Bishop Alexander J. R., Schiestl Robert H.
J Biomed Biotechnol. 2002;2(2):75-85. doi: 10.1155/S1110724302204052.
Cancer develops when cells no longer follow their normal pattern of controlled growth. In the absence or disregard of such regulation, resulting from changes in their genetic makeup, these errant cells acquire a growth advantage, expanding into precancerous clones. Over the last decade, many studies have revealed the relevance of genomic mutation in this process, be it by misreplication, environmental damage, or a deficiency in repairing endogenous and exogenous damage. Here, we discuss homologous recombination as another mechanism that can result in a loss of heterozygosity or genetic rearrangements. Some of these genetic alterations may play a primary role in carcinogenesis, but they are more likely to be involved in secondary and subsequent steps of carcinogenesis by which recessive oncogenic mutations are revealed. Patients, whose cells display an increased frequency of recombination, also have an elevated frequency of cancer, further supporting the link between recombination and carcinogenesis.
当细胞不再遵循其正常的受控生长模式时，癌症就会发生。由于其基因组成的变化，在缺乏或无视这种调控的情况下，这些异常细胞获得生长优势，扩展为癌前克隆。在过去十年中，许多研究揭示了基因组突变在这一过程中的相关性，无论是通过错误复制、环境损伤，还是修复内源性和外源性损伤的缺陷。在这里，我们讨论同源重组作为另一种可导致杂合性丧失或基因重排的机制。其中一些基因改变可能在致癌过程中起主要作用，但它们更可能参与致癌的继发性及后续步骤，通过这些步骤隐性致癌突变得以显现。细胞显示出重组频率增加的患者，患癌频率也会升高，这进一步支持了重组与致癌之间的联系。
