癌可能是我们最古老的进化祖先

sunsong7

【摘译】原文：Cancerous tumors might be our oldest evolutionary ancestors    http://www.abovetopsecret.com/forum/thread675117/pg10 m# Z8 x# r1 k  W
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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。& ]% Y" ]' W/ i7 s, [' Q/ |

' b! J$ d( b7 f, P, H! Y% s 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。 . F; [: l# ?. n% x) ]8 o7 b# t, ~
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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。 + H  l; l6 z  w

4 h& \% g4 u! 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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4 B" l7 j$ {4 B2 Y6 a2 M% _8 Y. s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。 9 F: m! V# d# o3 X7 b
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。 1 L- P8 }/ B7 J, o. j: b/ ]7 u

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Tumours could be the ancestors of animals
+ C% m, ^6 X4 l$ H/ o$ i11 March 2011 by Colin Barras  
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( G7 @! g3 }& jCANCER 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.9 Z1 G1 `7 F7 y1 P" v
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Astrobiologists 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.
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; c6 ^* t+ o) d) E) I( ]Their 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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; q/ y  M& K, }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.% ^; ]! \+ a( v  i- b
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The 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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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.
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" s2 a6 L: A; e9 f0 i) WConsequently, 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)." l2 R6 E  q& d, G

) z( P# y1 N: f! k; |" m( zReactions 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.0 Y' T7 C. Y9 p1 ~7 |, ]

* Z( X8 C# u2 _7 p. t  J' B4 [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."  t5 ^8 H* r$ R* a- n5 K$ S

% K& e. Z% ^) K* U' GLineweaver 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."
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) e7 t: `, ?* p  P# jGenetic 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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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.' r; o* v( B5 w5 z

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sunsong7

* g2 ~9 L1 Z& h( n' wVolume 584, Issue 17, Pages 3741-3751 (10 September 2010)
5 r0 t. ^/ p8 A: X9 g6 _( u8 W2 jTelomere biology in Metazoa (后生动物端粒生物学)
" m# V7 n/ K* C) x5 T4 pEdited by Wilhelm Just3 N/ m5 H. e# f2 i5 H2 k
Nuno M.V. Gomes, Jerry W. Shay, Woodring E. Wright: j2 e: X& j9 C  d" T8 Z, F
Received 2 July 2010; received in revised form 19 July 2010; accepted 20 July 2010. published online 23 July 2010.+ X; B1 i! J  ?' V# v. U0 p# C
Abstract
! }( P; Y! t4 XIn this review we present critical overview of some of the available literature on the fundamental biology of telomeres and telomerase in Metazoan. With the exception of Nematodes and Arthropods, the (TTAGGG)n sequence is conserved in most Metazoa. Available data show that telomerase-based end maintenance is a very ancient mechanism in unicellular and multicellular organisms. In invertebrates, fish, amphibian, and reptiles persistent telomerase activity in somatic tissues might allow the maintenance of the extensive regenerative potentials of these species. Telomerase repression among birds and many mammals suggests that, as humans, they may use replicative aging as a tumor protection mechanism.
$ R5 I* z( z. s/ Dhttp://www.febsletters.org/article/S0014-5793(10)00589-2/abstract
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癌干细胞标记驱动正常细胞转录——HAT复合物存在于后生动物
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1 I' _! L5 E4 `3 f  @% G* G论文作者：Steven B. McMahon等 期刊：《分子细胞》
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1月18日的《分子细胞》（Molecular Cell）上刊载了2项独立的研究，将近来发现的一种多面的转录复合物的功能与控制正常细胞及癌干细胞基因表达联系起来。这些研究使我们了解了一种在进化上保守的、与转录调节复合物有联系的新型亚单位，并披露了一种以前没有被描述过的正常细胞内核受体及肿瘤细胞内 MYC 肿瘤蛋白全部活性所需的染色质功能。1 Z2 K* m: m. E) ~

