Homologous Recombination and Its Role in Carcinogenesis.
Homologous Recombination and Its Role in Carcinogenesis.
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同源重组及其在癌变中的作用。
DOI：
10.1155/s1110724302204052
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发表时间：
2002
影响因子：
--
通讯作者：
Schiestl, Robert H.
中科院分区：
文献类型：
--
作者：
Bishop, Alexander J. R.;Schiestl, Robert H.
当细胞不再遵循正常的控制生长模式时，癌症就会发生。由于基因组成的变化，在缺乏或无视这种调节的情况下，这些错误的细胞获得了生长优势，扩展成癌前克隆。在过去的十年中，许多研究揭示了基因组突变在这一过程中的相关性，可能是由于错误复制、环境损伤或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机制，可以导致杂合性或遗传重排的损失。其中一些基因改变可能在癌变中起主要作用，但它们更有可能参与继发性和后续的癌变步骤，从而揭示隐性致癌突变。细胞重组频率增加的患者，患癌症的频率也会增加，这进一步支持了重组与致癌之间的联系。
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.