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

Chen W; Kumar AR; Hudson WA; Li Q; Wu B; Staggs RA; Lund EA; Sam TN; Kersey JH

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

机译：由Mll-AF9引发的恶性转化：基因剂量和关键靶细胞。

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The pathways by which oncogenes, such as MLL-AF9, initiate transformation and leukemia in humans and mice are incompletely defined. In a study of target cells and oncogene dosage, we found that Mll-AF9, when under endogenous regulatory control, efficiently transformed LSK (Lin(-)Sca1(+)c-kit(+)) stem cells, while committed granulocyte-monocyte progenitors (GMPs) were transformation resistant and did not cause leukemia. Mll-AF9 was expressed at higher levels in hematopoietic stem (HSC) than GMP cells. Mll-AF9 gene dosage effects were directly shown in experiments where GMPs were efficiently transformed by the high dosage of Mll-AF9 resulting from retroviral transduction. Mll-AF9 upregulated expression of 192 genes in both LSK and progenitor cells, but to higher levels in LSKs than in committed myeloid progenitors.

机译：致癌基因（例如MLL-AF9）在人类和小鼠中引发转化和白血病的途径尚未完全定义。在对靶细胞和致癌基因剂量的研究中，我们发现Mll-AF9在内源性调控下可有效转化LSK（Lin（-）Sca1（+）c-kit（+））干细胞，同时将粒细胞-单核细胞定型祖细胞（GMP）具有转化抗性，不会引起白血病。 Mll-AF9在造血干细胞（HSC）中的表达水平高于GMP细胞。在通过逆转录病毒转导产生的高剂量Mll-AF9有效转化GMP的实验中，直接显示了Mll-AF9基因的剂量效应。 Mll-AF9在LSK和祖细胞中均上调192个基因的表达，但在LSK中的水平要高于定型的髓祖细胞中的水平。

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《Cancer Cell》 |2008年第5期|共9页
作者
Chen W; Kumar AR; Hudson WA; Li Q; Wu B; Staggs RA; Lund EA; Sam TN; Kersey JH;
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正文语种 eng
中图分类肿瘤学;
关键词
Animals; Cell Division; Cell Transformation; Neoplastic; Gene Dosage; Gene Expression Regulation; Neoplastic; 动物; 细胞分裂; 细胞转化; 肿瘤; 基因剂量; 基因表达调控; 肿瘤; 造血干细胞;

机译：Animals;Cell Division;Cell Transformation;Neoplastic;Gene Dosage;Gene Expression Regulation;Neoplastic;动物;细胞分裂;细胞转化;肿瘤;基因剂量;基因表达调控;肿瘤;造血干细胞;

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专利

1. Malignant transformation initiated by Mll-AF9: gene dosage and critical target cells. [J] . Chen W, Kumar AR, Hudson WA, Cancer Cell . 2008,第5期

机译：由Mll-AF9引发的恶性转化：基因剂量和关键靶细胞。
2. Degree of Recruitment of DOT1L to MLL-AF9 Defines Level of H3K79 Di- and Tri-methylation on Target Genes and Transformation Potential [J] . Aravinda Kuntimaddi, Nicholas?J. Achille, Jeremy Thorpe, Cell Reports . 2015,第5期

机译：DOT1L对MLL-AF9的募集程度定义了靶基因和转化电位上的H3K79二 - 甲基化水平和三甲基化
3. Estrogen potentiates reactive oxygen species (ROS) tolerance to initiate carcinogenesis and promote cancer malignant transformation [J] . Tian Hui, Gao Zhen, Wang Gang, Tumour biology : . 2016,第1期

机译：雌激素可增强活性氧（ROS）的耐受性，从而启动致癌作用并促进癌症恶性转化
4. A model of phenotypic state dynamics initiates a promising approach to control heterogeneous malignant cell populations [C] . Margaret P. Chapman, Tyler T. Risom, Anil Aswani, IEEE Conference on Decision and Control . 2016

机译：表型状态动力学模型启动了一种有前途的方法来控制异种恶性细胞群体
5. N-Myc—A critical target of the proliferative response initiated by the multiple endocrine neoplasia type II A oncogene - Ret2A [D] . Kulkarni, Mandar V. 2007

机译：N-Myc-由多发性内分泌肿瘤IIA型致癌基因-Ret2A引发的增殖反应的关键目标
6. Malignant transformation initiated by Mll-AF9: Gene dosage and critical target cells [O] . Weili Chen, Ashish R. Kumar, Wendy A. Hudson, -1

机译：Mll-AF9启动的恶性转化：基因剂量和关键靶细胞
7. Malignant Transformation Initiated by Mll-AF9: Gene Dosage and Critical Target Cells [O] . Chen Weili, Kumar Ashish R., Hudson Wendy A., 2008

机译：Mll-AF9启动的恶性转化：基因剂量和关键靶细胞。
8. Ras-Directed N-Glycoproteins Are Novel Early Biomarkers for Tumorigenesis and Malignant Transformation and Therapeutic Targets of Neurofibromatosis Type 1. [R] . Zhu, Q. 2014

机译：Ras指导的N-糖蛋白是用于肿瘤发生和恶性转化的新型早期生物标志物和1型神经纤维瘤病的治疗靶点。

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

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