2022年经济学人 为什么大象很少患癌症？(1)（在线收听）

Science & technology

科技板块

Oncology

肿瘤学

Protein shake-up

蛋白质重组

Why elephants so rarely get cancer

为什么大象很少患癌症

Elephants have always presented a paradox to biologists.

对于生物学家来说，大象一直是一个悖论。

They are much larger than humans and live for a similar length of time, yet they only rarely develop cancer.

它们比人类大得多，寿命也差不多，但它们很少患上癌症。

That is odd.

这很奇怪。

Cancer, after all, is something of a numbers game: the more cells, the more replications.

毕竟，在某种程度上癌症是一个数字游戏：细胞越多，复制就越多。

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.

复制越多，随机DNA损伤和细胞失控的可能性就越大，无法被检测到，最终开始向肿瘤扩散的失控过程。

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.

巴塞罗那自治大学的Konstantinos Karakostis领导的研究发表在《分子生物学与进化》上，这项研究指出了皮托悖论的答案，至少对大象来说是这样。

This absence of size-to-cancer correlation is named after Sir Richard Peto, a British epidemiologist who first noted it in 1977.

大小与癌症之间没有相关性的现象，是以英国流行病学家理查德·皮托爵士的名字命名的，他在1977年首次发现这一现象。

Their investigations began with p53, a transcription factor.

他们的研究始于转录因子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.

当DNA被转录成RNA时，这些蛋白质参与其中，控制着哪些基因被激活以及激活多长时间。

But p53 is also in the business of marshalling resources in the service of quality control.

但P53也在为质量控制服务中调集资源。

When it encounters damaged dna, it fails to bind to yet another protein called mdm2.

当它遇到受损的DNA时，它无法与另一种名为MDM2的蛋白质结合。

That in turn sets off a chain of events that stimulates a cell to repair any damage.

进而引发了一系列事件，刺激细胞修复任何损伤。

If that fails, p53 initiates a different chain that makes the cell destroy itself.

如果失败，p53会启动不同的链条，使细胞自我毁灭。

P53, then, is a potent anti-cancer agent in the body’s arsenal.

因此，p53是人体基因库中一种有效的抗癌剂。

But cancer, in many creatures, is a potent adversary.

但在许多生物体中，癌症是一个强劲的对手。

Cancer cells have damaged dna but have ways to ensure the binding to mdm2 happens without a hitch.

癌细胞破坏了DNA，但有办法确保与MDM2的结合顺利进行。