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癌可能是我们最古老的进化祖先 [复制链接]

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楼主
发表于 2011-4-17 16:50 |只看该作者 |倒序浏览 |打印
【摘译】原文:Cancerous tumors might be our oldest evolutionary ancestors    http://www.abovetopsecret.com/forum/thread675117/pg19 S# Z& S4 z% k5 @: B, p: J
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癌症是医学科学史上所面对最困难的敌人之一,但一个有争议的新想法可能为我们打通胜利的道路。一个科学家小组证据显示,癌症可能是一种将我们退化到最遥远的动物的祖先机制。9 p+ p6 T6 R" v

0 g$ Y( d- f8 a9 A 天体生物学家澳大利亚国立大学Charles Lineweaver和亚利桑那州的Paul Davies 提出,癌细胞是一个所谓的“活化石”,来自距今约600万年前一个关键的进化接缝的最后残余。 癌症可以追溯到多细胞动物的开始,此前需要进行一个进化的创新,即每当细胞想要开始与其他有机体协调时要停止复制。
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1 F. K3 T$ ~5 I4 B) @" ^. x癌症发生于这些非常古老的细胞复制控制故障,导致失控的细胞复制。但这里Lineweaver和Davies有了进一步的想法——他们认为癌症实际上是我们的最早的动物祖先。 他们指出,这些生物最早拥有了一些对细胞复制的控制措施,但他们缺乏对细胞生长更精确的控制。 ! e, J# b  D, h, r$ M7 e) N

4 H  ^* x* R0 Q$ [  M0 q3 c/ A这一假说,他们认为,比那些认为所有癌细胞都是特立独行的观点能更好地解释肿瘤的行为。他们指出血管生成,癌细胞建设血管网络将养料运入肿瘤,这表明细胞之间的合作。事实上,癌细胞可以转移到其他组织的地区,如果所有的细胞都是特立独行的癌转移行为是很难解释的。
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有时为了击败你的敌人,你必须成为你自己的敌人,用这种方式看待癌症正是我们在做的。 4 X1 @# g* L# \# [4 t$ r" N3 }
显然,辐射、或遗传因素等种种因素可以导致癌症,因此绝不会有“痊愈”。然而,这可能意味着将有一个标准的过程最终被用于清除它。 一旦我们掌握了她的代码,我们就可以开始攻击它。
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Tumours could be the ancestors of animals
2 A* E/ K/ o5 a4 R0 K11 March 2011 by Colin Barras  & G/ s, b2 [( C0 y
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CANCER remains a formidable foe even 40 years after Richard Nixon officially declared war on it. A new and controversial hypothesis now offers hope that the war can ultimately be won. It suggests tumours have a limited ability to evade modern therapies - a consequence of the idea that cancer is our most distant animal ancestor, a "living fossil" from over 600 million years ago.
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Some cancers evolve resistance to a treatment within a few years. One possible explanation for this is that the cells within a tumour act independently, competing with one another via natural selection to evolve therapy-dodging innovations.
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: I  m2 i4 Y2 |+ Z6 G) vAstrobiologists Charles Lineweaver at the Australian National University in Canberra and Paul Davies at Arizona State University in Tempe have an alternative explanation. They say that evidence of basic cellular cooperation within tumours suggests cancers are a throwback from the origin of the animal kingdom - and that any ability to resist modern drugs relies on an ancient and ultimately limited array of survival tactics." k2 x; F2 s6 M. n2 ?3 U

7 R0 Q/ A5 y4 w$ pTheir hypothesis builds on an old idea that suggests a link between cancer and the origin of multicellular animals, sometime before 600 million years ago. For billions of years before that point, the animals' single-celled ancestors replicated with reckless abandon. Once organisms contained multiple cells, however, replication had to become more restrained, to avoid adverse effects on the organism.
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Cancer is thought to be triggered by a malfunction of the genes that try to hold back this uncontrolled replication. But Lineweaver and Davies go further: cancer is not simply linked to the evolution of animals - it was the earliest animals. They believe these organisms had cracked the problem of runaway replication but they still lacked total control over cell growth and proliferation.6 r1 {/ a- }. t

