Integrated genomic analysis illustrates the central role of JAK-STAT pathway activation in myeloproliferative neoplasm pathogenesis. - Wikidata - awgldk - TriplyDB

Integrated genomic analysis illustrates the central role of JAK-STAT pathway activation in myeloproliferative neoplasm pathogenesis.

Integrated genomic analysis illustrates the central role of JAK-STAT pathway activation in myeloproliferative neoplasm pathogenesis.

http://www.wikidata.org/entity/Q33697252

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Role of tyrosine-kinase inhibitors in myeloproliferative neoplasms: comparative lessons learned Recent advances in understanding myelofibrosis and essential thrombocythemia Overcoming treatment challenges in myelofibrosis and polycythemia vera: the role of ruxolitinib Genomic landscape of megakaryopoiesis and platelet function defects JAK kinase targeting in hematologic malignancies: a sinuous pathway from identification of genetic alterations towards clinical indications Long-term survival and blast transformation in molecularly annotated essential thrombocythemia, polycythemia vera, and myelofibrosis Managing Patients With Myelofibrosis in the Era of Janus Kinase Inhibitors Novel therapies for myelofibrosis The secret life of a megakaryocyte: emerging roles in bone marrow homeostasis control Calreticulin (CALR) mutation in myeloproliferative neoplasms (MPNs)Diagnosis, prevention, and management of bleeding episodes in Philadelphia-negative myeloproliferative neoplasms: recommendations by the Hemostasis Working Party of the German Society of Hematology and Medical Oncology (DGHO) and the Society of Thro Clinical effect of driver mutations of JAK2, CALR, or MPL in primary myelofibrosis Ruxolitinib: long-term management of patients with myelofibrosis and future directions in the treatment of myeloproliferative neoplasms X-linked thrombocytopenia with thalassemia displays bone marrow reticulin fibrosis and enhanced angiogenesis: comparisons with primary myelofibrosis.Efficacy, safety, and survival with ruxolitinib in patients with myelofibrosis: results of a median 3-year follow-up of COMFORT-I.ASXL1 mutations are frequent and prognostically detrimental in CSF3R-mutated chronic neutrophilic leukemia.Safety considerations when treating myelofibrosis.A phase I, open-label, dose-escalation, multicenter study of the JAK2 inhibitor NS-018 in patients with myelofibrosis Primary analysis of a phase II open-label trial of INCB039110, a selective JAK1 inhibitor, in patients with myelofibrosis.Anti-Platelet Factor 4/Heparin Antibody Formation Occurs Endogenously and at Unexpected High Frequency in Polycythemia Vera.Increased B cell activation is present in JAK2V617F-mutated, CALR-mutated and triple-negative essential thrombocythemia.CHZ868, a Type II JAK2 Inhibitor, Reverses Type I JAK Inhibitor Persistence and Demonstrates Efficacy in Myeloproliferative Neoplasms.Distinct effects of concomitant Jak2V617F expression and Tet2 loss in mice promote disease progression in myeloproliferative neoplasms.Central role of ULK1 in type I interferon signaling Differential clinical effects of different mutation subtypes in CALR-mutant myeloproliferative neoplasms.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.Mutant Calreticulin Requires Both Its Mutant C-terminus and the Thrombopoietin Receptor for Oncogenic Transformation Mutant calreticulin-expressing cells induce monocyte hyperreactivity through a paracrine mechanism Tyrosine 625 plays a key role and cooperates with tyrosine 630 in MPL W515L-induced signaling and myeloproliferative neoplasms.Efficacy and safety of ruxolitinib in the treatment of patients with myelofibrosis.Role of neoplastic monocyte-derived fibrocytes in primary myelofibrosis Novel insights into the biology and treatment of chronic myeloproliferative neoplasms.Neutrophil extracellular trap formation and circulating nucleosomes in patients with chronic myeloproliferative neoplasms.Molecular determinants of pathogenesis and clinical phenotype in myeloproliferative neoplasms.Driver mutations (JAK2V617F, MPLW515L/K or CALR), pentraxin-3 and C-reactive protein in essential thrombocythemia and polycythemia vera.BET protein bromodomain inhibitor-based combinations are highly active against post-myeloproliferative neoplasm secondary AML cells.Efficacy of ALK5 inhibition in myelofibrosis.A novel signalling screen demonstrates that CALR mutations activate essential MAPK signalling and facilitate megakaryocyte differentiation.Is there a role for JAK inhibitors in BCR-ABL1-negative myeloproliferative neoplasms other than myelofibrosis?Reducing symptom burden in patients with myeloproliferative neoplasms in the era of Janus kinase inhibitors.

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Integrated genomic analysis illustrates the central role of JAK-STAT pathway activation in myeloproliferative neoplasm pathogenesis.

http://www.wikidata.org/entity/Q33697252

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2014 nî lūn-bûn

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2014 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2014 թվականի ապրիլին 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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name

Integrated genomic analysis il ...... erative neoplasm pathogenesis.

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Integrated genomic analysis il ...... erative neoplasm pathogenesis.

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Integrated genomic analysis il ...... erative neoplasm pathogenesis.

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Integrated genomic analysis il ...... erative neoplasm pathogenesis.

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Integrated genomic analysis il ...... erative neoplasm pathogenesis.

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Integrated genomic analysis il ...... erative neoplasm pathogenesis.

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P2860

Profiling critical cancer gene mutations in clinical tumor samples

Impaired hydroxylation of 5-methylcytosine in myeloid cancers with mutant TET2

Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles.

Somatic CALR mutations in myeloproliferative neoplasms with nonmutated JAK2

JAK2 exon 12 mutations in polycythemia vera and idiopathic erythrocytosis

Genetic characterization of TET1, TET2, and TET3 alterations in myeloid malignancies

Prognostic relevance of integrated genetic profiling in acute myeloid leukemia.

Oncogenic CSF3R mutations in chronic neutrophilic leukemia and atypical CML

A comparison of normalization methods for high density oligonucleotide array data based on variance and bias

Molecular classification of cancer: class discovery and class prediction by gene expression monitoring

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