The catch is that the respite does not last. Typically, someone will respond for about a year,but after that his tumour starts growing again and the disease continues on its course. This isa pattern seen again and again with the new generation of drugs that genomics has helped tocreate. They slow the disease, but only for a few months. The presumption is that furthermutations are arising in a tumour all the time, and that eventually one of them makes amolecular change that nullifies the effect of the drug. Researchers would dearly like to find a wayto deal with this.
但问题是Xalkori对病情的缓解作用持续时间不长。一般来说,持续服药一年后患者将产生抗药性,体内癌细胞恢复增长导致病情恶化。这是一代代利用基因组学开发出的药物共同的治疗效果变化模式,最终都只能短暂地缓解病情。其机制可能是,癌细胞会不断地产生新的突变体,最终其中的某个突变体编码产生了使药物作用失效的蛋白分子。研究人员正致力于找出对付这种机制的办法。
One who is trying to do so is Ren Bernards of theNetherlands Cancer Institute. On September 18th hetold a meeting of the American Association forCancer Research, held in San Francisco, about a waythat the sensitivity of tumour cells to Xalkori mightbe restored. More important than that, though, isthe way he discovered the solutionfor this couldbe applied to many other cases in which an anti-cancer drug is having its useful life curtailed by thedevelopment of resistance.
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