Berns A, Jaenisch R
Proc Natl Acad Sci U S A. 1976 Jul;73(7):2448-52. doi: 10.1073/pnas.73.7.2448.
AKR mice produce, from shortly after birth, high titers of their endogenous Gross type murine leukemia virus, and develop a thymus-derived leukemia at 7-9 months of age. We show that this oncogenesis is accompanied by an increase in the number of AKR-specific DNA sequences in the tumor tissues, whereas the "non-target" organs are not affected. Sequence increase was determined by kinetic analysis of DNA reassociation using an AKR-murine leukemia virus (MuLV)-specific cDNA and also by hybridization with excess AKR cDNA. The AKR cDNA was selected to recognize AKR sequences without significant crossreaction with DNA sequences of other endogenous viruses. The results show that during the development of the leukemia, the number of AKR-MuLV-specific genes increases in tumor tissues by a factor of 1 1/2 to 2.
AKR小鼠从出生后不久就会产生高滴度的内源性格罗斯型鼠白血病病毒,并在7至9个月大时发生胸腺源性白血病。我们发现,这种肿瘤发生伴随着肿瘤组织中AKR特异性DNA序列数量的增加,而“非靶”器官则不受影响。通过使用AKR-鼠白血病病毒(MuLV)特异性cDNA对DNA复性进行动力学分析,以及与过量的AKR cDNA杂交,确定了序列增加。选择AKR cDNA以识别与其他内源性病毒的DNA序列无明显交叉反应的AKR序列。结果表明,在白血病发展过程中,肿瘤组织中AKR-MuLV特异性基因的数量增加了1.5至2倍。