Mäkelä T P, Saksela K, Alitalo K
Department of Virology, University of Helsinki, Finland.
Mutat Res. 1992 May;276(3):307-15. doi: 10.1016/0165-1110(92)90017-4.
DNA amplification of cellular proto-oncogenes is a well-established and common mechanism of oncogene activation in several types of human tumors, including the rapidly fatal small-cell lung cancer (SCLC). Approximately one fourth of primary SCLC tumors contain amplified copies of one of the three myc proto-oncogenes. Occasionally DNA amplification of the myc genes is associated with DNA rearrangements. Specifically, a novel locus named rlf is often involved in intrachromosomal L-myc rearrangements in SCLC. The structurally similar rearrangements are probably due to a highly repetitive region upstream of the L-myc gene, and result in the formation of a chimeric rlf-L-myc fusion protein. The consistent finding of the rlf-L-myc rearrangement in SCLC suggests that it may provide a selective advantage to the cells harboring it.
细胞原癌基因的DNA扩增是多种人类肿瘤中癌基因激活的一种已确立的常见机制，包括快速致死性的小细胞肺癌（SCLC）。大约四分之一的原发性SCLC肿瘤含有三种myc原癌基因之一的扩增拷贝。偶尔，myc基因的DNA扩增与DNA重排有关。具体而言，一个名为rlf的新位点经常参与SCLC中染色体内部L-myc的重排。结构相似的重排可能是由于L-myc基因上游的一个高度重复区域，导致形成嵌合的rlf-L-myc融合蛋白。在SCLC中一致发现rlf-L-myc重排表明它可能为携带它的细胞提供选择性优势。
