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Science & technology
科技板塊
Oncology
腫瘤學
Protein shake-up
蛋白質重組
Why elephants so rarely get cancer
為什么大象很少患癌癥
Elephants have always presented a paradox to biologists.
對于生物學家來說，大象一直是一個悖論。
They are much larger than humans and live for a similar length of time, yet they only rarely develop cancer.
它們比人類大得多，壽命也差不多，但它們很少患上癌癥。
That is odd.
這很奇怪。
Cancer, after all, is something of a numbers game: the more cells, the more replications.
畢竟，在某種程度上癌癥是一個數字游戲：細胞越多，復制就越多。
The more replications, the greater the likelihood of random dna damage and a cell going rogue, failing to be detected and ultimately starting the runaway process towards a tumour.
復制越多，隨機DNA損傷和細胞失控的可能性就越大，無法被檢測到，最終開始向腫瘤擴散的失控過程。
Work led by Konstantinos Karakostis of the Autonomous University of Barcelona and published in Molecular Biology and Evolution, points to an answer, for elephants at least, to Peto’s paradox.
巴塞羅那自治大學的Konstantinos Karakostis領導的研究發表在《分子生物學與進化》上，這項研究指出了皮托悖論的答案，至少對大象來說是這樣。
This absence of size-to-cancer correlation is named after Sir Richard Peto, a British epidemiologist who first noted it in 1977.
大小與癌癥之間沒有相關性的現象，是以英國流行病學家理查德·皮托爵士的名字命名的，他在1977年首次發現這一現象。
Their investigations began with p53, a transcription factor.
他們的研究始于轉錄因子P53。
These are the proteins that are in attendance as dna is transcribed into rna, controlling which genes are switched on and for how long.
當DNA被轉錄成RNA時，這些蛋白質參與其中，控制著哪些基因被激活以及激活多長時間。
But p53 is also in the business of marshalling resources in the service of quality control.
但P53也在為質量控制服務中調集資源。
When it encounters damaged dna, it fails to bind to yet another protein called mdm2.
當它遇到受損的DNA時，它無法與另一種名為MDM2的蛋白質結合。
That in turn sets off a chain of events that stimulates a cell to repair any damage.
進而引發了一系列事件，刺激細胞修復任何損傷。
If that fails, p53 initiates a different chain that makes the cell destroy itself.
如果失敗，p53會啟動不同的鏈條，使細胞自我毀滅。
P53, then, is a potent anti-cancer agent in the body’s arsenal.
因此，p53是人體基因庫中一種有效的抗癌劑。
But cancer, in many creatures, is a potent adversary.
但在許多生物體中，癌癥是一個強勁的對手。
Cancer cells have damaged dna but have ways to ensure the binding to mdm2 happens without a hitch.
癌細胞破壞了DNA，但有辦法確保與MDM2的結合順利進行。
