Radford I R
Radiation Oncology Division, Peter MacCallum Cancer Centre, St Andrews Place, East Melbourne, Victoria 3002, Australia.
Int J Radiat Biol. 2004 Aug;80(8):543-57. doi: 10.1080/09553000412331283489.
To develop a model for the initiation of human tumourigenesis that is consistent with various observations that are difficult to reconcile with current models.
A novel model of tumourigenesis was developed that includes three basic postulates: (1) tumourigenesis is initiated by recombinogenic DNA lesions, (2) potentially recombinogenic DNA lesions in transcribed regions of the genome can be converted into chromosomal rearrangements and (3) chromosomal rearrangements alone are insufficient for tumourigenesis but can initiate a mutator/recombinator phenotype.
建立一个人类肿瘤发生起始模型,该模型与各种难以与当前模型相协调的观察结果相一致。
开发了一种新的肿瘤发生模型,该模型包括三个基本假设:(1)肿瘤发生由重组性DNA损伤引发;(2)基因组转录区域中潜在的重组性DNA损伤可转化为染色体重排;(3)单独的染色体重排不足以引发肿瘤发生,但可引发突变/重组表型。