Mutations in oncogenes or tumour suppressor genes cause increases in cell growth capacity. In some cases, fully malignant cancer cells develop after additional mutations occur in initially mutated cells. In such instances, the risk of cancer would increase in response to growth of these initially mutated cells. To ascertain whether such a situation might occur in cultured cells, three independent cultures of human lymphoblastoid GM00130 cells were treated with N-ethyl-N-nitrosourea to induce mutations, and the cells were maintained for 12 weeks. Mutant frequencies and spectra of the cells at the MspI and HaeIII restriction sites located at codons 247-250 of the TP53 gene were examined. Mutant frequencies at both sites in the gene exhibited a declining trend during cell culture and reached background levels after 12 weeks; this was also supported by mutation spectra findings. These results indicate that the mutations detected under our assay conditions are disadvantageous to cell growth.

中文翻译：

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在ENU突变的人类淋巴母细胞细胞培养过程中，TP53热点突变频率的变化。

癌基因或肿瘤抑制基因的突变引起细胞生长能力的增加。在某些情况下，在最初突变的细胞中发生其他突变后，会发展出完全恶性的癌细胞。在这种情况下，响应于这些最初突变的细胞的生长，癌症的风险将增加。为了确定在培养的细胞中是否可能发生这种情况，用N-乙基-N-亚硝基脲处理人淋巴母细胞样GM00130细胞的三个独立培养物以诱导突变，并将细胞维持12周。检查了位于TP53基因第247-250位密码子的MspI和HaeIII限制性位点的细胞的突变频率和光谱。基因的两个位点的突变频率在细胞培养过程中均呈下降趋势，并在12周后达到背景水平。突变光谱的发现也证明了这一点。这些结果表明，在我们的测定条件下检测到的突变对细胞生长不利。