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首页> 外文期刊>Molecular and Cellular Biology >Progression of the transformed phenotype in clonal lines of Abelson virus-infected lymphocytes.
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Progression of the transformed phenotype in clonal lines of Abelson virus-infected lymphocytes.

机译：Abelson病毒感染的淋巴细胞的克隆系中转化表型的进展。

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Some molecular changes which correlate with the tumorigenic progression of neoplastic cells can best be studied with in vitro cell lines that represent each stage in the progression. Lymphoid cells infected by Abelson murine leukemia virus exhibit a wide range of growth potential in vitro and in vivo. Uncloned populations that are poorly oncogenic early after infection become progressively more oncogenic with successive passages of the cells in culture. In such mass cultures, it is difficult to evaluate whether a rare subpopulation of highly oncogenic cells becomes dominant in the culture or whether the individual cells progress in oncogenic phenotype. To examine this latter possibility, Abelson virus-infected lymphoid cells were cloned by limiting-dilution culture 10 days postinfection. We isolated two clones that grew poorly in agar, required feeder layers of adherent bone marrow cells for growth in liquid culture, and were extremely slow to form tumors in syngeneic animals. Both clones, after passage in the presence of adherent feeder layers for 3 months, grew well in liquid and agar-containing cultures in the absence of feeder layers and formed tumors in animals at a rapid rate. The progression of these clonal cell lines to a more malignant growth phenotype occurred in the absence of detectable changes in the concentration, half-life, phosphorylation, in vitro kinase activity, or cell localization of the Abelson virus-encoded transforming protein. No change in the concentration or arrangement of integrated Abelson viral DNA sequences was detected in either clone. Thus, perhaps changes in the expression of cellular genes would appear to alter the growth properties of lymphoid cells after their initial transformation by Abelson virus. Such cellular changes could complement the activity of the Abelson virus transforming protein in producing the fully malignant growth phenotype.
机译：与肿瘤细胞的肿瘤发生发展相关的一些分子变化，可以用代表进展过程各个阶段的体外细胞系进行研究。受Abelson鼠白血病病毒感染的淋巴细胞在体外和体内均具有广泛的生长潜力。感染后致癌性较差的未克隆种群随着培养细胞的连续传代而逐渐变得更具致癌性。在这样的大规模培养中，很难评估高致癌细胞的稀有亚群是否在培养中占优势，或者单个细胞是否在致癌表型上发展。为了检验后者的可能性，在感染后10天通过有限稀释培养克隆了感染了Abelson病毒的淋巴样细胞。我们分离了两个克隆，这些克隆在琼脂中生长较差，需要粘附的骨髓细胞饲养层才能在液体培养中生长，并且在同系动物中形成肿瘤的速度非常慢。两个克隆在附着的饲养层存在下传代3个月后，在没有饲养层的液体和琼脂培养液中生长良好，并在动物中迅速形成肿瘤。在无浓度，半衰期，磷酸化，体外激酶活性或Abelson病毒编码的转化蛋白的细胞定位检测不到变化的情况下，这些克隆细胞系发展为更具恶性的生长表型。在任一克隆中均未检测到整合的Abelson病毒DNA序列的浓度或排列发生变化。因此，也许细胞基因表达的改变似乎会在阿贝尔森病毒最初转化后改变淋巴样细胞的生长特性。此类细胞变化可能会补充Abelson病毒转化蛋白在产生完全恶性生长表型中的活性。

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