Kondo S
Differentiation. 1983;24(1):1-8. doi: 10.1111/j.1432-0436.1983.tb01294.x.
From reports on fish, mice, rats, and humans, it can be concluded that at early developmental stages, especially stages before organogenesis, vertebrates are resistant to the induction of tumors by carcinogens. This conclusion and results on the molecular biology of chemical carcinogenesis in mice support the hypothesis that carcinogenesis of an organ is initiated by mutation of its stem cells formed during organogenesis. Convincing support for the existence of mutations that cause development of tumors is that heritable tumors are induced in mice and Drosophila by exposure of germ cells to radiation and chemicals. Various lines of evidence support the notion that tumor genes, which increase the predisposition of their carriers to develop tumors, are at least partly regulatory mutations. In this paper, the interrelation of tumorigenesis and teratogenesis, the high susceptibility of growing or regenerating organs to induction of tumors by carcinogens, and the latent period of induced neoplasms are discussed in relation to the stem-cell-mutation hypothesis.
从有关鱼类、小鼠、大鼠和人类的报告中可以得出结论，在早期发育阶段，尤其是器官发生之前的阶段，脊椎动物对致癌物诱导肿瘤具有抗性。这一结论以及小鼠化学致癌分子生物学的研究结果支持了这样一种假说，即器官的致癌作用是由器官发生过程中形成的干细胞突变引发的。对导致肿瘤发生的突变存在的令人信服的支持证据是，通过使生殖细胞暴露于辐射和化学物质，在小鼠和果蝇中诱发了可遗传的肿瘤。各种证据支持这样一种观点，即肿瘤基因至少部分是调节性突变，其会增加携带者患肿瘤的易感性。在本文中，结合干细胞突变假说，讨论了肿瘤发生与致畸作用的相互关系、生长或再生器官对致癌物诱导肿瘤的高度敏感性以及诱导肿瘤的潜伏期。
