Distinct effects of concomitant Jak2V617F expression and Tet2 loss in mice promote disease progression in myeloproliferative neoplasms. - Wikidata - awgldk - TriplyDB

Distinct effects of concomitant Jak2V617F expression and Tet2 loss in mice promote disease progression in myeloproliferative neoplasms.

Distinct effects of concomitant Jak2V617F expression and Tet2 loss in mice promote disease progression in myeloproliferative neoplasms.

http://www.wikidata.org/entity/Q34876785

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Rationale for revision and proposed changes of the WHO diagnostic criteria for polycythemia vera, essential thrombocythemia and primary myelofibrosis Role of TET enzymes in DNA methylation, development, and cancer Frequencies, Laboratory Features, and Granulocyte Activation in Chinese Patients with CALR-Mutated Myeloproliferative Neoplasms.Gene expression profiling of loss of TET2 and/or JAK2V617F mutant hematopoietic stem cells from mouse models of myeloproliferative neoplasms DNMT3A(R882H) mutant and Tet2 inactivation cooperate in the deregulation of DNA methylation control to induce lymphoid malignancies in mice Myeloproliferative neoplasms: A decade of discoveries and treatment advances.Overview of Transgenic Mouse Models of Myeloproliferative Neoplasms (MPNs).Hmga2 promotes the development of myelofibrosis in Jak2V617F knockin mice by enhancing TGF-β1 and Cxcl12 pathways.Contemporary insights into the pathogenesis and treatment of chronic myeloproliferative neoplasms.Dysregulation of TET2 in hematologic malignancies.Myeloproliferative neoplasm stem cells.Epigenetic dysregulation of hematopoietic stem cells and preleukemic state.Clonal hematopoiesis as determined by the HUMARA assay is a marker for acquired mutations in epigenetic regulators in older women.The loss of Ezh2 drives the pathogenesis of myelofibrosis and sensitizes tumor-initiating cells to bromodomain inhibition.Alterations in DNA methylation/demethylation intermediates predict clinical outcome in chronic lymphocytic leukemia JAK2/IDH-mutant-driven myeloproliferative neoplasm is sensitive to combined targeted inhibition.Integrated genomic analysis identifies deregulated JAK/STAT-MYC-biosynthesis axis in aggressive NK-cell leukemia.Mutations in myeloproliferative neoplasms - their significance and clinical use.Epigenetic Regulations in Neural Stem Cells and Neurological Diseases.

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P2860

Distinct effects of concomitant Jak2V617F expression and Tet2 loss in mice promote disease progression in myeloproliferative neoplasms.

http://www.wikidata.org/entity/Q34876785

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2014 nî lūn-bûn

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2014 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

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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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Distinct effects of concomitan ...... myeloproliferative neoplasms.

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Distinct effects of concomitan ...... myeloproliferative neoplasms.

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Distinct effects of concomitan ...... myeloproliferative neoplasms.

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Amy Ko

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Benjamin L Ebert

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Edwin Chen

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Emily A Rosen

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Shannon Elf

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P2860

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

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

Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation

Mouse models of myeloproliferative neoplasms: JAK of all grades

Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis

Genomic and epigenomic landscapes of adult de novo acute myeloid leukemia.

A gain-of-function mutation of JAK2 in myeloproliferative disorders

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