STUDIES ON THE ACTIVATION OF ONCOGENES IN VIRUSES AND HUMAN TUMORS

我们之前发现了OVC，一种激活的人类转化序列 在DNA转染过程中，并从人卵巢癌细胞中获得 线路，OVCAR3。这些序列的一部分映射到9号染色体上， 在被测试的转化细胞系的子集中表达。我们已经分析了 从30例不同类型卵巢和卵巢癌的临床标本中提取DNA 女性生殖道肿瘤，并已检测到10至15倍 在一例转移性、低分化的患者中扩增这些序列 腺癌。 进一步分析了限制RD114生长的机理。 猫成纤维细胞中的病毒。虽然报告基因的表达 RD114 LTR不受限制，出现完整的RD114病毒RNA表达 无论基因组是通过感染还是通过感染引入的 转染法。这表明，除了LTR外，病毒成分还包括 在转录水平上参与了RD114的细胞限制。 我们已经分析了高度多样性的毒性和细胞抑制效应。 含mos癌基因的Mo-MuSV感染。不同品系的 含有MOS的病毒似乎阻止了成纤维细胞的细胞增殖， 而无辅助剂的m1菌株既有毒性，又有生长。 抑制力。毒性伴随着在体内诱导的异常 核和染色体结构。

We had previously identified ovc, a human transforming sequence activated during DNA transfection and derived from the human ovarian carcinoma cell line, OVCAR3. A portion of these sequences map to chromosome 9 and is expressed in a subset of transformed cell lines tested. We have analyzed the DNA obtained from 30 clinical samples of various types of ovarian and female reproductive tract tumors, and have detected a 10- to 15-fold amplification of these sequences in one metastatic, poorly differentiated adenocarcinoma. We have further analyzed the mechanism of restriction of growth of RD114 virus in feline fibroblasts. Although expression of reporter genes of the RD114 LTR is not restricted, expression of intact RD114 viral RNA appears to be reduced whether the genome is introduced by infection or transfection. This suggests viral components, in addition to the LTR, are involved in cellular restriction of RD114 at the transcriptional level. We have analyzed the toxic and cytostatic effects of high multiplicity infection of Mo-MuSV containing the mos oncogene. Different strains of mos-containing viruses appear to block cell proliferation in fibroblasts, and helper-free stocks of the ml strain induce both toxicity and growth inhibition. Toxicity is accompanied by the induction of abnormalities in nuclear and chromosomal structure.