( Q6 F6 c, L8 y1 Y$ K转录过程的启动需要对许多不同调节因子进行精密复杂的协调。共激活因子是有多种亚单位的复合物，它们可以通过与RNA聚合酶及普通转录因子相互作用而直接易化转录过程的启动，或以间接的方式来影响染色质。例如，组蛋白乙酰转移酶（HAT）复合物被认为是通过修饰与染色质相连的被称作组蛋白的蛋白质来激活基因表达的过程，而组蛋白的功能是被当作让DNA缠绕的线轴。, T0 h' U: m; a2 _( O

9 P" R/ p  ^0 u( [% t! }  V存在于酵母菌中的SAGA复合物及其存在于后生动物中的同源物TFTC/STAGA（又被称为hSAGA）皆为含有HAT的复合物，其功能是通过组蛋白的乙酰化作用来易化普通转录因子与DNA的接触。尽管hSAGA被认为是被充分研究过的酵母菌SAGA复合物的同源物，但人们对其亚单位的组成及功能并不十分了解。法国斯特拉斯堡遗传学与分子及细胞生物学研究所的Dr. Didier Devys及其同僚确认了3个新型的亚单位：ATXN7L3, USP22 和 ENY2。 这些亚单位与从前描述过的存在于酵母菌SAGA复合物中的亚单位为同源物。
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* p+ b( H# G+ c3 @- f7 |研究人员证明，这些新确认的亚单位通过协同作用来去除单残基泛素化组蛋白H2B中的泛素部分，该作用与先前描述过的在酵母菌中的过程类似，但其还可去除单残基泛素化组蛋白H2A中的泛素部分。后一种修饰方式不存在于酵母菌中，但它在哺乳动物中却比单残基泛素H2B的存在更为普遍。重要的是，果蝇TFTC/STAGA复合物的去泛素化模块乃是位置效应花斑的增强子，它能对抗异染色质沉默。而果蝇及人类的去泛素化模块为雄激素受体所致的完全的转录激活所必需。这一发现具有临床意义，因为，在前列腺癌中，雄激素受体的活性常常不受调节。
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Dr. Devys说：“在hSAGA复合物中，HAT与去泛素化活性两者间的关联提出了一种诱人的机制，即这种在特定组蛋白标记之间的所谓的‘对话’是在同一个调节复合物中进行协调的。必须对该机制开展进一步的研究来检测这些活性与其它染色质修饰复合物之间的关联原委，这样才能了解这些顺序发生的事件是如何参与染色质重构及基因激活的过程。”
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在一项同时并行的研究中，由费城托马斯•杰斐逊大学的Dr. Steven B. McMahon领导的第二个研究小组也确认了USP22 为hSAGA家族的一员。先前的研究已经确认了USP22 是一种有11个基因的癌干细胞标记的一部份，它能精确地将那些肿瘤最终会转移的病人与肿瘤保持局部化的病人区分开来。Dr. McMahon解释说：“与这种癌干细胞标记的其他基因不同，还没有人将USP22 与人类癌症进行直接的机制性关联”。McMahon的小组证明，由MYC肿瘤蛋白激活的标靶基因转录需要USP22，而USP22的耗损将危及MYC的功能，其中包括哺乳动物细胞转化过程将受到损害，及导致细胞周期的停滞。
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综上所述，这些结果披露了hSAGA组蛋白乙酰转移酶复合物同时也具有将组蛋白去泛素化的能力，因而大大增进了人们对转录调节过程的精微调节机制的理解。这些发现提供了人们关键性的新资讯，即在控制正常细胞基因表达时的染色质修饰的时机与顺序的重要性，帮助人们更好地了解癌干细胞标记与hSAGA 亚单位 USP22的生物化学功能，并确认其为一种可能的治疗标靶。（来源：EurekAlert!中文版）
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（《分子细胞》（Molecular Cell），Vol 29, 102-111，Xiao-Yong Zhang，Steven B. McMahon）
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（《分子细胞》（Molecular Cell），Vol 29, 92-101，Yue Zhao，Didier Devys）( W7 B3 S: y- S0 ~8 q
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原癌基因RAS的系统发育分析$ m: S- }, h) w) M& Z  B6 `
Analyses of the System Development of the Proto-oncogene" U7 A7 Z# j8 u
广东农工商职业技术学院学报  2009, 25(2)
5 n# S/ i& P, H3 c7 z+ D作者： 刘光华    何淼    刘永生    LIU Guang-hua    HE Miao    LIU Yong-sheng  
' ^6 T1 x7 Q& q; \9 t. l* K作者单位： 刘光华,LIU Guang-hua(广东农工商职业技术学院,热带作物研究所,广东,广州,510507)4 I6 ]  E6 s# `* W7 {! H

