Heterodimeric JAK-STAT activation as a mechanism of persistence to JAK2 inhibitor therapy. - Wikidata - awgldk - TriplyDB

Heterodimeric JAK-STAT activation as a mechanism of persistence to JAK2 inhibitor therapy.

Heterodimeric JAK-STAT activation as a mechanism of persistence to JAK2 inhibitor therapy.

http://www.wikidata.org/entity/Q38824881

about

JAK kinase targeting in hematologic malignancies: a sinuous pathway from identification of genetic alterations towards clinical indications Clinical potential of pacritinib in the treatment of myelofibrosis JAK2 activation by growth hormone and other cytokines Signal transduction in the chronic leukemias: implications for targeted therapies A Pilot Study of Quantitative MRI Parametric Response Mapping of Bone Marrow Fat for Treatment Assessment in Myelofibrosis.Contribution of chaperones to STAT pathway signaling.Novel therapies for myelofibrosis Systems biology of cancer: entropy, disorder, and selection-driven evolution to independence, invasion and "swarm intelligence"Divergent modulation of Src-family kinase regulatory interactions with ATP-competitive inhibitors.Targeting substrate-site in Jak2 kinase prevents emergence of genetic resistance Efficacy of ruxolitinib for myelofibrosis.Safety evaluation of ruxolitinib for treating myelofibrosis.Safety considerations when treating myelofibrosis.A phase I, open-label, dose-escalation, multicenter study of the JAK2 inhibitor NS-018 in patients with myelofibrosis ALOX5 exhibits anti-tumor and drug-sensitizing effects in MLL-rearranged leukemia.Mechanistic insights into activation and SOCS3-mediated inhibition of myeloproliferative neoplasm-associated JAK2 mutants from biochemical and structural analyses The molecular regulation of Janus kinase (JAK) activation Co-targeting the PI3K/mTOR and JAK2 signalling pathways produces synergistic activity against myeloproliferative neoplasms Combination treatment for myeloproliferative neoplasms using JAK and pan-class I PI3K inhibitors.Acylglycerol kinase augments JAK2/STAT3 signaling in esophageal squamous cells The arrival of JAK inhibitors: advancing the treatment of immune and hematologic disorders.CHZ868, a Type II JAK2 Inhibitor, Reverses Type I JAK Inhibitor Persistence and Demonstrates Efficacy in Myeloproliferative Neoplasms.Investigational Janus kinase inhibitors.Enu mutagenesis identifies a novel platelet phenotype in a loss-of-function Jak2 allele.Evaluation of the in vitro and in vivo efficacy of the JAK inhibitor AZD1480 against JAK-mutated acute lymphoblastic leukemia.Emerging therapeutic paradigms to target the dysregulated Janus kinase/signal transducer and activator of transcription pathway in hematological malignancies RAS signaling promotes resistance to JAK inhibitors by suppressing BAD-mediated apoptosis.A method for screening and validation of resistant mutations against kinase inhibitors Janus kinase inhibitors and allogeneic stem cell transplantation for myelofibrosis Discovery of a drug targeting microenvironmental support for lymphoma cells by screening using patient-derived xenograft cells Activity of the Type II JAK2 Inhibitor CHZ868 in B Cell Acute Lymphoblastic Leukemia.Mesenchymal Cell Reprogramming in Experimental MPLW515L Mouse Model of Myelofibrosis.Tumor-specific HSP90 inhibition as a therapeutic approach in JAK-mutant acute lymphoblastic leukemias.The PIM inhibitor AZD1208 synergizes with ruxolitinib to induce apoptosis of ruxolitinib sensitive and resistant JAK2-V617F-driven cells and inhibit colony formation of primary MPN cells.Establishing the role of tyrosine kinase 2 in cancer.Single agent BMS-911543 Jak2 inhibitor has distinct inhibitory effects on STAT5 signaling in genetically engineered mice with pancreatic cancer Intrinsic resistance to JAK2 inhibition in myelofibrosis.New Strategies in Myeloproliferative Neoplasms: The Evolving Genetic and Therapeutic Landscape.Efficacy and safety of ruxolitinib in the treatment of patients with myelofibrosis.Advances in myelofibrosis: a clinical case approach.

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Heterodimeric JAK-STAT activation as a mechanism of persistence to JAK2 inhibitor therapy.

http://www.wikidata.org/entity/Q38824881

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Abby Weinstein

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Ann Mullally

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Aviva Goel

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Benjamin L Ebert

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Bradley E Bernstein

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Fan Liu

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Laura Leung

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Lindsay M Saunders

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Mazhar Adli

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Mithat Gönen

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P2860

KRAS mutations and primary resistance of lung adenocarcinomas to gefitinib or erlotinib

Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation

Genome-wide maps of chromatin state in pluripotent and lineage-committed cells

Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain

Modulation of Activation-Loop Phosphorylation by JAK Inhibitors Is Binding Mode Dependent

EGFR mutation and resistance of non-small-cell lung cancer to gefitinib.

MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling.

Inhibition of Mutated, Activated BRAF in Metastatic Melanoma

Gefitinib or carboplatin-paclitaxel in pulmonary adenocarcinoma

A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera

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155-159

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10.1038/NATURE11303

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7414

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489

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Gabriela Chiosis

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Srdan Verstovsek

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2012-09-01T00:00:00Z

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229436278

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22820254

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3991463

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