Pecenka V, Dvorák M, Karafiát V, Sloncová E, Hlozánek I, Trávnícek M, Ríman J
Institute of Molecular Genetics, Czechoslovak Academy of Sciences, Praha.
Folia Biol (Praha). 1988;34(3):147-69.
To demonstrate the existence of a common site of integration in independent tumour clones, restriction mapping of the vicinity of integrated MAV-2 proviruses in nephroblastoma DNA was performed, using Southern hybridization with an MAV-2 specific probe U3(pAT). The results have shown that (1) nephroblastomas are of semiclonal origin. (2) Nephroblastoma cells contain an average of 5 clonally located integrated proviruses per diploid genome; they do not contain any detectable amount of non-integrated proviruses. (3) In the DNA from independent nephroblastoma clones, there appear at an increased frequency Tth111I fragments of 14.6 and 17.8 kb that hybridize with the U3(pAT) probe. Considering a random selection of integration sites, such coincidence is of little probability. Thus we suppose that these fragments represent a common site(s) of integration with an MAV-2 proviral insert. Two hypotheses concerning possible mechanisms of nephroblastoma induction are discussed: proto-oncogene insertional activation and anti-oncogene insertional inactivation.
为了证明在独立肿瘤克隆中存在一个共同的整合位点，利用与MAV - 2特异性探针U3(pAT)的Southern杂交技术，对肾母细胞瘤DNA中整合的MAV - 2前病毒附近区域进行了限制性图谱分析。结果表明：(1)肾母细胞瘤起源于半克隆。(2)肾母细胞瘤细胞每个二倍体基因组平均含有5个克隆定位的整合前病毒；它们不含任何可检测到的非整合前病毒。(3)在来自独立肾母细胞瘤克隆的DNA中，出现频率增加的与U3(pAT)探针杂交的14.6和17.8 kb的Tth111I片段。考虑到整合位点的随机选择，这种巧合的概率很小。因此我们推测这些片段代表了MAV - 2前病毒插入的一个共同整合位点。讨论了关于肾母细胞瘤诱导可能机制的两种假说：原癌基因插入激活和抗癌基因插入失活。
