Elwood N J, Cook W D, Metcalf D, Begley C G
Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Parkville, Victoria, Australia.
Oncogene. 1993 Nov;8(11):3093-101.
SCL (TAL-1) is implicated in the generation of human T-cell acute lymphoblastic leukaemia. To directly examine the role of this putative oncogene, an SCL retrovirus was constructed and used to infect a v-ABL transformed T-lymphocyte cell line. Thirteen independent SCL-infected and four control cell lines were established and injected subcutaneously into syngeneic mice. Mice injected with SCL-infected clonal cell lines died significantly more rapidly than control animals. By day 200 46% (40/87) of animals injected with SCL-infected cell lines had died due to disseminated transplantable lymphoid tumours. In contrast only 22% of control mice were dead by day 200 (P < 0.0015). Of possible relevance to the enhanced tumourigenesis, some SCL-infected cell lines displayed increased clonogenicity in agar. Increased cell growth was even more striking when ex-vivo tumour-derived cell lines were studied. Thus, SCL can co-operate with v-ABL to hasten T-cell tumourigenesis. This is the first direct evidence demonstrating that SCL can behave as an oncogene.
SCL（TAL-1）与人类T细胞急性淋巴细胞白血病的发生有关。为了直接研究这个假定的癌基因的作用，构建了一种SCL逆转录病毒并用于感染v-ABL转化的T淋巴细胞系。建立了13个独立的SCL感染细胞系和4个对照细胞系，并将其皮下注射到同基因小鼠体内。注射SCL感染的克隆细胞系的小鼠死亡速度明显比对照动物快。到第200天时，注射SCL感染细胞系的动物中有46%（40/87）因转移性可移植性淋巴瘤而死亡。相比之下，到第200天时，只有22%的对照小鼠死亡（P<0.0015）。与肿瘤发生增强可能相关的是，一些SCL感染的细胞系在琼脂中显示出克隆形成能力增加。当研究体外肿瘤来源的细胞系时，细胞生长增加更为显著。因此，SCL可以与v-ABL协同作用以加速T细胞肿瘤发生。这是证明SCL可作为癌基因的首个直接证据。
