生物谷報(bào)道：癌細(xì)胞的恒久生命與導(dǎo)致人死亡的衰老過程看起來似乎是相對(duì)立的,。但令人吃驚的是，癌細(xì)胞和衰老過程的生物學(xué)基礎(chǔ)卻是相合的,?；蚪M不穩(wěn)定、端粒功能和自噬作用等在關(guān)于癌癥和衰老的論文中都能見到,。研究人員已經(jīng)在腫瘤發(fā)生與細(xì)胞衰老之間發(fā)現(xiàn)了聯(lián)系,。線粒體代謝對(duì)這兩個(gè)現(xiàn)象來說都是中心內(nèi)容。Finkel等人發(fā)表在最新一期《自然》雜志上的一篇綜述,，從歷史角度向我們介紹了癌癥和衰老的共同生物學(xué)基礎(chǔ)：從第一次意識(shí)到人類癌細(xì)胞—HeLa細(xì)胞—在培養(yǎng)中有可能繼續(xù)分裂一直談到系統(tǒng)生物學(xué)方法的問世,。

 
FIGURE 1. The potential interplay between stem cells, stress, ageing and cancer.
During normal ageing, stem cells accumulate damage and subsequent stress-dependent changes (for example, de-repression of the CDKN2a (INK4a/ARF) locus or telomere shortening). This leads to the increasing abundance of senescent cells (large blue cells) within differentiated tissues. Incipient tumours, arising directly from stem cells or from more committed cells, undergo rapid proliferation (small red cells). These pre-malignant tumour cells rapidly accumulate damage, in part owing to the presence of oncogenes, leading to a higher proportion of tumour cells becoming senescent (small blue cells). Tumour progression to full malignancy is favoured when tumour cells acquire mutations that impair the senescence program (for example, mutations in Trp53 or CDKN2a).

原文出處：

Nature       Volume 448 Number 7155

The common biology of cancer and ageing p767
Toren Finkel, Manuel Serrano & Maria A. Blasco

doi:10.1038/nature05985

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See also: Editor's summary

作者簡(jiǎn)介：
Toren Finkel