As they report in Nature, he and his team discovered 18 genes that were often mutated.Some were the usual suspects of cancer genetics. These included p53, a gene that, whenworking properly, suppresses cancer by regulating DNA repair, cell division and cellularsuicide, and MAP3K1 and MAP2K4, which both promote cell growth. Others, though, were asurprise. At the top of that list were five which had previously been linked to leukaemia, butwere not thought to affect solid tumours.

　　正如他们在《自然》杂志中所报告的那样，埃利斯和他的团队发现了18种经常发生突变的基因，其中有些是癌症遗传学通常怀疑的对象。这中间包括p53，这种基因在正常工作时通过调节DNA对的修复、细胞分裂和细胞自杀来抑制癌症;还有MAP3K1和MAP2K4，它们都能促进细胞生长。但也有些令人吃惊的其他结果。高踞名单前列的5种基因是人们过去认为与白血病有关的，没想到它们也会影响实体瘤。

　　By combining their newly acquired genetic data with clinical data from the participants, DrEllis and his colleagues showed that those whose tumours carried mutations in p53 were less likely to have responded to letrozole than women whose tumours hadnormal p53. Conversely, those whose tumours had changes in either MAP3K1 or MAP2K4 had better than average responses to the drug.

　　将他们新得到的基因数据与参与试验者的临床数据结合，埃利斯博士等人证明了，来曲唑对肿瘤中有p53基因突变的病人的疗效不如对肿瘤中p53基因正常的病人那样显著。与此相反，这一药物对肿瘤中MAP3K1或MAP2K4有变化的病人的疗效高于平均水平。

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