Inhibition of the Bcr-Abl tyrosine kinase as a therapeutic strategy for CML. - Wikidata - wikimedia - TriplyDB

Inhibition of the Bcr-Abl tyrosine kinase as a therapeutic strategy for CML.

Inhibition of the Bcr-Abl tyrosine kinase as a therapeutic strategy for CML.

http://www.wikidata.org/entity/Q35022505

about

The GIST of targeted therapy for malignant melanoma Dissecting therapeutic resistance to RAF inhibition in melanoma by tumor genomic profiling.Imagine a world without cancer Principles of cancer therapy: oncogene and non-oncogene addiction Misfolding, Aggregation, and Disordered Segments in c-Abl and p53 in Human Cancer.S-glutathionylated serine proteinase inhibitors as plasma biomarkers in assessing response to redox-modulating drugs Abl-kinase-sensitive levels of ERK5 and its intrinsic basal activity contribute to leukaemia cell survival Quantitative methods for the analysis of protein phosphorylation in drug development.Heterogeneity of gene expression in murine squamous cell carcinoma development-the same tumor by different means.Selective tyrosine kinase inhibition by imatinib mesylate for the treatment of autoimmune arthritis The EGF receptor family--multiple roles in proliferation, differentiation, and neoplasia with an emphasis on HER4 Hepatic stellate cells: central modulators of hepatic carcinogenesis.The p63/p73 network mediates chemosensitivity to cisplatin in a biologically defined subset of primary breast cancers A derivative of epigallocatechin-3-gallate induces apoptosis via SHP-1-mediated suppression of BCR-ABL and STAT3 signalling in chronic myelogenous leukaemia American Society of Clinical Oncology policy statement update: the critical role of phase I trials in cancer research and treatment.PDGF in gliomas: more than just a growth factor?The serum tryptase test: an emerging robust biomarker in clinical hematology.Extended adjuvant therapy with imatinib in patients with gastrointestinal stromal tumors : recommendations for patient selection, risk assessment, and molecular response monitoring.Mechanisms leading to nonrandom, nonhomologous chromosomal translocations in leukemia Combination of rapamycin and protein tyrosine kinase (PTK) inhibitors for the treatment of leukemias caused by oncogenic PTKs.Toward 'SMART' stem cells.Apoptosis and autophagy: BIM as a mediator of tumour cell death in response to oncogene-targeted therapeutics.Real-time nanoscale proteomic analysis of the novel multi-kinase pathway inhibitor rigosertib to measure the response to treatment of cancer.Imatinib enhances human melanoma cell susceptibility to TRAIL-induced cell death: Relationship to Bcl-2 family and caspase activation.Pharmacologic inhibition of mTOR antagonizes the cytotoxic activity of pemetrexed in non-small cell lung cancer.Downregulation of NPM-ALK by siRNA causes anaplastic large cell lymphoma cell growth inhibition and augments the anti cancer effects of chemotherapy in vitro.Arsenic trioxide and proteasome inhibitor bortezomib synergistically induce apoptosis in leukemic cells: the role of protein kinase Cdelta.FOXO3a induces differentiation of Bcr-Abl-transformed cells through transcriptional down-regulation of Id1.Specific killing of Rb mutant cancer cells by inactivating TSC2.Defective cell cycle checkpoints as targets for anti-cancer therapies.Chronic myeloproliferative disorders with rearrangement of the platelet-derived growth factor alpha receptor: a new clinical target for STI571/Glivec.Do cells need CDK2 and ... Bcr-Abl?Suppression of vascular endothelial growth factor (VEGF) expression by targeting the Bcr-Abl oncogene and protein tyrosine kinase activity in Bcr-Abl-positive leukaemia cells.Induction of apoptosis by shikonin through a ROS/JNK-mediated process in Bcr/Abl-positive chronic myelogenous leukemia (CML) cells.Leukemic cells with increased telomerase activity exhibit resistance to imatinib.Nilotinib-induced vasculopathy: identification of vascular endothelial cells as a primary target site.Kinase impact assessment in the landscape of fusion genes that retain kinase domains: a pan-cancer study.Progressive peripheral arterial occlusive disease and other vascular events during nilotinib therapy in CML.

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P2860

Inhibition of the Bcr-Abl tyrosine kinase as a therapeutic strategy for CML.

http://www.wikidata.org/entity/Q35022505

description

2002 nî lūn-bûn

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2002 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2002 թվականի դեկտեմբերին հրատարակված գիտական հոդված

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2002年の論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年论文

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name

Inhibition of the Bcr-Abl tyrosine kinase as a therapeutic strategy for CML.

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Inhibition of the Bcr-Abl tyrosine kinase as a therapeutic strategy for CML.

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type

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Inhibition of the Bcr-Abl tyrosine kinase as a therapeutic strategy for CML.

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Inhibition of the Bcr-Abl tyrosine kinase as a therapeutic strategy for CML.

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Inhibition of the Bcr-Abl tyrosine kinase as a therapeutic strategy for CML.

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Inhibition of the Bcr-Abl tyrosine kinase as a therapeutic strategy for CML.

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Inhibition of the Bcr-Abl tyrosine kinase as a therapeutic strategy for CML.

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P2860

Lessons learned from the development of an abl tyrosine kinase inhibitor for chronic myelogenous leukemia

Structural mechanism for STI-571 inhibition of abelson tyrosine kinase

Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells

Neonatal lethality and lymphopenia in mice with a homozygous disruption of the c-abl proto-oncogene

Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia

Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia

Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors

Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification

Structural requirements for function of the Crkl adapter protein in fibroblasts and hematopoietic cells.

Activity of a specific inhibitor of the BCR-ABL tyrosine kinase in the blast crisis of chronic myeloid leukemia and acute lymphoblastic leukemia with the Philadelphia chromosome.

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8541-8546

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scholarly article

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10.1038/SJ.ONC.1206081

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56

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21

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Brian J. Druker

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2002-12-01T00:00:00Z

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10996466

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