Human AML1/MDS1/EVI1 fusion protein induces an acute myelogenous leukemia (AML) in mice: a model for human AML - Wikidata - awgldk - TriplyDB

Human AML1/MDS1/EVI1 fusion protein induces an acute myelogenous leukemia (AML) in mice: a model for human AML

Human AML1/MDS1/EVI1 fusion protein induces an acute myelogenous leukemia (AML) in mice: a model for human AML

http://www.wikidata.org/entity/Q37116614

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Evi-1 transforming and repressor activities are mediated by CtBP co-repressor proteins SALL4, a novel oncogene, is constitutively expressed in human acute myeloid leukemia (AML) and induces AML in transgenic mice Cooperation of BCR-ABL and AML1/MDS1/EVI1 in blocking myeloid differentiation and rapid induction of an acute myelogenous leukemia The RUNX genes: gain or loss of function in cancer Allele-specific KRT1 expression is a complex trait.RUNX1-ETO and RUNX1-EVI1 Differentially Reprogram the Chromatin Landscape in t(8;21) and t(3;21) AML.AML1-ETO expression is directly involved in the development of acute myeloid leukemia in the presence of additional mutations A murine model of CML blast crisis induced by cooperation between BCR/ABL and NUP98/HOXA9 Chromatin modification, leukaemia and implications for therapy.Dissecting the molecular mechanism of chronic myelogenous leukemia using murine models.Functionally deregulated AML1/RUNX1 cooperates with BCR-ABL to induce a blastic phase-like phenotype of chronic myelogenous leukemia in mice.The molecular mechanism of chronic myelogenous leukemia and its therapeutic implications: studies in a murine model.Animal models of acute myelogenous leukaemia - development, application and future perspectives.Gatekeeper pathways and cellular background in the pathogenesis and therapy of AML.Altered myelopoiesis and the development of acute myeloid leukemia in transgenic mice overexpressing cyclin A1.RUNX1-Evi-1 fusion gene inhibited differentiation and apoptosis in myelopoiesis: an in vivo study.FoxO1-dependent induction of acute myeloid leukemia by osteoblasts in mice Review: genetic models of acute myeloid leukaemia.The role of aberrant transcription factor in the progression of chronic myeloid leukemia.A novel rapid-onset high-penetrance plasmacytoma mouse model driven by deregulation of cMYC cooperating with KRAS12V in BALB/c mice.MYC and PIM2 co-expression in mouse bone marrow cells readily establishes permanent myeloid cell lines that can induce lethal myeloid sarcoma in vivo The leukemic fusion gene AML1-MDS1-EVI1 suppresses CEBPA in acute myeloid leukemia by activation of Calreticulin.RUNX1 translocations and fusion genes in malignant hemopathies.EVI1 induces myelodysplastic syndrome in mice.The leukemia-associated transcription repressor AML1/MDS1/EVI1 requires CtBP to induce abnormal growth and differentiation of murine hematopoietic cells.The t(3;21) fusion product, AML1/Evi-1 blocks AML1-induced transactivation by recruiting CtBP.Hypomethylation and Over-Expression of the Beta Isoform of BLIMP1 is Induced by Epstein-Barr Virus Infection of B Cells; Potential Implications for the Pathogenesis of EBV-Associated Lymphomas.Both AML1 and EVI1 oncogenic components are required for the cooperation of AML1/MDS1/EVI1 with BCR/ABL in the induction of acute myelogenous leukemia in mice.Consistent up-regulation of Stat3 Independently of Jak2 mutations in a new murine model of essential thrombocythemia.Fadd and Skp2 are possible downstream targets of RUNX1-EVI1.Entinostat prevents leukemia maintenance in a collaborating oncogene-dependent model of cytogenetically normal acute myeloid leukemia.

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Human AML1/MDS1/EVI1 fusion protein induces an acute myelogenous leukemia (AML) in mice: a model for human AML

http://www.wikidata.org/entity/Q37116614

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article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on February 2000

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Human AML1/MDS1/EVI1 fusion pr ...... in mice: a model for human AML

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Human AML1/MDS1/EVI1 fusion protein induces an acute myelogenous leukemia

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Human AML1/MDS1/EVI1 fusion pr ...... in mice: a model for human AML

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Human AML1/MDS1/EVI1 fusion protein induces an acute myelogenous leukemia

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prefLabel

Human AML1/MDS1/EVI1 fusion pr ...... in mice: a model for human AML

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Human AML1/MDS1/EVI1 fusion protein induces an acute myelogenous leukemia

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Proceedings of the National Academy of Sciences of the United States of America

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Human AML1/MDS1/EVI1 fusion pr ...... in mice: a model for human AML

@en

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G M Cuenco

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G Nucifora

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

R Ren

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P2860

Fusion between transcription factor CBF beta/PEBP2 beta and a myosin heavy chain in acute myeloid leukemia

Intergenic splicing of MDS1 and EVI1 occurs in normal tissues as well as in myeloid leukemia and produces a new member of the PR domain family

The PEBP2betaMYH11 fusion created by Inv(16)(p13;q22) in myeloid leukemia impairs neutrophil maturation and contributes to granulocytic dysplasia

Fusion of the TEL gene on 12p13 to the AML1 gene on 21q22 in acute lymphoblastic leukemia

The 3;21 translocation in myelodysplasia results in a fusion transcript between the AML1 gene and the gene for EAP, a highly conserved protein associated with the Epstein-Barr virus small RNA EBER 1

AML1, the target of multiple chromosomal translocations in human leukemia, is essential for normal fetal liver hematopoiesis

Retroviral activation of a novel gene encoding a zinc finger protein in IL-3-dependent myeloid leukemia cell lines

AML1 and the 8;21 and 3;21 translocations in acute and chronic myeloid leukemia

Hematopoiesis in the fetal liver is impaired by targeted mutagenesis of a gene encoding a non-DNA binding subunit of the transcription factor, polyomavirus enhancer binding protein 2/core binding factor

Bcr-Abl with an SH3 deletion retains the ability To induce a myeloproliferative disease in mice, yet c-Abl activated by an SH3 deletion induces only lymphoid malignancy

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1760-1765

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scholarly article

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10.1073/PNAS.030421197

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4

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97

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2000-02-01T00:00:00Z

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12636973

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10677531

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26509

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