Conditional expression of oncogenic K-ras from its endogenous promoter induces a myeloproliferative disease. - Wikidata - wikimedia - TriplyDB

Conditional expression of oncogenic K-ras from its endogenous promoter induces a myeloproliferative disease.

Conditional expression of oncogenic K-ras from its endogenous promoter induces a myeloproliferative disease.

http://www.wikidata.org/entity/Q36056927

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The molecular mechanisms that control thrombopoiesis Engineering mouse models with myelodysplastic syndrome human candidate genes; how relevant are they?Juvenile myelomonocytic leukemia: molecular pathogenesis informs current approaches to therapy and hematopoietic cell transplantation Oncogenic Kras initiates leukemia in hematopoietic stem cells RAS oncogenes: weaving a tumorigenic web RAS diseases in children Developmental and species-divergent globin switching are driven by BCL11A Knock-in of an internal tandem duplication mutation into murine FLT3 confers myeloproliferative disease in a mouse model A retroviral library genetic screen identifies IRF-2 as an inhibitor of N-ras-induced growth suppression in leukemic cells.Ral is both necessary and sufficient for the inhibition of myeloid differentiation mediated by Ras Genome profiling of chronic myelomonocytic leukemia: frequent alterations of RAS and RUNX1 genes.Loss of the Gata1 gene IE exon leads to variant transcript expression and the production of a GATA1 protein lacking the N-terminal domain Oncogenic RAS enables DNA damage- and p53-dependent differentiation of acute myeloid leukemia cells in response to chemotherapy.Combined MEK and JAK inhibition abrogates murine myeloproliferative neoplasm.Copy-neutral loss of heterozygosity is prevalent and a late event in the pathogenesis of FLT3/ITD AML Ras activation of Erk restores impaired tonic BCR signaling and rescues immature B cell differentiation.Mutant Ikzf1, KrasG12D, and Notch1 cooperate in T lineage leukemogenesis and modulate responses to targeted agents.Inhibition of the Gab2/PI3K/mTOR signaling ameliorates myeloid malignancy caused by Ptpn11 (Shp2) gain-of-function mutations.Use of chromosome engineering to model a segmental deletion of chromosome band 7q22 found in myeloid malignancies.p53 loss promotes acute myeloid leukemia by enabling aberrant self-renewal.Identification of K-ras as the major regulator for cytokine-dependent Akt activation in erythroid progenitors in vivo.Constitutive MAP kinase activation in hematopoietic stem cells induces a myeloproliferative disorder.Germline CBL mutations cause developmental abnormalities and predispose to juvenile myelomonocytic leukemia.STAT3 supports experimental K-RasG12D-induced murine myeloproliferative neoplasms dependent on serine phosphorylation.A germline gain-of-function mutation in Ptpn11 (Shp-2) phosphatase induces myeloproliferative disease by aberrant activation of hematopoietic stem cells.Harnessing preclinical mouse models to inform human clinical cancer trials.Endogenous oncogenic Nras mutation promotes aberrant GM-CSF signaling in granulocytic/monocytic precursors in a murine model of chronic myelomonocytic leukemia Lyn- and PLC-beta3-dependent regulation of SHP-1 phosphorylation controls Stat5 activity and myelomonocytic leukemia-like disease.Pathogenesis of acute myeloid leukaemia and inv(16)(p13;q22): a paradigm for understanding leukaemogenesis?The Lkb1 metabolic sensor maintains haematopoietic stem cell survival.K-RasV14I recapitulates Noonan syndrome in mice.Hematopoiesis and leukemogenesis in mice expressing oncogenic NrasG12D from the endogenous locus.Combining ATR suppression with oncogenic Ras synergistically increases genomic instability, causing synthetic lethality or tumorigenesis in a dosage-dependent manner.PML-RARA can increase hematopoietic self-renewal without causing a myeloproliferative disease in mice.Germinal center B-cells resist transformation by Kras independently of tumor suppressor Arf Loss of Apc allows phenotypic manifestation of the transforming properties of an endogenous K-ras oncogene in vivo Systemic activation of K-ras rapidly induces gastric hyperplasia and metaplasia in mice Activating the expression of human K-rasG12D stimulates oncogenic transformation in transgenic goat fetal fibroblast cells.Endogenous oncogenic Nras mutation initiates hematopoietic malignancies in a dose- and cell type-dependent manner.The prognostic impact of K-RAS mutations in adult acute myeloid leukemia patients treated with high-dose cytarabine

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Conditional expression of oncogenic K-ras from its endogenous promoter induces a myeloproliferative disease.

http://www.wikidata.org/entity/Q36056927

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2004 nî lūn-bûn

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Conditional expression of onco ...... a myeloproliferative disease.

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Conditional expression of onco ...... a myeloproliferative disease.

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Conditional expression of onco ...... a myeloproliferative disease.

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Journal of Clinical Investigation

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Conditional expression of onco ...... a myeloproliferative disease.

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D Gary Gilliland

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Hirokazu Shigematsu

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Ifor R Williams

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Iris T Chan

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Jeffery L Kutok

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Koichi Akashi

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Lauren Kelly

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Leisa Johnson

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Sarah Cohen

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Tyler Jacks

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P2860

Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a

NF1 tumor suppressor gene function: narrowing the GAP

Role of phosphoinositide 3-OH kinase in cell transformation and control of the actin cytoskeleton by Ras

Nf1 deficiency causes Ras-mediated granulocyte/macrophage colony stimulating factor hypersensitivity and chronic myeloid leukaemia

Targeted deletion of the H-ras gene decreases tumor formation in mouse skin carcinogenesis

Tumour predisposition in mice heterozygous for a targeted mutation in Nf1

Critical role for Gab2 in transformation by BCR/ABL

Inducible gene targeting in mice

A clonogenic common myeloid progenitor that gives rise to all myeloid lineages

Fusion of ETV6 to neurotrophin-3 receptor TRKC in acute myeloid leukemia with t(12;15)(p13;q25).

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338267

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