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| 購買進(jìn)口儀器、試劑和耗材——就在始于2001年的畢特博生物 effectnews.cn |
英國科學(xué)家找到了“急性癌癥”的形成原因：細(xì)胞內(nèi)的染色體發(fā)生“爆炸”破壞了DNA，從而讓人有可能在短時(shí)間內(nèi)患上癌癥。相關(guān)論文發(fā)表于Cell。 傳統(tǒng)理論認(rèn)為癌癥是人體經(jīng)歷成千上萬次的細(xì)胞突變后，慢慢演化的結(jié)果。但英國著名的疾病研究機(jī)構(gòu)桑格研究所的新發(fā)現(xiàn)推翻了這種看法。這暗示了不管人們怎么努力保持身體健康，也不能保證命運(yùn)不會(huì)拿他們開玩笑。同時(shí)還說明了為什么有些人在體檢時(shí)根本沒發(fā)現(xiàn)癌癥痕跡，但數(shù)月后突然就被診斷患上這種疾病了。 桑格學(xué)院的科學(xué)家是通過研究750個(gè)腫瘤的遺傳缺陷后得出以上結(jié)論的。其中大部分的案例都與傳統(tǒng)理論相符，染色體的損壞是常年累積的結(jié)果。然而，其中至少有1/40的腫瘤不符合“標(biāo)準(zhǔn)模式”，有的染色體似乎是在一夜之間遭到破壞的。 參與此項(xiàng)研究的坎貝爾博士稱：“測驗(yàn)結(jié)果太讓我們驚訝了。在一個(gè)細(xì)胞里面，染色體經(jīng)過一次或者是多次爆炸成為碎片。如果這個(gè)細(xì)胞開始笨拙地修補(bǔ)，把碎片雜亂的縫合起來，這樣就破壞了原來的DNA結(jié)構(gòu)，為癌癥的快速形成提供了條件。” 坎貝爾博士表示：“這個(gè)細(xì)胞應(yīng)該說‘好吧，我放棄’，而不是像對待昂貴的瓷器一樣，把染色體拼接回去。細(xì)胞試圖修復(fù)一個(gè)不可修復(fù)的東西，最后造出一個(gè)災(zāi)難性的、能讓癌癥更快形成的基因組。” 這種“急性癌癥”在骨癌里面特別常見，大概1/4的患者身上都能看到明顯的染色體受損特征模式?？茖W(xué)家目前還不能肯定是什么引起了這種染色體“爆炸”，但有嫌疑的罪魁禍?zhǔn)装╔光和曬傷?？藏悹柌┦糠Q：“如果我們能了解根本的病因，或許就可以防止患上這種癌癥。” 推薦原文出處： Cell doi:10.1016/j.cell.2010.11.055 Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development Philip J. Stephens, Chris D. Greenman, Beiyuan Fu, Fengtang Yang, Graham R. Bignell, Laura J. Mudie, Erin D. Pleasance, King Wai Lau, David Beare, Lucy A. Stebbings, Stuart McLaren, Meng-Lay Lin, David J. McBride, Ignacio Varela, Serena Nik-Zainal, Catherine Leroy, Mingming Jia, Andrew Menzies, Adam P. Butler, Jon W. Teague, Michael A. Quail, John Burton, Harold Swerdlow, Nigel P. Carter, Laura A. Morsberger, Christine Iacobuzio-Donahue, George A. Follows, Anthony R. Green, Adrienne M. Flanagan, Michael R. Stratton, P. Andrew Futreal, Peter J. Campbell Highlights 2%–3% cancers show 10–100 s of rearrangements localized to specific genomic regions Genomic features imply chromosome breaks occur in one-off crisis (“chromothripsis”) Found across all tumor types, especially common in bone cancers (up to 25%) Can generate several genomic lesions with potential to drive cancer in single event Summary Cancer is driven by somatically acquired point mutations and chromosomal rearrangements, conventionally thought to accumulate gradually over time. Using next-generation sequencing, we characterize a phenomenon, which we term chromothripsis, whereby tens to hundreds of genomic rearrangements occur in a one-off cellular crisis. Rearrangements involving one or a few chromosomes crisscross back and forth across involved regions, generating frequent oscillations between two copy number states. These genomic hallmarks are highly improbable if rearrangements accumulate over time and instead imply that nearly all occur during a single cellular catastrophe. The stamp of chromothripsis can be seen in at least 2%–3% of all cancers, across many subtypes, and is present in ～25% of bone cancers. We find that one, or indeed more than one, cancer-causing lesion can emerge out of the genomic crisis. This phenomenon has important implications for the origins of genomic remodeling and temporal emergence of cancer. |
購買進(jìn)口儀器、試劑和耗材——就在始于2001年的畢特博生物
effectnews.cn |
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