格拉菲鼠白血病病毒前病毒整合导致髓系白血病中的癌基因激活。
Oncogene activation in myeloid leukemias by Graffi murine leukemia virus proviral integration.
作者信息
Denicourt C, Edouard E, Rassart E
机构信息
Laboratoire de Biologie Moléculaire, Département des Sciences Biologiques, Université du Québec à Montréal, Montréal, Québec H3C 3P8, Canada.
出版信息
J Virol. 1999 May;73(5):4439-42. doi: 10.1128/JVI.73.5.4439-4442.1999.
Abstract
The Graffi murine leukemia virus (MuLV) is a nondefective retrovirus that induces granulocytic leukemia in BALB/c and NFS mice. To identify genes involved in Graffi MuLV-induced granulocytic leukemia, tumor cell DNAs were examined for genetic alterations at loci described as common proviral integration sites in MuLV-induced myeloid, lymphoid, and erythroid leukemias. Southern blot analysis revealed rearrangements in c-myc, Fli-1, Pim-1, and Spi-1/PU.1 genes in 20, 10, 3.3, and 3.3% of the tumors tested, respectively. These results demonstrate for the first time the involvement of those genes in granulocytic leukemia.
摘要
格拉菲鼠白血病病毒（MuLV）是一种无缺陷逆转录病毒，可在BALB/c和NFS小鼠中诱发粒细胞白血病。为了鉴定参与格拉菲MuLV诱导的粒细胞白血病的基因，研究人员检查了肿瘤细胞DNA在MuLV诱导的髓系、淋巴系和红系白血病中被描述为常见原病毒整合位点的基因座处的遗传改变。Southern印迹分析显示，在分别检测的20%、10%、3.3%和3.3%的肿瘤中，c-myc、Fli-1、Pim-1和Spi-1/PU.1基因发生了重排。这些结果首次证明了这些基因参与粒细胞白血病。
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