著名科学家提出癌症成因新解

中国教育装备采购网2011-08-02 16:37围观120次我要分享

  

著名科学家提出癌症成因新解

  中国教育装备采购网讯:据上海卡努生物科技有限公司消息,随着老龄化的加剧,癌症的发生率以及死亡率都急剧攀升,这使得癌症研究变得更加迫切。对于癌症生物学的研究让科学家们了解更多癌症的真相,比如说,多种遗传变异,多种表观遗传学变异等等,但是至今科学家们还并不清楚到底癌症如何形成的。

  在最近的《Cell Cycle》杂志上,来自加州大学伯克利分校的研究人员发表了题为“Is carcinogenesis a form of speciation?”的文章,提出癌症是新进化寄生物种,认为癌症的形成实际上就是一个新寄生物种的进化过程。

  这篇文章由加州大学伯克利分校Peter Duesberg博士领衔完成,这位著名的病毒学家是艾滋病研究领域备受争议的人物,数十年来,他一直质疑艾滋病的元凶是HIV病毒,并认为艾滋病可以不用药治愈的。

  在最新这篇文章中,Duesberg博士则提出了一个新的癌症成因观点——癌症是新进化寄生物种,其实这一观点说新也不新,研究人员之前就提出了癌症是进化作用的结果。这一观点代表了对癌症这一疾病的一项重要反思。进化生物学家朱利安·S·赫胥黎在1956年率先提出自生的肿瘤是一种新物种。

  但主流观点认为癌症是癌基因和抗癌基因突变的结果。Duesberg博士自己在1970年曾首先鉴别并克隆出第一个癌基因,但是他现在认为非整倍体(异常数目的染色体)是癌症的真正元凶。

  Duesberg博士认为被称作非整倍体的染色体突变是癌症的起因,这一突变破坏了染色体组型的稳定性。一些紊乱的染色体能够分裂,埋下了癌症的种子。结果形成一种不同于我们自己的新染色体组型。

  他提出就像寄生物一样,癌肿依赖宿主获得营养。这就是为什么阻断癌肿的治疗方法能够非常有效。由于这种寄生物与宿主的关系,癌肿能够自己决定生长方式和生长位置。癌细胞的生存不依赖其他细胞,而且它们形成与其人类宿主不同的染色体组型。因此,它们是新物种。

  Duesberg博士希望能这一理论将引导新的癌症诊断和治疗方法。染色体化验有可能很早就挑出非整倍体,比如在受损染色体有机会分裂之前。此外,新的治疗方法有可能瞄准染色体紊乱,而非清除或者关闭基因。

  不过由于Duesberg博士的主流观点,他自从怀疑HIV与艾滋病之间的关系后,再也没有得到政府基金的资助。他认为“同行评议导致基金不会资助那些挑战他们利益的申请”。

  (生物通:万纹)

  原文摘要:

  Cell Cycle. 2011 Jul 1;10(13).

  Is carcinogenesis a form of speciation?

  Duesberg P, Mandrioli D, McCormack A, Nicholson JM.

  SourceUniversity of California at Berkeley; Berkeley, CA USA.

  Abstract

  Since cancers have individual clonal karyotypes, are immortal and evolve from normal cells treated by carcinogens only after exceedingly long latencies of many months to decades-we deduce that carcinogenesis may be a form of speciation. This theory proposes that carcinogens initiate carcinogenesis by causing aneuploidy, i.e., losses or gains of chromosomes. Aneuploidy destabilizes the karyotype, because it unbalances thousands of collaborating genes including those that synthesize, segregate and repair chromosomes. Driven by this inherent instability aneuploid cells evolve ever-more random karyotypes automatically. Most of these perish, but a very small minority acquires reproductive autonomy-the primary characteristic of cancer cells and species. Selection for autonomy stabilizes new cancer species against the inherent instability of aneuploidy within specific margins of variation. The speciation theory explains five common characteristics of cancers: (1) species-specific autonomy; (2) karyotypic and phenotypic individuality; (3) flexibility by karyotypic variations within stable margins of autonomy; (4) immortality by replacing defective karyotypes from constitutive pools of competent variants or subspecies generated by this flexibility; and (5) long neoplastic latencies by the low probability that random karyotypic alterations generate new autonomous species. Moreover, the theory explains phylogenetic relations between cancers of the same tissue, because carcinogenesis is restricted by tissue-specific transcriptomes. The theory also solves paradoxes of other cancer theories. For example, "aneuploidy" of cancers is now said to be a "paradox" or "cancers fatal flaw," because aneuploidy impairs normal growth and development. But if the "aneuploidies" of cancers are in effect the karyotypes of new species, this paradox is solved.

来源:上海卡努生物科技有限公司作者:上海卡努生物科技有限公司

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