's in the bag

Blood, 2010
Abstract 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 ...
Duncan R. Hewett, Junia V. Melo
openaire   +3 more sources

Response: too much BCR-ABL to live on, but too little BCR-ABL to die on? [PDF]

open access: possibleBlood, 2012
The 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
openaire   +1 more source

BCR/ABL: The Clonal Bully

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
openaire   +2 more sources

BCR/ABL signal transduction.

International journal of hematology, 1995
A strong association between the Philadelphia chromosome (Ph1) and chronic myelogenous leukemia (CML) suggests that the Ph1 translocation plays a significant role in pathogenesis of CML. For this reason, Ph1-positive leukemias have been well studied from the molecular, clinical and cell biological perspective.
Hal E. Broxmeyer, Tetsuzo Tauchi
openaire   +2 more sources

Mechanisms of Transformation by the BCR/ABL Oncogene

International Journal of Hematology, 2001
The 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.
James D. Griffin, Martin Sattler
openaire   +3 more sources

BCR-ABL and Human Cancer [PDF]

open access: possible, 2007
The BCR-ABL oncogene was the first chromosomal abnormality shown to be associated with a specific human malignancy, the chronic myelogenous leukemia (CML), resulting from a reciprocal t(9;22) translocation characterized by the formation of a shortened chromosome, named Philadelphia chromosome (Ph), in which the tyrosine kinase of c-ABL is ...
Maria Perez-Caro   +1 more
openaire   +1 more source

2 BCR-ABL gene variants

Baillière's Clinical Haematology, 1997
The BCR-ABL hybrid gene, the main product of the t(9;22)(q34;q11) translocation, is found in the leukaemic clone of at least 95% of CML patients. The fusion protein encoded by BCR-ABL varies in size, depending on the breakpoint in the BCR gene. Three breakpoint cluster regions have been characterized to date: major (M-bcr), minor (m-bcr) and micro (mu ...
openaire   +3 more sources

Bcr-Abl and Signal Transduction [PDF]

open access: possible, 2007
The BCR-ABL oncogene is generated by the Philadelphia (Ph) chromosome translocation, fusing the BCR to the ABL gene. The Bcr-Abl fusion protein has constitutive and deregulated tyrosine kinase activity that is critical for transformation of hematopoietic cells.
Giuseppe Saglio, Daniela Cilloni
openaire   +1 more source

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