Milo G E, Casto B C
Cancer Lett. 1986 Apr;31(1):1-13. doi: 10.1016/0304-3835(86)90161-8.
Low passage (low population doubling) human diploid fibroblasts respond to carcinogen and mutagen treatment, with higher passage level human cells remaining refractory to the insult. A cell cycle dependency for an optimize response to the carcinogen of competent responsive low passage cells is associated with early S phase. The process of fixation of the damage in dividing young cells could be more efficient due to intrinsic sensitivity of young cells towards carcinogens. However, specific DNA-carcinogen adduct analysis does not reveal any qualitative or quantitative difference. These low passage carcinogen initiated human cells progress towards the expression of a malignant phenotype. There is little evidence to suggest that these abnormal phenotypes exhibit an infinite lifespan using the selection pressures for isolation of the transformed phenotypes. However, the lifespan of these treated cells is extended beyond those of the untreated cells. In conclusion, criteria can be established to measure the expression of progression of these carcinogen initiated cells towards a malignant phenotype.
低代次（低群体倍增）的人二倍体成纤维细胞对致癌物和诱变剂处理有反应，而高代次的人细胞对这种损伤仍具有抗性。有能力做出反应的低代次细胞对致癌物的最佳反应存在细胞周期依赖性，且与早期S期相关。由于年轻细胞对致癌物具有内在敏感性，在分裂的年轻细胞中损伤的固定过程可能更有效。然而，特定的DNA-致癌物加合物分析并未揭示任何定性或定量差异。这些低代次致癌物引发的人细胞会朝着恶性表型的表达发展。几乎没有证据表明这些异常表型在用于分离转化表型的选择压力下具有无限寿命。然而，这些处理过的细胞的寿命比未处理的细胞延长了。总之，可以建立标准来衡量这些致癌物引发的细胞向恶性表型发展的进程表达。
