K-RasG12D-induced T-cell lymphoblastic lymphoma/leukemias harbor Notch1 mutations and are sensitive to gamma-secretase inhibitors. - Wikidata - awgldk - TriplyDB

K-RasG12D-induced T-cell lymphoblastic lymphoma/leukemias harbor Notch1 mutations and are sensitive to gamma-secretase inhibitors.

K-RasG12D-induced T-cell lymphoblastic lymphoma/leukemias harbor Notch1 mutations and are sensitive to gamma-secretase inhibitors.

http://www.wikidata.org/entity/Q36941105

about

Oncogenic Kras initiates leukemia in hematopoietic stem cells Simvastatin enhances bone marrow stromal cell differentiation into endothelial cells via notch signaling pathway.Phenotypic analysis of images of zebrafish treated with Alzheimer's gamma-secretase inhibitors.Murine models of acute leukemia: important tools in current pediatric leukemia research.Mutant Ikzf1, KrasG12D, and Notch1 cooperate in T lineage leukemogenesis and modulate responses to targeted agents.Impact of complex NOTCH1 mutations on survival in paediatric T-cell leukaemia.Notch signalling in T-cell lymphoblastic leukaemia/lymphoma and other haematological malignancies.Endogenous oncogenic Nras mutation promotes aberrant GM-CSF signaling in granulocytic/monocytic precursors in a murine model of chronic myelomonocytic leukemia Role of Notch and its oncogenic signaling crosstalk in breast cancer.Endogenous oncogenic Nras mutation initiates hematopoietic malignancies in a dose- and cell type-dependent manner.Notch1 inhibition targets the leukemia-initiating cells in a Tal1/Lmo2 mouse model of T-ALL.A complex Polycomb issue: the two faces of EZH2 in cancer.Co-targeting of Akt and Myc inhibits viability of lymphoma cells from Lck-Dlx5 mice.Targeting oncogenic Ras signaling in hematologic malignancies.Impact of PTEN abnormalities on outcome in pediatric patients with T-cell acute lymphoblastic leukemia treated on the MRC UKALL2003 trial Intracellular Signaling Pathways Involved in Childhood Acute Lymphoblastic Leukemia; Molecular Targets Loss of CD44 attenuates aberrant GM-CSF signaling in Kras G12D hematopoietic progenitor/precursor cells and prolongs the survival of diseased animals.Transcription factor Foxp1 exerts essential cell-intrinsic regulation of the quiescence of naive T cells Defective K-Ras oncoproteins overcome impaired effector activation to initiate leukemia in vivo Notch1 gene mutations target KRAS G12D-expressing CD8+ cells and contribute to their leukemogenic transformation.A double-edged sword: how oncogenes and tumor suppressor genes can contribute to chromosomal instability NK/T-cell lymphomas in children Inactivation of SHIP1 in T-cell acute lymphoblastic leukemia due to mutation and extensive alternative splicing.Rasgrp1 mutation increases naive T-cell CD44 expression and drives mTOR-dependent accumulation of Helios⁺ T cells and autoantibodies.STAT5 is crucial to maintain leukemic stem cells in acute myelogenous leukemias induced by MOZ-TIF2.NOTCH and phosphatidylinositide 3-kinase/phosphatase and tensin homolog deleted on chromosome ten/AKT/mammalian target of rapamycin (mTOR) signaling in T-cell development and T-cell acute lymphoblastic leukemia.The molecular basis of T cell acute lymphoblastic leukemia Ras/Raf/MEK/ERK Pathway Activation in Childhood Acute Lymphoblastic Leukemia and Its Therapeutic Targeting Interaction of Ras with p110γ is required for thymic β-selection in the mouse.Epigenetic regulation of the Ink4a-Arf (Cdkn2a) tumor suppressor locus in the initiation and progression of Notch1-driven T cell acute lymphoblastic leukemia.Bortezomib suppresses the growth of leukemia cells with Notch1 overexpression in vivo and in vitro.Aberrant expression of RasGRP1 cooperates with gain-of-function NOTCH1 mutations in T-cell leukemogenesis.TRIB2 regulates normal and stress-induced thymocyte proliferation.Aberrant Signaling Pathways in T-Cell Acute Lymphoblastic Leukemia.Cutting Edge: Codeletion of the Ras GTPase-Activating Proteins (RasGAPs) Neurofibromin 1 and p120 RasGAP in T Cells Results in the Development of T Cell Acute Lymphoblastic Leukemia.MEK and PI3K-AKT inhibitors synergistically block activated IL7 receptor signaling in T-cell acute lymphoblastic leukemia.High selective pressure for Notch1 mutations that induce Myc in T-cell acute lymphoblastic leukemia.Mice expressing KrasG12D in hematopoietic multipotent progenitor cells develop neonatal myeloid leukemia.Inactivation of Capicua in adult mice causes T-cell lymphoblastic lymphoma.Wild-type KRAS inhibits oncogenic KRAS-induced T-ALL in mice.

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P2860

K-RasG12D-induced T-cell lymphoblastic lymphoma/leukemias harbor Notch1 mutations and are sensitive to gamma-secretase inhibitors.

http://www.wikidata.org/entity/Q36941105

description

2008 nî lūn-bûn

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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2008年论文

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2008年论文

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name

K-RasG12D-induced T-cell lymph ...... to gamma-secretase inhibitors.

@en

type

label

K-RasG12D-induced T-cell lymph ...... to gamma-secretase inhibitors.

@en

prefLabel

K-RasG12D-induced T-cell lymph ...... to gamma-secretase inhibitors.

@en

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K-RasG12D-induced T-cell lymph ...... to gamma-secretase inhibitors.

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P2093

Benjamin H Lee

http://www.w3.org/2001/XMLSchema#string

Claudia Scholl

http://www.w3.org/2001/XMLSchema#string

D Gary Gilliland

http://www.w3.org/2001/XMLSchema#string

Dena S Leeman

http://www.w3.org/2001/XMLSchema#string

J Erika Haydu

http://www.w3.org/2001/XMLSchema#string

Jianing Liu

http://www.w3.org/2001/XMLSchema#string

Melanie G Cornejo

http://www.w3.org/2001/XMLSchema#string

Stefan Fröhling

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Thomas Kindler

http://www.w3.org/2001/XMLSchema#string

P2860

RAS mutation in acute myeloid leukemia is associated with distinct cytogenetic subgroups but does not influence outcome in patients younger than 60 years.

The GTPase superfamily: conserved structure and molecular mechanism

Proteins regulating Ras and its relatives

Phospholipase C(epsilon): a novel Ras effector

Disordered T-cell development and T-cell malignancies in SCL LMO1 double-transgenic mice: parallels with E2A-deficient mice

Activating mutations of NOTCH1 in human T cell acute lymphoblastic leukemia

Hyperactive Ras in developmental disorders and cancer

Phosphatidylinositol-3-OH kinase as a direct target of Ras

Ras caught in another affair: the exchange factors for Ral.

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3373-3382

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8

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112

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23133751

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18663146

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2569181

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