Malignant transformation initiated by Mll-AF9: gene dosage and critical target cells. - Wikidata - awgldk - TriplyDB

Malignant transformation initiated by Mll-AF9: gene dosage and critical target cells.

Malignant transformation initiated by Mll-AF9: gene dosage and critical target cells.

http://www.wikidata.org/entity/Q36726183

about

Dual function of histone H3 lysine 36 methyltransferase ASH1 in regulation of Hox gene expression PIM serine/threonine kinases in the pathogenesis and therapy of hematologic malignancies and solid cancers Mouse models to interrogate the implications of the differentiation status in the ontogeny of gliomas Engineering mouse models with myelodysplastic syndrome human candidate genes; how relevant are they?It takes two to tango, a dance between the cells of origin and cancer stem cells in the Drosophila larval brain Hijacked in cancer: the KMT2 (MLL) family of methyltransferases Update on acute myeloid leukemia stem cells: New discoveries and therapeutic opportunities The PIM kinases in hematological cancers Environmental and chemotherapeutic agents induce breakage at genes involved in leukemia-causing gene rearrangements in human hematopoietic stem/progenitor cells.Transformation of quiescent adult oligodendrocyte precursor cells into malignant glioma through a multistep reactivation process Epigenetics in normal and malignant hematopoiesis: An overview and update 2017.Transforming human blood stem and progenitor cells: a new way forward in leukemia modeling.MLL-AF9-induced leukemogenesis requires coexpression of the wild-type Mll allele.Hsp90 directly modulates the spatial distribution of AF9/MLLT3 and affects target gene expression.Induction of autophagy and inhibition of melanoma growth in vitro and in vivo by hyperactivation of oncogenic BRAF.PAFc, a key player in MLL-rearranged leukemogenesis.Induction of histiocytic sarcoma in mouse skeletal muscle.Concise review: preleukemic stem cells: molecular biology and clinical implications of the precursors to leukemia stem cells Single unpurified breast tumor-initiating cells from multiple mouse models efficiently elicit tumors in immune-competent hosts.Mapping cancer origins.MEIS1 regulates an HLF-oxidative stress axis in MLL-fusion gene leukemia.Cell of origin strongly influences genetic selection in a mouse model of T-ALL Evi1 is essential for hematopoietic stem cell self-renewal, and its expression marks hematopoietic cells with long-term multilineage repopulating activity MLL fusions: pathways to leukemia EVI1, a target gene for amplification at 3q26, antagonizes transforming growth factor-β-mediated growth inhibition in hepatocellular carcinoma.EVI1 is critical for the pathogenesis of a subset of MLL-AF9-rearranged AMLs.Acute myeloid leukemia stem cells and CD33-targeted immunotherapy MLL leukemia induction by genome editing of human CD34+ hematopoietic cells.Stress hematopoiesis reveals abnormal control of self-renewal, lineage bias, and myeloid differentiation in Mll partial tandem duplication (Mll-PTD) hematopoietic stem/progenitor cells PML-RARA requires DNA methyltransferase 3A to initiate acute promyelocytic leukemia.Meis1 preserves hematopoietic stem cells in mice by limiting oxidative stress.Identification of MLL-fusion/MYC⊣miR-26⊣TET1 signaling circuit in MLL-rearranged leukemia.Core Circadian Clock Genes Regulate Leukemia Stem Cells in AML The trithorax protein partner menin acts in tandem with EZH2 to suppress C/EBPα and differentiation in MLL-AF9 leukemia.A decade of genome-wide gene expression profiling in acute myeloid leukemia: flashback and prospects.Leukaemia cell of origin identified by chromatin landscape of bulk tumour cells.A role for MEIS1 in MLL-fusion gene leukemia Supraphysiologic levels of the AML1-ETO isoform AE9a are essential for transformation.Essential role of PR-domain protein MDS1-EVI1 in MLL-AF9 leukemia.CBX8, a component of the Polycomb PRC1 complex, modulates DOT1L-mediated gene expression through AF9/MLLT3

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P2860

Malignant transformation initiated by Mll-AF9: gene dosage and critical target cells.

http://www.wikidata.org/entity/Q36726183

description

2008 nî lūn-bûn

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2008年论文

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2008年论文

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name

Malignant transformation initiated by Mll-AF9: gene dosage and critical target cells.

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Malignant transformation initiated by Mll-AF9: gene dosage and critical target cells.

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type

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Malignant transformation initiated by Mll-AF9: gene dosage and critical target cells.

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Malignant transformation initiated by Mll-AF9: gene dosage and critical target cells.

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Malignant transformation initiated by Mll-AF9: gene dosage and critical target cells.

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Malignant transformation initiated by Mll-AF9: gene dosage and critical target cells.

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J.CCR.2008.03.005

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Malignant transformation initiated by Mll-AF9: gene dosage and critical target cells.

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Ashish R Kumar

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Erik A Lund

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John H Kersey

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Quanzhi Li

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Rodney A Staggs

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Thien N Sam

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Weili Chen

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Wendy A Hudson

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P2860

Genome-wide analysis of menin binding provides insights into MEN1 tumorigenesis.

Global and Hox-specific roles for the MLL1 methyltransferase

Significance analysis of microarrays applied to the ionizing radiation response

Modulation of cell cycle by graded expression of MLL-AF4 fusion oncoprotein

A clonogenic common myeloid progenitor that gives rise to all myeloid lineages

MLL translocations, histone modifications and leukaemia stem-cell development

The mll-AF9 gene fusion in mice controls myeloproliferation and specifies acute myeloid leukaemogenesis.

MLLT3 gene on 9p22 involved in t(9;11) leukemia encodes a serine/proline rich protein homologous to MLLT1 on 19p13.

Similar MLL-associated leukemias arising from self-renewing stem cells and short-lived myeloid progenitors.

An Mll-AF9 fusion gene made by homologous recombination causes acute leukemia in chimeric mice: a method to create fusion oncogenes.

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432-440

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10.1016/J.CCR.2008.03.005

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5

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13

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5397910

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18455126

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2430522

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