癌症基因疗法取得新突破_BEC初级作文

癌症基因疗法取得新突破

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, Dr Ellis and his colleagues showed that those whose tumours carried mutations in p53 (16% of the total) were less likely to have responded to letrozole than women whose tumours had normal p53. Conversely, those whose tumours had changes in either MAP3K1 or MAP2K4 (another 16%) 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（占总数的16%）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（也占总数的16%）的疗效高于平均水平。

This sort of information has obvious implications for treatment. And the cheapness of modern gene-sequencing methods, particularly those that are looking for specific mutations suspected in advance, means that a tumour's mutational complement can be worked out easily in an appropriately equipped pathology laboratory. In the case of oestrogen-receptor-positive breast cancer, the genetic analysis has not yet gone so far as to be able to say with certainty which drug will produce the best result for a given individual, but Dr Ellis's result lays a foundation on which such an edifice might be built for breast cancer and perhaps for other types of tumour, too.