2012年8月13日 訊 /生物谷BIOON/ --近日，來(lái)自科羅拉多大學(xué)癌癥中心的一篇研究綜述揭示了癌癥是和年齡相關(guān)的,，癌癥在老年人中的發(fā)病頻率比在年輕人中高許多,。相關(guān)研究成果刊登在了國(guó)際雜志Oncogene上,，文章中研究者反對(duì)傳統(tǒng)的觀點(diǎn)，傳統(tǒng)觀點(diǎn)認(rèn)為老年人癌癥發(fā)生是由于引發(fā)癌癥突變的積累所導(dǎo)致的,。
組織紋理的改變和非必要的致癌突變的積累可以驅(qū)動(dòng)老年人的高癌癥風(fēng)險(xiǎn)
研究者James表示,，如今的米克-賈格爾(Mick Jagger，滾石樂(lè)隊(duì)主唱)和其1960年的對(duì)比,，你會(huì)發(fā)現(xiàn)現(xiàn)在的他的機(jī)體組織紋理發(fā)生了明顯的改變,。這種改變并不是促使癌癥突變因子的積累所導(dǎo)致的，但是其可以促使其癌癥發(fā)病比率升高,?；谧C據(jù)，研究者首次指出,，等我們?cè)谖覀兦嗌倌晖砥谕Ｖ股L(zhǎng)的時(shí)候,，我們已經(jīng)積累了我們一生的一大群突變，突變曲線和癌癥曲線的錯(cuò)配意味著癌癥如果已經(jīng)達(dá)到了一個(gè)臨界點(diǎn),，也就是說(shuō)5-6個(gè)突變,，這樣我們就會(huì)看到20多歲人群高的癌癥發(fā)病風(fēng)險(xiǎn)。
研究者同樣指出,，甚至是健康的組織也會(huì)有許多致癌的突變,。如果癌基因能夠圍繞在組織周圍，那么向老鼠干細(xì)胞中引入癌基因可以幫助小鼠的組織細(xì)胞生存,，而且干細(xì)胞可以包裹癌基因使得癌基因快速被淘汰,。
我們健康的細(xì)胞會(huì)達(dá)到最優(yōu)化狀態(tài)來(lái)完成維持機(jī)體健康的任務(wù)，如果改變了這種平衡，比如發(fā)生致癌的突變,，那么機(jī)體中的健康細(xì)胞便會(huì)迅速反應(yīng)戰(zhàn)勝致癌突變的細(xì)胞,。但是如果組織變老了，健康細(xì)胞便不能完美勝任機(jī)體賦予其的責(zé)任了,，此時(shí)突變或許會(huì)幫助癌細(xì)胞來(lái)適應(yīng)機(jī)體,，發(fā)生癌癥。（生物谷Bioon.com）
編譯自：Why cancer rate increases with age (it's not what you think)
doi:10.1038/onc.2012.281
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PMID:
Challenging the axiom: does the occurrence of oncogenic mutations truly limit cancer development with age?
J DeGregori
A widely accepted paradigm in cancer research holds that the development of cancers is rate limited by the occurrence of oncogenic mutations. In particular, the exponential rise in the incidence of most cancers with age is thought to reflect the time required for cells to accumulate the multiple oncogenic mutations needed to confer the cancer phenotype. Here I will argue against the axiom that the occurrence of oncogenic mutations limits cancer incidence with age, based on several observations, including that the rate of mutation accumulation is maximal during ontogeny, oncogenic mutations are frequently detected in normal tissues, the evolution of complex multicellularity was not accompanied by reductions in mutation rates, and that many oncogenic mutations have been shown to impair stem cell activity. Moreover, although evidence that has been used to support the current paradigm includes increased cancer incidence in individuals with inherited DNA repair deficiencies or exposed to mutagens, the pleotropic effects of these contexts could enhance tumorigenesis at multiple levels. I will further argue that age-dependent alteration of selection for oncogenic mutations provides a more plausible explanation for increased cancer incidence in the elderly. Although oncogenic mutations are clearly required for cancer evolution, together these observations counter the common view that age dependence of cancers is largely explained by the time required to accumulate sufficient oncogenic mutations.
