p53 signaling in response to increased DNA damage sensitizes AML1-ETO cells to stress-induced death - Wikidata - wikimedia - TriplyDB

p53 signaling in response to increased DNA damage sensitizes AML1-ETO cells to stress-induced death

p53 signaling in response to increased DNA damage sensitizes AML1-ETO cells to stress-induced death

http://www.wikidata.org/entity/Q36445874

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Aging of hematopoietic stem cells: DNA damage and mutations?In vitro transformation of primary human CD34+ cells by AML fusion oncogenes: early gene expression profiling reveals possible drug target in AML The rate of spontaneous mutations in human myeloid cells Recurrent CDC25C mutations drive malignant transformation in FPD/AML.Contribution of an aged microenvironment to aging-associated myeloproliferative disease.N-Ras(G12D) induces features of stepwise transformation in preleukemic human umbilical cord blood cultures expressing the AML1-ETO fusion gene Identification of the Adapter Molecule MTSS1 as a Potential Oncogene-Specific Tumor Suppressor in Acute Myeloid Leukemia The thrombopoietin/MPL/Bcl-xL pathway is essential for survival and self-renewal in human preleukemia induced by AML1-ETO.Thrombopoietin/MPL participates in initiating and maintaining RUNX1-ETO acute myeloid leukemia via PI3K/AKT signaling.Gene and protein analysis reveals that p53 pathway is functionally inactivated in cytogenetically normal Acute Myeloid Leukemia and Acute Promyelocytic Leukemia Stem Cell-Specific Mechanisms Ensure Genomic Fidelity within HSCs and upon Aging of HSCs.UBASH3B/Sts-1-CBL axis regulates myeloid proliferation in human preleukemia induced by AML1-ETO.AML1-ETO mediates hematopoietic self-renewal and leukemogenesis through a COX/β-catenin signaling pathway Transcription factor RUNX1 promotes survival of acute myeloid leukemia cells Mouse models of human AML accurately predict chemotherapy response Supraphysiologic levels of the AML1-ETO isoform AE9a are essential for transformation.Targeting autophagic pathways for cancer drug discovery Core binding factor at the crossroads: determining the fate of the HSC.Molecular pathogenesis of core binding factor leukemia: current knowledge and future prospects.DNA damage accumulation and repair defects in acute myeloid leukemia: implications for pathogenesis, disease progression, and chemotherapy resistance.Mouse models for core binding factor leukemia.Identifying high-risk adult AML patients: epigenetic and genetic risk factors and their implications for therapy.RUNX1 and its fusion oncoprotein derivative, RUNX1-ETO, induce senescence-like growth arrest independently of replicative stress.Acute B lymphoblastic leukaemia-propagating cells are present at high frequency in diverse lymphoblast populations.Autophagy is dispensable for Kmt2a/Mll-Mllt3/Af9 AML maintenance and anti-leukemic effect of chloroquine.Activating c-KIT mutations confer oncogenic cooperativity and rescue RUNX1/ETO-induced DNA damage and apoptosis in human primary CD34+ hematopoietic progenitors.Acute myeloid leukemia with the t(8;21) translocation: clinical consequences and biological implications.Immortalization of human AE pre-leukemia cells by hTERT allows leukemic transformation.ETV6/RUNX1 induces reactive oxygen species and drives the accumulation of DNA damage in B cells.The leukemia-associated RUNX1/ETO oncoprotein confers a mutator phenotype.OGG1 is a novel prognostic indicator in acute myeloid leukaemia.Dysfunctional diversity of p53 proteins in adult acute myeloid leukemia: projections on diagnostic workup and therapy.Ruxolitinib-induced defects in DNA repair cause sensitivity to PARP inhibitors in myeloproliferative neoplasms.RUNX1 Mutations in Inherited and Sporadic Leukemia.A Regulatory Role for RUNX1, RUNX3 in the Maintenance of Genomic Integrity.RUNX1-ETO Leukemia.Chromatin modifications induced by the AML1-ETO fusion protein reversibly silence its genomic targets through AML1 and Sp1 binding motifs.MAPK8-mediated stabilization of SP1 is essential for RUNX1-RUNX1T1 - driven leukaemia.C-terminal mutation of RUNX1 attenuates the DNA-damage repair response in hematopoietic stem cells.Tyrosine kinase inhibitor-induced defects in DNA repair sensitize FLT3(ITD)-positive leukemia cells to PARP1 inhibitors.

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p53 signaling in response to increased DNA damage sensitizes AML1-ETO cells to stress-induced death

http://www.wikidata.org/entity/Q36445874

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2007 nî lūn-bûn

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2007年の論文

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2007年学术文章

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David Schleimer

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

Hartmut Geiger

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James C Mulloy

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Mark Wunderlich

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Michael Jansen

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Ondrej Krejci

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Paul R Andreassen

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P2860

The t(8;21) translocation in acute myeloid leukemia results in production of an AML1-MTG8 fusion transcript

Exploration, normalization, and summaries of high density oligonucleotide array probe level data

DNA double-stranded breaks induce histone H2AX phosphorylation on serine 139

Identification of breakpoints in t(8;21) acute myelogenous leukemia and isolation of a fusion transcript, AML1/ETO, with similarity to Drosophila segmentation gene, runt

Modeling pO(2) distributions in the bone marrow hematopoietic compartment. II. Modified Kroghian models

Production of large amounts of hydrogen peroxide by human tumor cells

Prenatal origin of childhood AML occurs less frequently than in childhood ALL.

AML1-ETO expression is directly involved in the development of acute myeloid leukemia in the presence of additional mutations

Modeling pO(2) distributions in the bone marrow hematopoietic compartment. I. Krogh's model.

AML1 and the AML1-ETO fusion protein in the pathogenesis of t(8;21) AML.

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2190-2199

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2234055

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