Birnbaum M, Spiess E
Institute of Cell and Tumor Biology, German Cancer Research Center, Heidelberg.
Anticancer Res. 1988 Nov-Dec;8(6):1185-91.
Metastatic (ASML 14-1, ASmv) and non metastatic (AS17-4) cell lines of the rat BSp73 pancreatic adenocarcinoma were investigated for amplification and expression of oncogene DNA. The c-myc gene was amplified, but only in one metastatic variant, ASML. The degree of amplification (3.5-fold) increased after prolongued in vitro cultivation (17.5-fold). All three tumor cell lines expressed c-myc and ras mRNA. Ras expression was at the same level as in rat liver. C-myc expression was considerably above the level in rat liver, but also differed considerably between the metastatic variants. In the metastatic ASML cells the c-myc gene was localized by in situ hybridization on a marker chromosome derived from chromosome 7. The karyotypes of the metastatic variants are different and have no common marker chromosomes. Our results obtained with the BSp73 tumor model do not support a role of the c-myc gene in the metastatic process.
对大鼠BSp73胰腺腺癌的转移性细胞系(ASML 14-1、ASmv)和非转移性细胞系(AS17-4)进行了癌基因DNA扩增和表达的研究。c-myc基因存在扩增,但仅在一种转移性变体ASML中出现。延长体外培养后,扩增程度(3.5倍)增加(至17.5倍)。所有三种肿瘤细胞系均表达c-myc和ras mRNA。Ras表达水平与大鼠肝脏中的相同。C-myc表达明显高于大鼠肝脏中的水平,但在转移性变体之间也存在显著差异。在转移性ASML细胞中,通过原位杂交将c-myc基因定位在一条源自7号染色体的标记染色体上。转移性变体的核型不同,没有共同的标记染色体。我们在BSp73肿瘤模型中获得的结果不支持c-myc基因在转移过程中起作用。