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在双表型白血病细胞系RED-3中,c-myc扩增与激活型N-ras点突变共存。

c-myc amplification coexistent with activating N-ras point mutation in the biphenotypic leukemic cell line RED-3.

作者信息

Mallet M K, Mane S M, Meltzer S J, Needleman S W

机构信息

Department of Medicine, University of Maryland Hospital, Baltimore 21201.

出版信息

Leukemia. 1989 Jul;3(7):511-5.

PMID:2659902
Abstract

While activation of the protooncogene c-N-ras is observed regularly in acute myelogenous leukemia, amplification of c-myc in AML cells or derived lines is uncommon. In particular, concurrent ras/myc activation, which has been shown to be critical in several elegant models of malignancy, has been demonstrated in a very small number of human tumors or derivative cell lines. A cell line, RED-3, is described which was derived from cells of a patient with aggressive acute leukemia which exhibits many markers of lineage infidelity. DNA from this cell line contains an activating point mutation of c-N-ras as well as 20-30-fold amplification of c-myc. After HL-60, this is the second example of ras/myc activation in AML derived cells and demonstrates that this lesion is not unique to HL-60. Rather, it may be important in leukemogenesis in a small proportion of AML patients.

摘要

虽然在急性髓性白血病中经常观察到原癌基因c-N-ras的激活,但c-myc在AML细胞或衍生系中的扩增并不常见。特别是,ras/myc同时激活,这在几个精巧的恶性肿瘤模型中已被证明至关重要,但仅在极少数人类肿瘤或衍生细胞系中得到证实。本文描述了一种细胞系RED-3,它源自一名侵袭性急性白血病患者的细胞,该细胞系表现出许多谱系不忠实的标志物。该细胞系的DNA包含c-N-ras的激活点突变以及c-myc 20 - 30倍的扩增。继HL-60之后,这是AML衍生细胞中ras/myc激活的第二个例子,表明这种病变并非HL-60所特有。相反,它可能在一小部分AML患者的白血病发生中起重要作用。

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