) q3 n: o3 d7 z. H9 _0 w% }( Q% iThe hypothesis helps to explain some of the more unusual features of tumours, says Lineweaver. Some cancer cells build a network of blood vessels, a process known as angiogenesis, to bring nutrients into the tumour - evidence of tumour-wide cooperation. Other cells gain the ability to spread to other tissues, or metastasise, which is difficult to explain if all cancer cells act independently.
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: {, S0 X0 U/ l& Y- B; [) c  t. Z) }Lineweaver and Davies think the genetic toolkit at work in these first animals is buried within all of us. The genes that came later might have tinkered with it, but whenever those later additions malfunction the ancient genes can revert to their initial function.5 t5 B+ r( C+ O! y2 {

5 ]$ D$ O$ z( P" _" o1 r  AConsequently, a tumour is not a collection of independently evolving cells, like bacteria, with almost infinite potential to evolve resistance to therapy. It is a group of largely cooperating cells relying on a finite collection of survival strategies that were locked in place over half a billion years ago (Physical Biology, DOI: 10.1088/1478-3975/8/1/015001).# V: X. P. H# e+ a" N! h- F% ?/ h

# I! ]! a! v" y& vReactions to Lineweaver and Davies's idea vary from cautious enthusiasm to outright scepticism. Carlo Maley at the University of California in San Francisco, who studies the evolutionary processes at work in cancer, is receptive: "They make a bunch of interesting predictions," he says.! L% |% B2 a) r' s7 E
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Others are more guarded. It is an "imaginative metaphor", says Mansi Srivastava at the Whitehead Institute for Biomedical Research in Cambridge, Massachusetts, who studies the evolution of genes including those involved with cancer. However, she thinks the idea of cancer as a living fossil from the dawn of animal life is a step too far. "There is no evidence to believe that the ability to develop blood vessels is an ancient feature of animals."
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Lineweaver disagrees: "Fully developed angiogenesis had to have evolved from proto-angiogenesis," he says. "I think it's clear that some form of proto-angiogenesis was very important for the earliest animals."7 t3 J* N& H5 [) w! Q+ y

2 y, d" {; i8 q5 n7 h% lGenetic profiling may soon help to test the hypothesis, says Lineweaver. The ways a particular cancer responds to treatment in different people should correlate with each other, he says, because they should share strategies for dealing with toxins that were developed in the earliest animals.
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, G2 |: y' G$ D3 n' I4 E2 {Even if cancer does have a limited ability to resist treatment, though, Maley has a reality check. If the war on cancer has taught us anything, it is that battling even a predictable cancer will remain "plenty hard" in the short term.
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发表于 2011-4-17 17:12 |只看该作者
问一个问题:天体生物学是研究什么的?
+ b4 A7 u; M; }8 I/ \* l$ s: g有一个疑问:这篇paper是发在什么上的?
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藤椅
发表于 2011-4-17 18:10 |只看该作者
好科幻……

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板凳
发表于 2011-4-17 19:07 |只看该作者
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marrowstem 发表于 2011-4-17 17:12
; V4 p- M& F' x/ M8 T4 L& a问一个问题:天体生物学是研究什么的?' R+ T5 A: u8 g6 y8 t$ C
有一个疑问:这篇paper是发在什么上的?

7 h; J9 a% \0 b; U1 M该条消息相关论文参见Phys. Biol. 8 (2011) 0150018 R! G1 M5 R4 g" `2 z: a
http://www.stemcell8.cn/forum-re ... 073-pid-334478.html  s# W7 R1 ~( `9 M( ~
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天体生物学(astrobiology ):指研究天体上存在生物的条件及探测天体上是否有生物存在的学科。地外生物学(exobiology),又称外空生物学(xenobiology),在天文学中,是研究太阳系除地球外其他行星及其卫星上和其他恒星的行星系上可能存在生命现象的理论,以及探讨探测方法和手段的交叉学科。5 U; L- G# S* @3 b6 _+ \8 d
天体生物学综合天文学、生物学与地质学几方面。其研究焦点在探讨生命的起源、散布和演进。英文中的“astrobiology”来自希腊语的αστρον(astron= 星体),βιος(bios= 生命),以及 λογος(logos= 词/科学)。
( }0 L4 G( o  B' Y# ~1 z参见百度百科:http://baike.baidu.com/view/1062748.htm#sub10627489 C# w  x. |. p: W1 D
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发表于 2011-4-17 19:31 |只看该作者
天体生物学(astrobiology ):研究的内容是不是也包括寻找外星人在内。+ c. t  y/ U- @7 {9 w$ |# Q+ ~6 P
外星生物是不是也由细胞这个基本单位组成的,我想还是一个问题?
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地板
发表于 2011-4-17 20:00 |只看该作者
marrowstem 发表于 2011-4-17 19:31 0 N' u5 e5 R7 P* P
天体生物学(astrobiology ):研究的内容是不是也包括寻找外星人在内。
' n+ a" G* q& I9 j3 D) [9 K外星生物是不是也由细胞这个基本单 ...

