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浆细胞样淋巴肉瘤中病毒插入诱变激活c-myb基因座

Activation of the c-myb locus by viral insertional mutagenesis in plasmacytoid lymphosarcomas.

作者信息

Shen-Ong G L, Potter M, Mushinski J F, Lavu S, Reddy E P

出版信息

Science. 1984 Nov 30;226(4678):1077-80. doi: 10.1126/science.6093260.

DOI:10.1126/science.6093260
PMID:6093260
Abstract

Rearrangement in the c-myb locus of each of four independently derived BALB/c plasmacytoid lymphosarcoma (ABPL's) is due to the insertion of a defective Moloney murine leukemia virus (M-MuLV) into a 1.5-kilobase-pair stretch of cellular DNA at the 5' end of the v-myb-related sequences. This retroviral insertion is associated with abnormal transcription of myb sequences and probably represents a step in the neoplastic transformation of ABPL cells.

摘要

四个独立衍生的BALB/c浆细胞样淋巴肉瘤(ABPL)中每一个的c-myb基因座重排,是由于一种缺陷型莫洛尼鼠白血病病毒(M-MuLV)插入到v-myb相关序列5'端一段1.5千碱基对的细胞DNA中。这种逆转录病毒插入与myb序列的异常转录相关,并且可能代表ABPL细胞肿瘤转化过程中的一个步骤。

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Activation of the c-myb locus by viral insertional mutagenesis in plasmacytoid lymphosarcomas.浆细胞样淋巴肉瘤中病毒插入诱变激活c-myb基因座
Science. 1984 Nov 30;226(4678):1077-80. doi: 10.1126/science.6093260.
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