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Adult cells are constantly under strict control, Weil says. "Basically cancer is a loss of control of those cells."
“成年的细胞是被持续的严格控制的”，韦尔说，“基本上我们可以把癌症理解为对这些细胞失去了控制。”
Cancer can only grow in this uncontrolled fashion if some of the genes that usually stop any accidental cell growth – such as the p53 gene – get mutated in the cancer cells.
通常情况下我们人体内的某些基因会阻止细胞意外生长，比如 P53基因，但如果他们在癌细胞中发生突变，那么癌细胞就会在这种失控的模式下成长。
However, our bodies are pretty good at spotting these mutations. There are biological systems within us that step in to destroy most mutated cells before they can cause us harm.
当然我们的身体非常善于识别这些突变。我们身体内部的生物系统会在突变细胞对人体健康产生危害时摧毁突变最严重的细胞。
We have several "corrective" genes which send instructions to kill any corrupted cells. "There's millions of years of evolution that's gone into this," says Charles Swanton of the Francis Crick Institute in the UK. "It's pretty good but it's not quite perfect."
在我们身体内部有一些负责“纠正错误”的基因，他们会指导我们杀死那些腐坏的细胞。“上百万年的进化让我们的身体非常善于修正错误，”英国弗朗西斯•克里克研究所（Francis Crick Institute）的教授查尔斯.斯旺顿（CharlesSwanton）说到。“基因在这方面非常强大，但是并不完美。”
The threat comes from the tiny number of corrupt cells that do not get fixed. Over time, one of these cells can grow and divide into thousands, then tens of thousands of cancer cells. Eventually there may even be billions of cells in a tumour.
威胁就来自于这一小撮腐坏的但并没有得到应有的修复的细胞。某一个未修复的腐坏的细胞通过分裂会变成几千个，几万个癌细胞。最终，一个肿瘤中可能存活了几十亿个癌细胞。
This leads to a truly challenging problem. Once that initial corrupt cell has divided and multiplied into a tumour, a person will have cancer until every single one of the cancer cells has been obliterated. If just a few survive, they can rapidly multiply and regrow the tumour.
这引发了一个极具挑战的问题，当一个腐坏的细胞通过分裂，生长成一个肿瘤的时候，我们就需要消灭每一个单独的癌细胞，那么这个患癌的人才可以被治愈。只要腐坏的细胞存活，哪怕只是很少的一部分，都可以迅速生长并形成肿瘤。
Cancer cells are not all alike: far from it. Whenever a cancerous cell divides, it has the potential to pick up new mutations that affect its behaviour. In other words, they evolve.
癌细胞并不相似，而且是非常不同。每一次癌细胞分裂，他们都有潜在的可能重新变异，也就是说癌细胞在不断的进化。
As the cells inside a tumour mutate, they become ever more genetically diverse. Then evolution goes to work to find the most cancerous ones.
当癌细胞在肿瘤里变异，他们的基因会变得越来越多样化，在进化的作用下，变异就会主动去找这些细胞里边最恶性的细胞。
Genetic diversity is "the spice of life, it's the substrate upon which natural selection acts", says Swanton. By this he means evolution by natural selection, first proposed by Charles Darwin in 1859.
基因多样性是“生活的调味品”，这是大自然的一种进化选择的基础，斯旺顿说。他的意思是通过自然选择的进化，也就是查尔斯.达尔文在1859年首次提出的理论。
Just like individual species – humans, lions, frogs, even bacteria – gain genetic variation over time, so too do cancer cells. "Tumours don't evolve in a linear manner," says Swanton. "They evolve in a branched evolutionary manner, which means that no two cells in a tumour are the same."
癌症细胞通过进化而完成基因的多样性，正如个体物种例如人类、狮子、青蛙、甚至细菌的进化方式。“肿瘤并不是线性的进化，”斯旺顿说。“他们通过分支进化的方式演变，也就是说同一个肿瘤中没有两个完全一样的癌细胞。”
In effect, the cells of a tumour are evolving to become more cancerous. "Essentially we are dealing with branches of evolution that create diversity and that create fitness, and allow cell populations to survive therapy and ultimately outwit the clinician," says Swanton.
本质上，在肿瘤内的癌细胞会变得越来越致命。“实际上我们所做的就是针对进化中产生多样性与健康的细胞分支进程，使细胞群挺过癌症治疗并最终取得良好的临床结果，”斯旺顿说。
The fact that tumours are constantly changing their genetic makeup is one of the reasons why cancers are so hard to "kill".
癌症之所以很难消灭是因为肿瘤在持续不断的改变他们的基因结构。
It is for this reason that Swanton, and others in the field, take an evolutionary approach to tackling cancer. Swanton, who specialises in lung cancer, is both a clinician and a research scientist. His work has revealed something that he hopes will help create effective, targeted treatment.
这就是为什么斯旺顿和其他研究人员采用进化性的眼光探寻着解决癌症的办法。斯旺顿即是临床医生也是理论科学家，他的专长是肺癌领域。他的研究工作已经揭示了癌症的一些工作原理，他希望这些成果可以帮助他最终找到更有效的精准治疗癌症的方法。
Think of the evolution that goes on inside a cancer tumour as like a tree with many branches. At the base of the tree are the original mutations that triggered the tumour in the first place: mutations that should be shared by all of the cancer cells in the tumour.
我们可以把肿瘤内部的细胞进化过程想象为一个长满树枝的大树。树根是触动基因变异的机关：树根细胞的变异影响到肿瘤内的所有细胞。
In theory, a therapy that targets one of those base mutations should destroy every cell in the tumour. This is an approach that some therapies already use. For instance a drug called EGFR therapy targets lung cancer, and a BRAF inhibitor protein attacks the faulty gene which can lead to melanoma.
理论上来说，如果任何一个疗法可以精准定位这个树根主干突变，并且成功摧毁它，那么就应该治愈了整个肿瘤。这也是现在很多治疗使用的疗法。比如针对肺癌的EGFR靶向治疗药物，还有针对导致黑色素瘤变异基因的BRAF抑制剂基因疗法。
The trouble is, these therapies do not work as well as we might hope. Even in these targeted therapies, resistance often appears over time.
但是问题在于这些疗法并没有当初科学家们预期的有效，即使是在一些靶向治疗中，时间一长就会出现耐药性。
It occurs because there will be one or more cells in the tumour branches that has a resistance mutation that allows it to outwit the therapy, Swanton says.
“这是因为一个肿瘤里边有一个或多个的癌细胞分支发生了突变，产生了耐药性，因此治疗失去了效果。”斯旺顿说。
In other words, some of the branches of the cancer tree have evolved in a way that makes them less vulnerable to attack through the base mutation. They can dodge the therapy.
换句话说，一些在肿瘤里的分支癌细胞通过进化对针对于主干突变的疗法产生耐受性，因此躲过了靶向疗法。
Swanton and his colleagues have studied the problem to see if they can develop a therapy with a better outcome.
斯旺顿和他的同事们已经注意到了这个问题，并且正在寻找新的方法，希望能够得到更好的治愈办法。
An average tumour might contain something like a thousand billion cancer cells. Some of those cells might well have evolved in a way that makes them immune to attack through a specific basal mutation.
平均一个肿瘤里边会保存着万亿个癌细胞，很多癌细胞可以通过变异对主干突变的治疗产生免疫。
But what if a therapy targeted two of those basal mutations at the same time? Far fewer cells will have evolved in a way that makes them immune to both forms of attack.
但是如果我们采用一种可以同时治疗两种主干突变的疗法进行治疗呢？单个癌细胞成功规避二次靶向药物交叉攻击的机会非常罕见。
