Signaling in leukemia: which messenger to kill?
作者信息
Pear W S
机构信息
University of Pennsylvania, Department of Pathology, Institute for Medicine and Engineering, 611 Biomedical Research Building II/III, 421 Curie Boulevard, Philadelphia, Pennsylvania 19104-6160, USA.
出版信息
J Clin Invest. 2000 Feb;105(4):419-22. doi: 10.1172/JCI9461.
Abstract
摘要
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Signaling in leukemia: which messenger to kill?白血病中的信号传导：该阻断哪个信使分子？
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本文引用的文献
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Fatal myeloproliferation, induced in mice by TEL/PDGFbetaR expression, depends on PDGFbetaR tyrosines 579/581.由TEL/PDGFβR表达在小鼠中诱导产生的致命性骨髓增殖依赖于PDGFβR的酪氨酸579/581。
J Clin Invest. 2000 Feb;105(4):423-32. doi: 10.1172/JCI8902.
3
Lessons learned from the development of an abl tyrosine kinase inhibitor for chronic myelogenous leukemia.从一种用于慢性粒细胞白血病的 Abl 酪氨酸激酶抑制剂的研发中吸取的经验教训。
J Clin Invest. 2000 Jan;105(1):3-7. doi: 10.1172/JCI9083.
4
Diverse signaling pathways activated by growth factor receptors induce broadly overlapping, rather than independent, sets of genes.生长因子受体激活的多种信号通路会诱导出广泛重叠而非独立的基因集。
Cell. 1999 Jun 11;97(6):727-41. doi: 10.1016/s0092-8674(00)80785-0.
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The P190, P210, and P230 forms of the BCR/ABL oncogene induce a similar chronic myeloid leukemia-like syndrome in mice but have different lymphoid leukemogenic activity.BCR/ABL癌基因的P190、P210和P230形式在小鼠中诱导出类似慢性髓性白血病的综合征，但具有不同的淋巴细胞白血病致瘤活性。
J Exp Med. 1999 May 3;189(9):1399-412. doi: 10.1084/jem.189.9.1399.
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Bcr-Abl efficiently induces a myeloproliferative disease and production of excess interleukin-3 and granulocyte-macrophage colony-stimulating factor in mice: a novel model for chronic myelogenous leukemia.Bcr-Abl可有效诱导小鼠发生骨髓增殖性疾病，并产生过量的白细胞介素-3和粒细胞-巨噬细胞集落刺激因子：一种慢性粒细胞白血病的新模型。
Blood. 1998 Nov 15;92(10):3829-40.
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Signal transduction via platelet-derived growth factor receptors.通过血小板衍生生长因子受体的信号转导。
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TEL gene rearrangements in myeloid malignancy.髓系恶性肿瘤中的TEL基因重排
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