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摘要：原癌基因(proto-oncogene)是细胞的正常基因,其编码的蛋白质参与调节正常细胞的生长与分化,在控制细胞增殖的信号转导途径中起作用.一旦受到致癌因子的影响,其活性就会发生变化,引起细胞癌变.基于目前GenBank的数据,运用相关的生物信息分析工具和分析方法,可对Ras原癌基因的转录本序列进行比对、筛选.该文是在此基础上选用目前较常用的构建系统发育树方法,建出系统发育树.结果表明,构建出来的树有三个大分枝,在分类学上分别是真菌界(Fungi)、四足动物(Tetrapoda)、体腔动物(Coelomata).后两者又是处于后生动物,这样就可以初步确定Ras原8 \8 X" b/ A7 Y. p4 x
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sunsong7

来源 Nature 2008-10-30 9:06:55 . p+ n+ v% e# D9 p

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Nature：MicroRNAs是后生动物的一个早期特征

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  u- ]- O# V' F. s( y* U$ {微RNA（MicroRNAs）是1993年在线虫中发现的抑制性小RNA分子，广泛分布在复杂动物中。人们普遍假设，它们是当动物形成双侧对称性（即动物身体结构复杂到有前部和后部以及上部和下部）时作为微调基因表达的一种方式而出现的。: o1 N; \: c1 a1 x. j
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新的研究工作（这项工作是基于对三种“基底后生动物门”的代表动物（一种扁盘动物、一种海绵和一种海葵）及一种单细胞“领鞭毛虫”的总RNA内容所做测序进行的）表明，微RNA出现的时间要比人们以前所想的长得多。调控性微RNA通道似乎是在后生动物演化过程中非常早的时候出现的——是当多细胞生命方式出现时出现的，尽管这种机制后来在一些生命分支中丢失了。（生物谷Bioon.com）
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$ t- h" l# Q: f. r% H2 {  r生物谷推荐原始出处：% l! Y  b0 b7 N8 r6 j) `
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Nature 455, 1193-1197 (30 October 2008) | doi:10.1038/nature07415+ d+ X/ A# e& Z  i' A+ N3 j

' F' T& n' s) s/ r5 Y( c, L4 b5 ?Early origins and evolution of microRNAs and Piwi-interacting RNAs in animals' r/ t, ], }5 a

; r% V7 D0 f, y% g% Z  oAndrew Grimson1,2, Mansi Srivastava4, Bryony Fahey3, Ben J. Woodcroft3, H. Rosaria Chiang1,2, Nicole King4, Bernard M. Degnan3, Daniel S. Rokhsar4,5 & David P. Bartel1,2- q7 X9 w0 u6 `  k

