隨著老齡化的加劇,，癌癥的發(fā)生率以及死亡率都急劇攀升,，這使得癌癥研究變得更加迫切,。對于癌癥生物學(xué)的研究讓科學(xué)家們了解更多癌癥的真相,，比如說,，多種遺傳變異,，多種表觀遺傳學(xué)變異等等,，但是至今科學(xué)家們還并不清楚癌癥到底是如何形成的。
在最近的《細(xì)胞周期》（Cell Cycle）雜志上,，來自加州大學(xué)伯克利分校的研究人員發(fā)表了題為“Is carcinogenesis a form of speciation?”的文章,，提出癌癥是新進(jìn)化寄生物種，認(rèn)為癌癥的形成實(shí)際上就是一個新寄生物種的進(jìn)化過程,。
這篇文章由加州大學(xué)伯克利分校Peter Duesberg博士領(lǐng)銜完成,，這位著名的病毒學(xué)家是艾滋病研究領(lǐng)域備受爭議的人物，數(shù)十年來,，他一直質(zhì)疑艾滋病的元兇是HIV病毒,，并認(rèn)為艾滋病可以不用藥物治愈。
在這篇文章中,，Duesberg博士則提出了一個新的癌癥成因觀點(diǎn)——癌癥是新進(jìn)化寄生物種,，其實(shí)這一觀點(diǎn)說新也不新，研究人員之前就提出了癌癥是進(jìn)化作用的結(jié)果,。這一觀點(diǎn)代表了對癌癥這一疾病的一項(xiàng)重要反思,。進(jìn)化生物學(xué)家朱利安·S·赫胥黎在1956年率先提出自生的腫瘤是一種新物種。
但主流觀點(diǎn)認(rèn)為癌癥是癌基因和抗癌基因突變的結(jié)果,。Duesberg博士自己在1970年曾首先鑒別并克隆出第一個癌基因,，但是他現(xiàn)在認(rèn)為非整倍體（異常數(shù)目的染色體）是癌癥的真正元兇。
Duesberg博士認(rèn)為被稱作非整倍體的染色體突變是癌癥的起因,，這一突變破壞了染色體組型的穩(wěn)定性,。一些紊亂的染色體能夠分裂,，埋下了癌癥的種子。結(jié)果形成一種不同于我們自己的新染色體組型,。
他提出就像寄生物一樣,，癌腫依賴宿主獲得營養(yǎng)。這就是為什么阻斷癌腫的治療方法能夠非常有效,。由于這種寄生物與宿主的關(guān)系,，癌腫能夠自己決定生長方式和生長位置。癌細(xì)胞的生存不依賴其他細(xì)胞,，而且它們形成與其人類宿主不同的染色體組型,。因此，它們是新物種,。
Duesberg博士希望能以這一理論引導(dǎo)新的癌癥診斷和治療方法,。染色體化驗(yàn)有可能很早就挑出非整倍體，比如在受損染色體有機(jī)會分裂之前,。此外,，新的治療方法有可能瞄準(zhǔn)染色體紊亂，而非清除或者關(guān)閉基因,。
不過由于Duesberg博士的主流觀點(diǎn),，他自從懷疑HIV與艾滋病之間的關(guān)系后，再也沒有得到政府基金的資助,。他認(rèn)為“同行評議導(dǎo)致基金不會資助那些挑戰(zhàn)他們利益的申請”,。（生物谷 Bioon.com）
doi:10.4161/cc.10.13.16352
PMC:
PMID:
Is carcinogenesis a form of speciation?
Peter Duesberg, Daniele Mandrioli, Amanda McCormack and Joshua M. Nicholson
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 “cancer’s 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.
