Results 1 to 10 of about 1,603 (142)
Direct Binding of CRKL to BCR-ABL Is Not Required for BCR-ABL Transformation [PDF]
Blood, 1997 AbstractCRKL has previously been shown to be a major tyrosine phosphorylated protein in neutrophils of patients with BCR-ABL+ chronic myelogenous leukemia and in cell lines expressing BCR-ABL. CRKL and BCR-ABL form a complex as demonstrated by coimmunoprecipitation and are capable of a direct interaction in a yeast two-hybrid assay.
Brian J Druker, Kolibaba Kathryn
exaly +4 more sources
An In-house Method for Molecular Monitoring of BCR-ABL
Turkish Journal of Hematology, 2012 OBJECTIVE: At present in Turkey, centers that are able to give reliable RQ-PCR BCR-ABL results are limited in number. We aimed to describe a cost-effective, in-house method for BCR-ABL quantification and to illustrate an example for RQ-PCR validation ...
Hakkı Ogun Sercan +4 more
doaj +4 more sources
Plants, 2021 We will study the effects of the methanol extract of Sphagneticola trilobata (L.) Pruski (Asteraceae) (MeST) on the growth of leukemia cells that may contain the BCR/ABL gene. This study also clarifies the mechanism of this effect on these cells.
Hoang Thanh Chi +2 more
doaj +1 more source
Suppression of USP7 induces BCR-ABL degradation and chronic myelogenous leukemia cell apoptosis
Cell Death and Disease, 2021 Chronic myelogenous leukemia (CML) is a clonal malignancy of hematopoietic stem cells featured with the fusion protein kinase BCR-ABL. To elicit the mechanism underlying BCR-ABL stability, we perform a screen against a panel of deubiquitinating enzymes ...
Shuoyi Jiang +9 more
doaj +1 more source
BCR-ABL affects STAT5A and STAT5B differentially. [PDF]
PLoS ONE, 2014 Signal transducers and activators of transcription (STATs) are latent cytoplasmic transcription factors linking extracellular signals to target gene transcription. Hematopoietic cells express two highly conserved STAT5-isoforms (STAT5A/STAT5B), and STAT5
Michael Schaller-Schönitz +9 more
doaj +1 more source
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 +1 more source
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
doaj +1 more source
Target Inhibition of CBP Induced Cell Senescence in BCR-ABL- T315I Mutant Chronic Myeloid Leukemia
Frontiers in Oncology, 2021 The treatment of chronic myeloid leukemia (CML) with BCR-ABL tyrosine kinase inhibitors (TKIs), such as imatinib, has yielded clinical success. However, the direct targeting of BCR-ABL does not eradicate CML cells expressing mutant BCR-ABL, especially ...
Ke Yang +10 more
doaj +1 more source
Molecular Therapy: Oncolytics, 2020 Chronic myeloid leukemia (CML) is caused by the Philadelphia (Ph+) chromosome carrying the BCR-ABL oncogene, a constitutively active tyrosine kinase. The discovery of imatinib represents a major success story in the treatment against CML.
Liuya Wei +13 more
doaj +1 more source
Molecular Pathways: BCR-ABL [PDF]
Clinical Cancer Research, 2012 Abstract Aberrant tyrosine kinase activity plays a critical role in many hematologic disorders, including chronic myeloid leukemia characterized by the constitutive activity of BCR-ABL. ABL therefore represents a crucial target for new therapeutic strategies.
Daniela, Cilloni, Giuseppe, Saglio
openaire +2 more sources