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Effects of Tyrosine Kinase Inhibitors on the Th1 and Treg Cells of CML Patients.

07:00 EST 1st February 2019 | BioPortfolio

Summary of "Effects of Tyrosine Kinase Inhibitors on the Th1 and Treg Cells of CML Patients."

To compare the immunomodulatory effects of the 2nd generation of tyrosine kinase inhibitors (TKIs)-dasatinib and nilotinib as well as the 1st generation of TKI-imatinib on chronic myeloid leukemia (CML) patients.

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Journal Details

This article was published in the following journal.

Name: Zhongguo shi yan xue ye xue za zhi
ISSN: 1009-2137
Pages: 25-32

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Medical and Biotech [MESH] Definitions

A protein kinase C subtype that was originally characterized as a CALCIUM-independent, serine-threonine kinase that is activated by PHORBOL ESTERS and DIACYLGLYCEROLS. It is targeted to specific cellular compartments in response to extracellular signals that activate G-PROTEIN-COUPLED RECEPTORS; TYROSINE KINASE RECEPTORS; and intracellular protein tyrosine kinase.

An eph family receptor found primarily in BRAIN and THYMUS. The EphB6 receptor is unusual in that its tyrosine kinase domain shares little homology with other members of this class. The unusual tyrosine kinase domain of this receptor appears to result in its lack of tyrosine kinase activity.

A receptor tyrosine kinase that is involved in HEMATOPOIESIS. It is closely related to FMS PROTO-ONCOGENE PROTEIN and is commonly mutated in acute MYELOID LEUKEMIA.

A receptor tyrosine kinase that transduces signals from EXTRACELLULAR MATRIX to the CYTOPLASM by binding ligands such as GALECTIN 3. It regulates many physiologic processes that include cell survival, migration, differentiation, and PHAGOCYTOSIS of apoptotic cells and ROD PHOTORECEPTORS in the RETINAL PIGMENT EPITHELIUM. Mutations in the MERTK gene are associated with type 38 RETINITIS PIGMENTOSA; it also plays a critical role as an inhibitor of TOLL-LIKE RECEPTORS signaling.

A protein-tyrosine kinase receptor that is specific for STEM CELL FACTOR. This interaction is crucial for the development of hematopoietic, gonadal, and pigment stem cells. Genetic mutations that disrupt the expression of PROTO-ONCOGENE PROTEINS C-KIT are associated with PIEBALDISM, while overexpression or constitutive activation of the c-kit protein-tyrosine kinase is associated with tumorigenesis.

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