Oncogenesis of T-ALL and nonmalignant consequences of overexpressing intracellular NOTCH1 - Wikidata - awgldk - TriplyDB

Oncogenesis of T-ALL and nonmalignant consequences of overexpressing intracellular NOTCH1

Oncogenesis of T-ALL and nonmalignant consequences of overexpressing intracellular NOTCH1

http://www.wikidata.org/entity/Q36979929

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Deletion of the RNA-binding proteins ZFP36L1 and ZFP36L2 leads to perturbed thymic development and T lymphoblastic leukemia A dominantly acting murine allele of Mcm4 causes chromosomal abnormalities and promotes tumorigenesis Therapeutic targeting of the cyclin D3:CDK4/6 complex in T cell leukemia.The PIAS-like Coactivator Zmiz1 Is a Direct and Selective Cofactor of Notch1 in T Cell Development and Leukemia Interconnecting molecular pathways in the pathogenesis and drug sensitivity of T-cell acute lymphoblastic leukemia Modeling T-cell acute lymphoblastic leukemia induced by the SCL and LMO1 oncogenes.ATM-deficient thymic lymphoma is associated with aberrant tcrd rearrangement and gene amplification.Notch ankyrin repeat domain variation influences leukemogenesis and Myc transactivation.Notch target gene deregulation and maintenance of the leukemogenic phenotype do not require RBP-J kappa in Ikaros null mice.The Notch/Hes1 pathway sustains NF-κB activation through CYLD repression in T cell leukemia.Notch dimerization is required for leukemogenesis and T-cell development.Notch signalling in T-cell lymphoblastic leukaemia/lymphoma and other haematological malignancies.Cyclin C is a haploinsufficient tumour suppressor.Long-range enhancer activity determines Myc sensitivity to Notch inhibitors in T cell leukemia Mutation of inhibitory helix-loop-helix protein Id3 causes γδ T-cell lymphoma in mice.The evolution of thymic lymphomas in p53 knockout mice GAS6 receptor status is associated with dormancy and bone metastatic tumor formation Growth factor independent-1 maintains Notch1-dependent transcriptional programming of lymphoid precursors.Constitutive Notch pathway activation in murine ZMYM2-FGFR1-induced T-cell lymphomas associated with atypical myeloproliferative disease.Repression of tumor suppressor miR-451 is essential for NOTCH1-induced oncogenesis in T-ALL.Notch1 inhibition targets the leukemia-initiating cells in a Tal1/Lmo2 mouse model of T-ALL.Notch Signaling in T-Cell Development and T-ALL Cell of origin strongly influences genetic selection in a mouse model of T-ALL Trib2 Suppresses Tumor Initiation in Notch-Driven T-ALL.The requirement for cyclin D function in tumor maintenance.Divergent effects of supraphysiologic Notch signals on leukemia stem cells and hematopoietic stem cells MicroRNAs and Glucocorticoid-Induced Apoptosis in Lymphoid Malignancies Characterization of transgenic mice expressing cancer-associated variants of human NOTCH1 Notch1 gene mutations target KRAS G12D-expressing CD8+ cells and contribute to their leukemogenic transformation.Pre-TCR signaling inactivates Notch1 transcription by antagonizing E2A.Irradiation alters selection for oncogenic mutations in hematopoietic progenitors.Stage-specific Arf tumor suppression in Notch1-induced T-cell acute lymphoblastic leukemia.Murine leukemia virus envelope gp70 is a shared biomarker for the high-sensitivity quantification of murine tumor burden.Prolyl-isomerase Pin1 controls normal and cancer stem cells of the breast.Oncogenic Notch signaling in T-cell and B-cell lymphoproliferative disorders.Loss of IP3R-dependent Ca2+ signalling in thymocytes leads to aberrant development and acute lymphoblastic leukemia.ZFX controls propagation and prevents differentiation of acute T-lymphoblastic and myeloid leukemia.Epigenetic regulation of the Ink4a-Arf (Cdkn2a) tumor suppressor locus in the initiation and progression of Notch1-driven T cell acute lymphoblastic leukemia.Notch signaling expands a pre-malignant pool of T-cell acute lymphoblastic leukemia clones without affecting leukemia-propagating cell frequency.High-level expression of Mastermind-like 2 contributes to aberrant activation of the NOTCH signaling pathway in human lymphomas.

P2860

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P2860

Oncogenesis of T-ALL and nonmalignant consequences of overexpressing intracellular NOTCH1

http://www.wikidata.org/entity/Q36979929

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

Oncogenesis of T-ALL and nonmalignant consequences of overexpressing intracellular NOTCH1

@en

type

label

Oncogenesis of T-ALL and nonmalignant consequences of overexpressing intracellular NOTCH1

@en

prefLabel

Oncogenesis of T-ALL and nonmalignant consequences of overexpressing intracellular NOTCH1

@en

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P1433

Journal of Experimental Medicine

P1476

Oncogenesis of T-ALL and nonmalignant consequences of overexpressing intracellular NOTCH1

@en

P2093

Alexei Protopopov

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

Fotini Gounari

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

Harald von Boehmer

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

Khashayarsha Khazaie

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

Xiaoyu Li

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

P2860

Notch signaling: cell fate control and signal integration in development

Analysis of C-MYC function in normal cells via conditional gene-targeted mutation

Requirement for cyclin D3 in lymphocyte development and T cell leukemias

Activating mutations of NOTCH1 in human T cell acute lymphoblastic leukemia

Characterization of the c-MYC-regulated transcriptome by SAGE: identification and analysis of c-MYC target genes

Reversible tumorigenesis by MYC in hematopoietic lineages.

Combined expression of pTalpha and Notch3 in T cell leukemia identifies the requirement of preTCR for leukemogenesis.

Disruption of pre-TCR expression accelerates lymphomagenesis in E2A-deficient mice

NOTCH1 directly regulates c-MYC and activates a feed-forward-loop transcriptional network promoting leukemic cell growth

Growth suppression of pre-T acute lymphoblastic leukemia cells by inhibition of notch signaling.

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2851-2861

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10.1084/JEM.20081561

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P433

12

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205

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2008-11-03T00:00:00Z

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23448610

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P698

18981238

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P932

2585834

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