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Swanton and his colleagues crunched the numbers to see how many base mutations in the cancer "trunk" they would have to target simultaneously to ensure that they could successfully destroy every one of the cancer cells. Three was the magic number. Their calculations suggest that targeting three base mutations at the same time will "chop the trunk down" and destroy every single cell in the tumour.
为此，斯旺顿和他的同事们精确的计算具体要同时进行多少种针对于主干突变的药物交叉攻击才能够彻底的消灭癌细胞。他们发现“三”是一个神奇的数字，他们的数据表明在同时攻击三个主干突变后，会成功摧毁“大树的主干”，并最终摧毁肿瘤内的每一个癌细胞。
However, this approach is not going to be cheap. To work, it requires the researchers to study a person's specific cancer to establish which base mutations their tumour has, so that the right cocktail of therapies can be applied.
当然这种治疗方法并不便宜，因为它需要研究者们研究病人的具体癌症情况，找到变异的主干，只有这样调制和使用合适有效的鸡尾酒合成疗法。
What we've come up with is an approach where we sequence tumours and produce the truncal antigens on a patient-by-patient basis, Swanton explains.
“我们采用了为肿瘤测序的方法，并针对每个病人生产不同主干抗原的办法，”斯旺顿说。
Colorectal cancer researcher Alberto Bardelli of the University of Turin in Italy, has also been using evolutionary theory as inspiration for a potential solution to overcoming drug resistance.
来自意大利都灵大学的阿尔贝托.巴尔代利（Alberto Bardelli）教授是大肠癌方面的权威，他从进化理论中得到灵感，寻找应对癌细胞耐药性的办法。
I was very disappointed by the fact that all tumours became resistant, he says of his previous work. Now Bardelli has used the reality of drug resistance to develop a new anti-cancer therapy.
“所有肿瘤都会产生耐药性，我为此感到失望和痛苦”，他说。巴尔代利教授目前基于这种耐药性开发新的治疗癌症的疗法。
He begins by teasing out the resistant cancerous cells, which he calls "clones". Patients are given a particular drug therapy and then monitored to see when a particular cancerous "clone" rises to dominance in the tumour because it has developed drug resistance.
他开始检测具有耐药性的癌细胞，他称这些细胞为“克隆”。在病人采用某种药物疗法的过程中，巴尔代利对这个过程进行监测，并观察具有耐药性的“克隆”细胞是否会成为肿瘤中的主宰细胞。
Then Bardelli stops treating the cancer with the drug. This removes the evolutionary pressure that allowed the clone to become so successful. Without that pressure, other types of cancer cell in the tumour also have a chance to flourish. They "fight back" against the dominant clone. In effect, the cancer effectively begins to war with itself.
这个时候，巴尔代利停止了对癌症的药物治疗，这样做的目的是为了使克隆细胞脱离所处的进化环境，该环境正是使得克隆细胞成为如此有耐药性的前提。这样肿瘤内的其他细胞也因此得到反扑的机会，普通的癌细胞开始与之前占主导的“克隆”癌细胞对抗，相互吞噬。这一结果导致的就是癌细胞自己开始内战了。
When some of those other clones have gained ground, it is time to administer the drugs again, as these new clones should not yet have developed resistance. Bardelli calls it "the war of clones".
当其他的克隆细胞占据优势之后，就是需要再次使用药物的时候，因为这些新的克隆细胞还没来得及产生耐药性。巴尔代利称之为“克隆之战”。
"We use clones against clones, we wait for the winners, then take out the pressure; the drug. The winners at this point are unfit and start to disappear, and then others take over. So we use the tumour against itself. "
“我们用新克隆细胞对付之前的旧克隆细胞，有了胜负之后，我们改变他们的生存环境，停止药物。胜出的癌细胞不适应新的环境，开始消失被其他细胞取代。你可以理解为我们引发不同性质的肿瘤细胞之间的相互对抗。
I want to use the portion of the cells that are not affected by the therapy to fight back the others."
“我们的目的就是激发那些对治疗方法无效的癌细胞去攻击其他的癌细胞。”
For now we do not know if this tactic will work or not. His team is starting a clinical trial in the summer of 2016.
目前来说这种方式是否有效还是一个未知数，巴尔代利和他的团队在2016年夏季开始临床试验。
These evolutionary approaches may show great promise, but at the same time it is important to better understand the many triggers that can cause cancer in the first place.
此类进化式的方法给癌症治疗带来了希望，但同时重要的是，我们需要增加对于引发癌症诱因的了解。
In 2013 one of the biggest genetic studies took an important step forward in doing so. Researchers scoured cancer patients' genomes to look at "signatures" of the 30 most common cancer mutations.
2013年一项大规模的基因研究在这个领域做出了重大的进展。研究者通过对癌症病人基因组的研究，探究30种最常见的癌症基因突变的生物标识。
