Hariharan I K, Adams J M, Cory S
Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Victoria, Australia.
Oncogene Res. 1988;3(4):387-99.
In chronic myeloid leukemia (CML), a chromosome translocation has fused the bcr gene to the c-abl oncogene, such that a chimeric bcr-abl polypeptide can be made. To explore the biological properties of bcr-abl and compare them with those of the Abelson virus (AMuLV) transforming gene (gag-v-abl), we have used either a synthetic bcr-v-abl gene that mimics the translocation product or, in some experiments, a bcr-c-abl cDNA. A new retroviral vector was used to introduce the genes into the factor-dependent myeloid line FDC-P1. Both bcr-abl and v-abl efficiently rendered the myeloid cells factor independent and tumorigenic. Their fully autonomous growth may be due to the myeloid growth factor interleukin-3 (IL-3) made in small amounts by the infected cells. Hence autocrine factor production may feature in CML development and Abelson virus transformation.
在慢性粒细胞白血病（CML）中，一种染色体易位使bcr基因与c-abl癌基因融合，从而可以产生一种嵌合的bcr-abl多肽。为了探索bcr-abl的生物学特性并将其与阿贝尔森病毒（AMuLV）转化基因（gag-v-abl）的特性进行比较，我们使用了模拟易位产物的合成bcr-v-abl基因，或者在某些实验中使用了bcr-c-abl cDNA。一种新的逆转录病毒载体被用于将这些基因导入依赖因子的髓系细胞系FDC-P1。bcr-abl和v-abl都能有效地使髓系细胞不依赖因子并具有致瘤性。它们完全自主生长可能是由于被感染细胞少量产生的髓系生长因子白细胞介素-3（IL-3）。因此，自分泌因子的产生可能在CML发展和阿贝尔森病毒转化中起作用。
