Sabatier L, Lebeau J, Dutrillaux B
Centre d'Etudes Nucleaires, DSV, DPTE, LCG BP6, Fontenay aux Roses, France.
Radiat Environ Biophys. 1995 Nov;34(4):229-32. doi: 10.1007/BF01209747.
In spite of a well-known relationship between exposure to radiation and increased risk for cancer development, the biological mechanisms involved in radiation-induced carcinogenesis remain poorly documented. Various hypotheses are discussed in this paper. It appears that radiation cannot be directly responsible for the numerous genetic alterations of cancer cells. Most of them occur during tumor progression. Only one or a very limited number of them was induced by radiation many years before tumor growth. This long delay is a major difficulty for experimental research and raises many questions. Recently, it has been shown that a genomic instability occurs after many generations in cells descending from irradiated cells. This instability leads to multiple genetic alterations and, preferentially, affects some chromosome structures, particularly telomeres. This kind of telomeric instability - related to the shortening of telomeric DNA sequences - has also been observed in senescent cells as well as in non-senescent cells from patients predisposed to cancer, and this process may possibly also occur in the progeny of irradiated cells.
尽管辐射暴露与癌症发生风险增加之间的关系已广为人知，但辐射致癌所涉及的生物学机制仍记录甚少。本文讨论了各种假说。似乎辐射并非癌细胞众多基因改变的直接原因。大多数基因改变发生在肿瘤进展过程中。其中只有一个或极少数是在肿瘤生长多年前由辐射诱导产生的。这种长时间的延迟是实验研究的一大难题，并引发了许多问题。最近有研究表明，受辐射细胞的后代在经过许多代后会出现基因组不稳定。这种不稳定性会导致多种基因改变，并优先影响某些染色体结构，尤其是端粒。这种与端粒DNA序列缩短相关的端粒不稳定性，在衰老细胞以及癌症易感患者的非衰老细胞中也有观察到，并且这个过程可能也会发生在受辐射细胞的后代中。
