Combined STAT3 and BCR-ABL1 inhibition induces synthetic lethality in therapy-resistant chronic myeloid leukemia - Wikidata - awgldk - TriplyDB

Combined STAT3 and BCR-ABL1 inhibition induces synthetic lethality in therapy-resistant chronic myeloid leukemia

Combined STAT3 and BCR-ABL1 inhibition induces synthetic lethality in therapy-resistant chronic myeloid leukemia

http://www.wikidata.org/entity/Q35102414

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Oncogenic kinase fusions: an evolving arena with innovative clinical opportunities Inhibition of STAT5: a therapeutic option in BCR-ABL1-driven leukemia Knockout Serum Replacement Promotes Cell Survival by Preventing BIM from Inducing Mitochondrial Cytochrome C Release Signal transducer and activator of transcription 3 (STAT3) inhibitor, S3I-201, acts as a potent and non-selective alkylating agent FTY720 inhibits proliferation and epithelial-mesenchymal transition in cholangiocarcinoma by inactivating STAT3 signaling shRNA library screening identifies nucleocytoplasmic transport as a mediator of BCR-ABL1 kinase-independent resistance.STAT3 pathway regulates lung-derived brain metastasis initiating cell capacity through miR-21 activation.CD133+ brain tumor-initiating cells are dependent on STAT3 signaling to drive medulloblastoma recurrence.A coiled-coil mimetic intercepts BCR-ABL1 dimerization in native and kinase-mutant chronic myeloid leukemia β-Catenin is required for intrinsic but not extrinsic BCR-ABL1 kinase-independent resistance to tyrosine kinase inhibitors in chronic myeloid leukemia.The Role of New Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia PPARγ ligands increase antileukemic activity of second- and third-generation tyrosine kinase inhibitors in chronic myeloid leukemia cells Applying Small Molecule Signal Transducer and Activator of Transcription-3 (STAT3) Protein Inhibitors as Pancreatic Cancer Therapeutics Constitutive activation of Pim1 kinase is a therapeutic target for adult T-cell leukemia.A role for FOXO1 in BCR-ABL1-independent tyrosine kinase inhibitor resistance in chronic myeloid leukemia Overexpression of RPS27a contributes to enhanced chemoresistance of CML cells to imatinib by the transactivated STAT3.Opportunities and challenges in combination gene cancer therapy.Patient-derived ovarian cancer xenografts re-growing after a cisplatinum treatment are less responsive to a second drug re-challenge: a new experimental setting to study response to therapy.Niclosamide inhibition of STAT3 synergizes with erlotinib in human colon cancer.Individualizing kinase-targeted cancer therapy: the paradigm of chronic myeloid leukemia.Chronic myeloid leukemia: advances in understanding disease biology and mechanisms of resistance to tyrosine kinase inhibitors.Single cell immune profiling by mass cytometry of newly diagnosed chronic phase chronic myeloid leukemia treated with nilotinib.A STAT inhibitor patent review: progress since 2011.Minimal Residual Disease Eradication in CML: Does It Really Matter?STAT3-Interacting Proteins as Modulators of Transcription Factor Function: Implications to Targeted Cancer Therapy.Disarming an Electrophilic Warhead: Retaining Potency in Tyrosine Kinase Inhibitor (TKI)-Resistant CML Lines While Circumventing Pharmacokinetic Liabilities Dysregulation of BCL-2 family proteins by leukemia fusion genes.The hOCT1 and ABCB1 polymorphisms do not influence the pharmacodynamics of nilotinib in chronic myeloid leukemia.Combined targeting of STAT3 and STAT5: a novel approach to overcome drug resistance in chronic myeloid leukemia.Emerging therapeutic targets in myeloproliferative neoplasms and peripheral T-cell leukemia and lymphomas.STAT3 inhibition as a therapeutic strategy for leukemia.Chronic myeloid leukemia: the paradigm of targeting oncogenic tyrosine kinase signaling and counteracting resistance for successful cancer therapy.Overexpression of Tpl2 is linked to imatinib resistance and activation of MEK-ERK and NF-κB pathways in a model of chronic myeloid leukemia.Effect of STAT3 inhibitor in chronic myeloid leukemia associated signaling pathway: a mathematical modeling, simulation and systems biology study.

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Combined STAT3 and BCR-ABL1 inhibition induces synthetic lethality in therapy-resistant chronic myeloid leukemia

http://www.wikidata.org/entity/Q35102414

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2014 nî lūn-bûn

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2014 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

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2014 թվականի օգոստոսին հրատարակված գիտական հոդված

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2014年の論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年论文

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Aleksandra Todic

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Alexander J Engar

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Anna Senina

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Anthony D Pomicter

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Brent D G Page

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Carolynn C Arpin

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Clinton C Mason

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David J Anderson

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Diana Resetca

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Ira L Kraft

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P2860

HER2 overexpression elicits a proinflammatory IL-6 autocrine signaling loop that is critical for tumorigenesis

AP24534, a pan-BCR-ABL inhibitor for chronic myeloid leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistance

Activation and association of Stat3 with Src in v-Src-transformed cell lines

Somatic STAT3 mutations in large granular lymphocytic leukemia

Stats: transcriptional control and biological impact

Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia

Stat3 as an oncogene

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

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

Disruption of transcriptionally active Stat3 dimers with non-phosphorylated, salicylic acid-based small molecules: potent in vitro and tumor cell activities.

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10.1038/LEU.2014.245

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29

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Richard Moriggl

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264904191

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25134459

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chronic myeloid leukemia

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4334758

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