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A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome.
The acquisition of a T674I resistance mutation at the time of relapse demonstrates that FIP1L1-PDGFRalpha is the target of imatinib, and data indicate that the deletion of genetic material may result in gain-of-function fusion proteins.
The roles of FLT3 in hematopoiesis and leukemia.
Results suggest that FLT3 is an attractive therapeutic target for kinase inhibitors or other approaches for patients with mutations of this gene, and preliminary studies suggest that mutantFLT3 cooperates with other leukemia oncogenes to confer a more aggressive phenotype.
Nilotinib in imatinib-resistant CML and Philadelphia chromosome-positive ALL.
Nilotinib has a relatively favorable safety profile and is active in imatinib-resistant CML, and common adverse events were myelosuppression, transient indirect hyperbilirubinemia, and rashes.
MAML1, a human homologue of Drosophila Mastermind, is a transcriptional co-activator for NOTCH receptors
Cl clone MAML1, a human homologue of the Drosophila gene Mastermind, and show that it encodes a protein of 130 kD localizing to nuclear bodies that functions as a transcriptional co-activator for NOTCH signalling.
Second generation inhibitors of BCR-ABL for the treatment of imatinib-resistant chronic myeloid leukaemia
The mechanism of action of imatinib in CML, the structural basis ofImatinib resistance, and the potential of second-generation BCR-ABL inhibitors to circumvent resistance are described.
JAK2 associates with the beta c chain of the receptor for granulocyte-macrophage colony-stimulating factor, and its activation requires the membrane-proximal region.
The studies described here demonstrate that GM-CSF stimulation of cells induces the tyrosine phosphorylation of JAK2 and activates its in vitro kinase activity and further support the hypothesis that the JAK family of kinase are critical to coupling cytokine binding to tyrosines phosphorylated and ultimately mitogenesis.
Functional screening identifies CRLF2 in precursor B-cell acute lymphoblastic leukemia
It is demonstrated that CRLF2 is overexpressed in approximately 15% of adult and high-risk pediatric B-ALL that lack MLL, TCF3, TEL, and BCR/ABL rearrangements, but not in B-all with these rearrangement or other lymphoid malignancies.