In fact, he found three. Mediator-12 , whichhelps to transcribe genes from DNA into RNAmessengers, was one. The other two were genesthat help maintain the structure of chromosomes.Presumably, resistance to Xalkori is being caused bydisabling mutations in one or more of these genes.
实际上,伯纳兹博士最后确认了三个。一个是Mediator-12,即控制基因转录成信使RNA的中介体复合物亚基12基因,其他两个是帮助维护持染色体结构的基因。可以推断,针对Xalkori的抗药性是由于这三个基因中的一个或多个发生了突变导致的结果。
That is interesting, but not of immediate assistance to the dying. What Dr Bernards and hiscolleagues did next, though, could be of such help. They looked for hairpin RNAs that restoredsensitivity to Xalkori in cells whose MED12 messengers were being blockedand they foundone. Disabling the messengers of the gene that encodes a receptor protein called TGF beta-R2, which is found on cell surfaces, caused cells that had once been resistant to Xalkori toshrivel in its presence. Moreover, treating these same Xalkori-resistant cells with anexperimental drug designed to block TGF beta-receptors restored sensitivity to Xalkori,though it had no effect on cancer-cell growth on its own.
这个发现十分有趣,但是对治疗患者没有直接帮助。伯纳兹博士与同事们接下来所做的工作正符合这个目的。他们尝试寻找能够拦截MED12基因的信使RNA 从而恢复细胞对Xalkori敏感性的发夹结构,并取得了成功。TGF beta-R2是一种存在于细胞表面的蛋白质受体,只要破坏编码这种受体DNA的信使RNA,就能消除细胞对Xalkori的抗药性。此外,设计药物针对同样的抗药细胞,使其表面的TGF beta受体被药物屏蔽,也会得到相同的实验结果,即使这种药物本身并没有阻止癌细胞增长的疗效。
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