* u/ E; Q" V) Y" ^你对天体生物学家的结论表示怀疑,那么,德国进化生物学家利用种群基因追踪(Phylostratigraphic tracking) 得到了相似的结论:提示癌基因的远古起源与后生动物的多细胞化相关:
0 E* ?+ b* ?. h2 d癌基因的远古起源:与后生动物的多细胞化相关  http://www.stemcell8.cn/thread-38158-1-1.html
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MBE:所有遗传疾病的基因有同一“祖先”http://www.stemcell8.cn/thread-38156-1-1.html
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发表于 2011-4-17 20:19 |只看该作者
本帖最后由 sunsong7 于 2011-4-17 20:21 编辑 ; d( a- D* g0 {0 l
marrowstem 发表于 2011-4-17 19:31
( e& L; D, L  x天体生物学(astrobiology ):研究的内容是不是也包括寻找外星人在内。6 a& `: o- U5 [8 o# t
外星生物是不是也由细胞这个基本单 ...

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# f  @" F( w/ x% L' G将殊途同归的两篇文章一起贴在这里,他们上个月他们几乎是同时发表文章揭示出癌的起源与后生动物(metazoa )相关。
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1 B7 m) j- K# }% l, _3 O" J澳大利亚天体生物学家文章:癌肿瘤是后生动物一代:远古祖先的攻丝基因) m) ]/ b- c' n1 r/ |
Cancer tumors as Metazoa 1.0: tapping genes of ancient ancestors7 r' A, s6 e: s# ?& m1 e
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PCWDavies1 and C H Lineweaver2! n2 B; a( ]' @% P/ Q3 J
Phys. Biol. 8 (2011) 015001
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, r, u  l+ T% d1 oThe genes of cellular cooperation that evolved with multicellularity about a billion years ago are the same genes that malfunction to cause cancer. We hypothesize that cancer is an atavistic  condition that occurs when genetic or epigenetic malfunction unlocks an ancient ‘toolkit’ of pre-existing adaptations, re-establishing the dominance of an earlier layer of genes that controlled loose-knit colonies of only partially differentiated cells, similar to tumors. The existence of such a toolkit implies that the progress of the neoplasm in the host organism differs distinctively from normal Darwinian evolution. Comparative genomics and the phylogeny of basal metazoans, opisthokonta and basal multicellular eukaryotes should help identify the relevant genes and yield the order in which they evolved. This order will be a rough guide to the reverse order in which cancer develops, as mutations disrupt the genes of cellular cooperation. Our proposal is consistent with current understanding of cancer and explains the paradoxical rapidity with which cancer acquires a suite of mutually-supportive complex abilities. Finally we make several predictions and suggest ways to test this model.
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德国进化生物学家文章:癌基因的远古起源:与后生动物的多细胞化相关  7 E/ _6 c8 b0 Y" X2 r+ _3 b
Phylostratigraphic tracking of cancer genes suggests a link to the emergence of multicellularity in metazoa  4 R5 }. z! ~$ U# t/ C
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Tomislav Domazet-Lošo1,2  and Diethard Tautz18 ?7 E( T% o1 s& }. h8 N
BMC Biology 2010,
: r3 v3 p; N: D: kBackground
7 H' i& z: y7 T/ c: D1 YPhylostratigraphy is a method used to correlate the evolutionary origin of founder genes (that is, functional founder protein domains) of gene families with particular macroevolutionary transitions. It is based on a model of genome evolution that suggests that the origin of complex phenotypic innovations will be accompanied by the emergence of such founder genes, the descendants of which can still be traced in extant organisms. The origin of multicellularity can be considered to be a macroevolutionary transition, for which new gene functions would have been required. Cancer should be tightly connected to multicellular life since it can be viewed as a malfunction of interaction between cells in a multicellular organism. A phylostratigraphic tracking of the origin of cancer genes should, therefore, also provide insights into the origin of multicellularity.
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Results
7 M; r7 ~! c3 C! oWe find two strong peaks of the emergence of cancer related protein domains, one at the time of the origin of the first cell and the other around the time of the evolution of the multicellular metazoan organisms. These peaks correlate with two major classes of cancer genes, the 'caretakers', which are involved in general functions that support genome stability and the 'gatekeepers', which are involved in cellular signalling and growth processes. Interestingly, this phylogenetic succession mirrors the ontogenetic succession of tumour progression, where mutations in caretakers are thought to precede mutations in gatekeepers.1 r+ y# f3 e0 P

