人類離贏得"癌症戰爭"勝利的距離(3)
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.
爲此，斯旺頓和他的同事們精確的計算具體要同時進行多少種針對於主幹突變的藥物交叉攻擊才能夠徹底的消滅癌細胞。他們發現“三”是一個神奇的數字，他們的數據表明在同時攻擊三個主幹突變後，會成功摧毀“大樹的主幹”，並最終摧毀腫瘤內的每一個癌細胞。
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.
當然這種治療方法並不便宜，因爲它需要研究者們研究病人的具體癌症情況，找到變異的主幹，只有這樣調製和使用合適有效的雞尾酒合成療法。
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.
“我們採用了爲腫瘤測序的方法，並針對每個病人生產不同主幹抗原的辦法，”斯旺頓說。
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.
來自意大利都靈大學的阿爾貝託.巴爾代利（Alberto Bardelli）教授是大腸癌方面的權威，他從進化理論中得到靈感，尋找應對癌細胞耐藥性的辦法。
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.
“所有腫瘤都會產生耐藥性，我爲此感到失望和痛苦”，他說。巴爾代利教授目前基於這種耐藥性開發新的治療癌症的療法。
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.
他開始檢測具有耐藥性的癌細胞，他稱這些細胞爲“克隆”。在病人採用某種藥物療法的過程中，巴爾代利對這個過程進行監測，並觀察具有耐藥性的“克隆”細胞是否會成爲腫瘤中的主宰細胞。
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.
這個時候，巴爾代利停止了對癌症的藥物治療，這樣做的目的是爲了使克隆細胞脫離所處的進化環境，該環境正是使得克隆細胞成爲如此有耐藥性的前提。這樣腫瘤內的其他細胞也因此得到反撲的機會，普通的癌細胞開始與之前佔主導的“克隆”癌細胞對抗，相互吞噬。這一結果導致的就是癌細胞自己開始內戰了。
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".
當其他的克隆細胞佔據優勢之後，就是需要再次使用藥物的時候，因爲這些新的克隆細胞還沒來得及產生耐藥性。巴爾代利稱之爲“克隆之戰”。
"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. "
“我們用新克隆細胞對付之前的舊克隆細胞，有了勝負之後，我們改變他們的生存環境，停止藥物。勝出的癌細胞不適應新的環境，開始消失被其他細胞取代。你可以理解爲我們引發不同性質的腫瘤細胞之間的相互對抗。
I want to use the portion of the cells that are not affected by the therapy to fight back the others."
“我們的目的就是激發那些對治療方法無效的癌細胞去攻擊其他的癌細胞。”
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.
目前來說這種方式是否有效還是一個未知數，巴爾代利和他的團隊在2016年夏季開始臨牀試驗。
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.
此類進化式的方法給癌症治療帶來了希望，但同時重要的是，我們需要增加對於引發癌症誘因的瞭解。
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年一項大規模的基因研究在這個領域做出了重大的進展。研究者通過對癌症病人基因組的研究，探究30種最常見的癌症基因突變的生物標識。
