STAT5 is crucial to maintain leukemic stem cells in acute myelogenous leukemias induced by MOZ-TIF2. - Test2 - elhamkhani - TriplyDB

STAT5 is crucial to maintain leukemic stem cells in acute myelogenous leukemias induced by MOZ-TIF2.

STAT5 is crucial to maintain leukemic stem cells in acute myelogenous leukemias induced by MOZ-TIF2.

http://www.wikidata.org/entity/Q37565082

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The Role of Histone Acetyltransferases in Normal and Malignant Hematopoiesis SEL120-34A is a novel CDK8 inhibitor active in AML cells with high levels of serine phosphorylation of STAT1 and STAT5 transactivation domains STAT activation status differentiates leukemogenic from non-leukemogenic stem cells in AML and is suppressed by arsenic in t(6;9)-positive AML Cooperation between RUNX1-ETO9a and novel transcriptional partner KLF6 in upregulation of Alox5 in acute myeloid leukemia.Emerging therapeutic paradigms to target the dysregulated Janus kinase/signal transducer and activator of transcription pathway in hematological malignancies Tetraspanin Family Member, CD82, Regulates Expression of EZH2 via Inactivation of p38 MAPK Signaling in Leukemia Cells.Hematopoietic Differentiation Is Required for Initiation of Acute Myeloid Leukemia.Potent co-operation between the NUP98-NSD1 fusion and the FLT3-ITD mutation in acute myeloid leukemia induction Reactive oxygen species in eradicating acute myeloid leukemic stem cells Oncogenic STAT5 signaling promotes oxidative stress in chronic myeloid leukemia cells by repressing antioxidant defenses.The Impact of FLT3 Mutations on the Development of Acute Myeloid Leukemias.Acetylation and deacetylation in cancer stem-like cells.A novel, dual pan-PIM/FLT3 inhibitor SEL24 exhibits broad therapeutic potential in acute myeloid leukemia.Cancer Stem Cells (CSCs) in Drug Resistance and their Therapeutic Implications in Cancer Treatment.

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STAT5 is crucial to maintain leukemic stem cells in acute myelogenous leukemias induced by MOZ-TIF2.

http://www.wikidata.org/entity/Q37565082

description

2012 nî lūn-bûn

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2012年の論文

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年學術文章

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2012年學術文章

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2012年學術文章

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name

STAT5 is crucial to maintain l ...... leukemias induced by MOZ-TIF2.

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STAT5 is crucial to maintain l ...... leukemias induced by MOZ-TIF2.

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type

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STAT5 is crucial to maintain l ...... leukemias induced by MOZ-TIF2.

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STAT5 is crucial to maintain l ...... leukemias induced by MOZ-TIF2.

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prefLabel

STAT5 is crucial to maintain l ...... leukemias induced by MOZ-TIF2.

@en

STAT5 is crucial to maintain l ...... leukemias induced by MOZ-TIF2.

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0008-5472.CAN-12-0255

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Cancer Research

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STAT5 is crucial to maintain l ...... leukemias induced by MOZ-TIF2.

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Andrea Schüler

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Andreas Kreft

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Benjamin H Lee

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D Gary Gilliland

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Daniel Sasca

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Gerlinde Wernig

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Gertraud W Robinson

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Glen Raffel

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Nan Zhu

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Patricia S Hähnel

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P2860

MOZ-TIF2 inhibits transcription by nuclear receptors and p53 by impairment of CBP function

MOZ and MORF, two large MYSTic HATs in normal and cancer stem cells

MOZ is essential for maintenance of hematopoietic stem cells

Knock-in of an internal tandem duplication mutation into murine FLT3 confers myeloproliferative disease in a mouse model

Monocytic leukemia zinc finger protein is essential for the development of long-term reconstituting hematopoietic stem cells

A novel fusion between MOZ and the nuclear receptor coactivator TIF2 in acute myeloid leukemia

FLT3 as a therapeutic target in AML: still challenging after all these years

Principles of cancer therapy: oncogene and non-oncogene addiction

Acute mixed lineage leukemia with an inv(8)(p11q13) resulting in fusion of the genes for MOZ and TIF2.

AML1-ETO and C-KIT mutation/overexpression in t(8;21) leukemia: implication in stepwise leukemogenesis and response to Gleevec.

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373-384

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10.1158/0008-5472.CAN-12-0255

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1

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Ernesto Bockamp

Lothar Hennighausen

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2012-11-13T00:00:00Z

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23149921

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