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% }3 b% n) S7 X7 t+ L$ b8 u% G" ^# LA link between multicellularity and formation of cancer has often been predicted. However, this has not so far been explicitly tested. Although we find that a significant number of protein domains involved in cancer predate the origin of multicellularity, the second peak of cancer protein domain emergence is, indeed, connected to a phylogenetic level where multicellular animals have emerged. The fact that we can find a strong and consistent signal for this second peak in the phylostratigraphic map implies that a complex multi-level selection process has driven the transition to multicellularity.( l6 J' H! y# A+ j
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发表于 2011-4-19 13:05 |只看该作者
回复 marrowstem 的帖子6 L+ C7 M( D) }2 [% _4 p; }

9 T! g4 `# u+ V$ u' K2 h( C% o# ?天体生物学不只研究外空生物,它还包括了对生命起源,生物体早期的进化,同时还涉及到生命体未来演变的方向,也包括探查生命的基础化学组成。譬如去年NASA声称发现“砷基生命(Arsenic-Based Life)”中砷元素取代了磷元素的作用,发表在《SCIENCE》A Bacterium That Can Grow by Using Arsenic Instead of Phosphorus  http://www.sciencemag.org/conten ... /01/science.1197258
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发表于 2011-4-19 13:14 |只看该作者
另外, 著名的寒武纪生命大爆发是1909年美国地质学家差尔斯·沃尔科特发现的,而云南“澄江动物群”是1984年我国地质古生物学家侯先光发现的。

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发表于 2011-4-19 13:38 |只看该作者
癌细胞的“自给播种”对肿瘤发展的决定性作用
; F2 U1 L, ]/ |8 f. F8 [4 d0 Z, _ 来源:生命经纬 | 2009-12-31 |
6 U7 s1 Z* l% o  J癌症的发展通常被认为是原始肿瘤的生长转移过程,在这个过程中癌细胞脱离原始的肿瘤并转移到其他的器官中。斯隆-凯特琳癌症中心的一项最新研究表明,流通的肿瘤细胞--癌细胞会脱离原始的肿瘤并散布到机体其他的区域,同样也能够再返回并在原始的地方生长,该过程科学家称之为“自给播种”( self-seeding)。
4 `5 a0 ]/ s5 K( x0 C这项研究结果发布在12月25日的《Cell》上,研究表明,自给播种能够增强肿瘤生长,这主要是通过释放能刺激血管再生,组织入侵和转移的信号进行调控的。
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这篇文章的第一作者Mi-Young Kim博士介绍说,该研究不仅仅为自给播种现象提供了证据,还揭示了这个过程的机制,同样阐明了自给播种在肿瘤发展过程中的可能角色。0 c& j  r9 N2 ~5 n
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在老鼠试验中,自给播种包含两种功能,即吸引肿瘤自身后代细胞的能力,使流通肿瘤细胞重新渗入肿瘤的能力,后者主要是为了应答吸引。研究人员识别了4个和这些功能执行有关的基因,其中基因IL-6和IL-8,能够吸引流动的肿瘤细胞群中最具侵略性的部分,基因FSCN1和MMP1,能调解流通肿瘤细胞的侵润。
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这项研究还发现,流通的乳癌细胞具有自给播种的能力,与乳腺癌细胞有着相似的基因表达模式,能够扩散到肺,骨骼和大脑中。另外的试验表明,自给播种能够发生在除了乳癌之外的其他许多不同类型的肿瘤中,比如结肠癌和黑素瘤。$ |( x+ ?/ E# [/ V: d3 t; ^; ]: v
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这项研究的负责人Joan Massagué博士介绍说,该研究结果为我们提供了开发新的靶向疗法的机会,或能干扰自给播种过程,减缓或预防肿瘤发展。
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