5 J2 K4 r; ?% T# x1 Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA; [& R! B5 I5 V8 R1 f. _& P3 B
2 Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
/ X% Y8 D1 {8 d. ?3 School of Integrative Biology, University of Queensland, Brisbane 4072, Australia
. d5 V( U6 m& v2 \4 Department of Molecular and Cell Biology and Center for Integrative Genomics, University of California at Berkeley, Berkeley, California 94720, USA* X6 U" E) f3 n# x1 a
5 Department of Energy, Joint Genome Institute, Walnut Creek, California 94598, USA: ?; i7 J5 R: V
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In bilaterian animals, such as humans, flies and worms, hundreds of microRNAs (miRNAs), some conserved throughout bilaterian evolution, collectively regulate a substantial fraction of the transcriptome. In addition to miRNAs, other bilaterian small RNAs, known as Piwi-interacting RNAs (piRNAs), protect the genome from transposons. Here we identify small RNAs from animal phyla that diverged before the emergence of the Bilateria. The cnidarian Nematostella vectensis (starlet sea anemone), a close relative to the Bilateria, possesses an extensive repertoire of miRNA genes, two classes of piRNAs and a complement of proteins specific to small-RNA biology comparable to that of humans. The poriferan Amphimedon queenslandica (sponge), one of the simplest animals and a distant relative of the Bilateria, also possesses miRNAs, both classes of piRNAs and a full complement of the small-RNA machinery. Animal miRNA evolution seems to have been relatively dynamic, with precursor sizes and mature miRNA sequences differing greatly between poriferans, cnidarians and bilaterians. Nonetheless, miRNAs and piRNAs have been available as classes of riboregulators to shape gene expression throughout the evolution and radiation of animal phyla.
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癌细胞的“自给播种”对肿瘤发展的决定性作用
- H; u0 _6 f: t0 Z( |% V 来源：生命经纬 | 2009-12-31 | # f" f  l) d5 P- |4 h* X1 `
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）。
) c: t$ z# P6 V8 c0 p* h2 u; u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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; V. u, W: B6 m& {. g/ l& d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。" J+ e5 Z' W0 d5 [* c5 C
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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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. I7 s6 `' S' d* N6 X5 R& \& M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。% G3 Y% A3 w; H8 z9 U% H

7 {) q0 b: l1 N# I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。6 m. A; _  k* R' d; _

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sunsong7

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。

sunsong7

回复 marrowstem 的帖子& N& ^" o, Q6 |3 j

; C$ @: u+ [: Z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

sunsong7

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marrowstem 发表于 2011-4-17 19:31
- U* w" H) y$ n4 k4 [* 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。
/ q+ Z/ M" B  }8 L( m外星生物是不是也由细胞这个基本单 ...

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% D+ p# C( `2 a5 z3 z5 O- g7 Q5 n; b6 F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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4 w" ^5 H8 z1 l/ Y$ o6 h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
8 _6 W0 {: ^2 p$ l" c' nCancer tumors as Metazoa 1.0: tapping genes of ancient ancestors' B6 P  c3 k# u) z

! x: v* T# {/ _: z4 UPCWDavies1 and C H Lineweaver2
; v# H$ x9 T* @Phys. Biol. 8 (2011) 015001
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1 B. Y. t; n+ A9 FAbstract; T1 b0 |0 m: I; A) a3 j
The 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  1 z$ N3 k9 Y& b' _2 q% c6 Y& Q7 x$ I
Phylostratigraphic tracking of cancer genes suggests a link to the emergence of multicellularity in metazoa  " a" \7 }7 O  {7 X

, F+ Z/ f! \+ NTomislav Domazet-Lošo1,2  and Diethard Tautz1, K" _/ V) U! @* R) D) j* O
BMC Biology 2010,
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- m" t) y& D2 f$ X* h1 M( Y* LPhylostratigraphy 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.6 j3 V! z; x4 T* i+ v3 F5 A2 Y
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Results1 i" h7 L1 G. X2 L% _7 a
We 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.
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% g1 I- E) R" P, b1 y  ~! T' F, gConclusions
& o& l& _+ p$ Z0 mA 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.; |  c( {. I  x- r# N

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sunsong7

marrowstem 发表于 2011-4-17 19:31 : m$ G6 y4 q+ c, G2 m8 Q8 k
天体生物学（astrobiology ）：研究的内容是不是也包括寻找外星人在内。8 R( }# ~4 E3 V2 y; q9 Z
外星生物是不是也由细胞这个基本单 ...

. t6 q1 [* {+ p/ G" i3 k! H% x% v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:
3 ~- [' ~" ]+ v& K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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