A Requirement for SOCS-1 and SOCS-3 Phosphorylation in Bcr-Abl-Induced Tumorigenesis
Neoplasia: An International Journal for Oncology Research, 2012 Suppressors of cytokine signaling 1 and 3 (SOCS-1 and SOCS-3) are inhibitors of the Janus tyrosine kinase (JAK)/signal transducers and activators of transcription (STAT) pathway and function in a negative feedback loop during cytokine signaling.
Xiaoxue Qiu +6 more
doaj +1 more source
Interactions of p62(dok) with p210(bcr-abl) and Bcr-Abl-associated proteins.
The Journal of biological chemistry, 1998 A 62-kDa Ras GTPase-activating protein (RasGAP)-associated protein is tyrosine-phosphorylated under a variety of circumstances including growth factor stimulation and in cells transformed by activated tyrosine kinases. A cDNA for p62(dok), reported to be the RasGAP-associated 62-kDa protein, was recently cloned from Abl-transformed cells. In this study,
A, Bhat +4 more
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Optimized Treatment Schedules for Chronic Myeloid Leukemia
, 2016 Over the past decade, several targeted therapies (e.g. imatinib, dasatinib, nilotinib) have been developed to treat Chronic Myeloid Leukemia (CML). Despite an initial response to therapy, drug resistance remains a problem for some CML patients.
Dingli, David +4 more
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e8a2 BCR–ABL: more frequent than other atypical BCR–ABL variants? [PDF]
Leukemia, 2005 DEMEHRI S +12 more
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Targeting HSPA8 to repress GPX4 and induce ferroptosis in BCR-ABL positive leukemia
Biomedical TechnologyBCR-ABL positive (BCR-ABL+) leukemia is driven by constitutive activation of tyrosine kinase activity, with tyrosine kinase inhibitors (TKIs) serving as the standard treatment. However, resistance to TKIs remains a significant clinical challenge. In this
Shuxin Zhong +12 more
doaj +1 more source
BCR-ABL activity and its response to drugs can be determined in CD34+ CML stem cells by CrkL phosphorylation status using flow cytometry. [PDF]
, 2006 In chronic myeloid leukaemia, CD34(+) stem/progenitor cells appear resistant to imatinib mesylate (IM) in vitro and in vivo. To investigate the underlying mechanism(s) of IM resistance, it is essential to quantify Bcr-Abl kinase status at the stem cell ...
Copland, M +6 more
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MicroRNAs act as decoy molecules to inhibit the function of RNA binding proteins [PDF]
, 2008 Professional Biological Sciences: 3rd Place (The Ohio State University Edward F. Hayes Graduate Research Forum)Altered microRNA (miRNA) expression contributes to aberrant post-transcriptional gene regulation in several types of cancers; however, their ...
Eiring, Anna M.
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eLifePhiladelphia chromosome-positive (Ph+) leukemia is a fatal hematological malignancy. Although standard treatments with tyrosine kinase inhibitors (TKIs) have achieved remarkable success in prolonging patient survival, intolerance, relapse, and TKI ...
Mengya Zhao +10 more
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BCR-ABL mutational studies for predicting the response of patients with chronic myeloid leukaemia to second-generation tyrosine kinase inhibitors after imatinib fail [PDF]
, 2009 Imatinib is the standard treatment for chronic myeloid leukaemia. BCR-ABL kinase domain mutation is the commonest mechanism implicated in imatinib resistance. In in-vitro studies, kinase domain mutations are variably resistant to second-line agents.
Chan, YY +8 more
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