埃利斯博士及其团队对46名身患雌激素受体阳性乳腺癌的妇女的癌组织和正常组织进行了全基因组测序。他们也对另外31名病人的基因组中含有基因的那些区域(约占整个DNA的1%)进行了测序,并对其他240名病人的这些部分做了部分测序。此后,为找出癌细胞中哪些基因发生了突变,他们比较了每个病人的健康和癌变基因组。
In this, they were following the normal protocol of the cancer genome consortium. The novelty of their approach was that the women in question had each been involved in one of two clinical trials of a drug called letrozole. These trials established letrozole as a standard treatment for people with this type of breast cancer, but not all patients benefit equally from the drug. Dr Ellis hoped to find out why.
他们在这一工作中是按癌症基因组协作组的标准程序操作的,但其方法的新颖之处是,他们还同时进行一种名为来曲唑的药物的临床试验。该试验有两种,每个病人都接受其中的一种。这些试验证实来曲唑是这类乳腺癌的标准治疗方法,但它对每个病人的疗效并不一样。埃利斯博士希望找出其原因。
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, when working properly, suppresses cancer by regulating DNA repair, cell division and cellular suicide, and MAP3K1 and MAP2K4, which both promote cell growth. Others, though, were a surprise. At the top of that list were five which had previously been linked to leukaemia, but were not thought to affect solid tumours.
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