Blick M B, Andersson B S, Gutterman J U, Keating A, Beran M
Leuk Res. 1986;10(12):1401-9. doi: 10.1016/0145-2126(86)90006-8.
Structural alterations of the oncogenes in human tumors are reported to result from a variety of mechanisms: point mutations, chromosomal translocations and gene amplifications. In over 90% of the cases of chronic myelogenous leukemia (CML), the c-abl oncogene is translocated from chromosome 9 to chromosome 22, and forms in part the Philadelphia (Ph1) chromosome. We have molecularly analysed a double Ph1-positive (Ph1+) cell line, KBM-5 that was established from a patient with CML in the blast-transformed phase (CML-BP). We report that the c-abl, bcr, and C lambda genes are amplified approximately eight-fold in the cell line but not in the fresh uncultured cells from which KBM-5 was derived.
据报道,人类肿瘤中癌基因的结构改变是由多种机制引起的:点突变、染色体易位和基因扩增。在超过90%的慢性粒细胞白血病(CML)病例中,c-abl癌基因从9号染色体易位至22号染色体,部分构成了费城(Ph1)染色体。我们对一个双Ph1阳性(Ph1+)细胞系KBM-5进行了分子分析,该细胞系是从一名处于急变期(CML-BP)的CML患者体内建立的。我们报告称,c-abl、bcr和Cλ基因在该细胞系中扩增了约8倍,但在KBM-5来源的新鲜未培养细胞中未扩增。