健康細(xì)胞轉(zhuǎn)變?yōu)榘┘?xì)胞的示意圖。
實(shí)證研究進(jìn)一步支持一種假設(shè)：散發(fā)性癌癥(sporadic form of cancer)是一種與年齡有關(guān)的代謝疾病,。該疾病特征在于(1)代謝失調(diào)(metabolic dysregulation),，同時(shí)線粒體DNA產(chǎn)生隨機(jī)性異常,；(2)代謝變化：補(bǔ)償性上調(diào)糖酵解代謝來(lái)彌補(bǔ)線粒體缺陷造成的氧化磷酸化作用下調(diào)，這樣癌細(xì)胞主要依靠糖酵解來(lái)獲取能量,。在這項(xiàng)研究中,，研究人員利用量子代謝理論(theory of quantum metabolism)和自然選擇法則(principles of natural selection)來(lái)給出一種定量分析癌癥起源和增殖的概念框架。
量子代謝理論用來(lái)描述量子過(guò)程，如量子糾纏,，如何影響細(xì)胞代謝,。這種理論給科學(xué)家們提供一種的新方法來(lái)解釋導(dǎo)致健康細(xì)胞轉(zhuǎn)變?yōu)榘┘?xì)胞的代謝變化。
這種轉(zhuǎn)變讓癌細(xì)胞在爭(zhēng)奪空間和營(yíng)養(yǎng)物過(guò)程中比健康細(xì)胞更有競(jìng)爭(zhēng)優(yōu)勢(shì),，從而導(dǎo)致癌癥產(chǎn)生和擴(kuò)散,。
研究人員聲稱，理解這種轉(zhuǎn)變的量子代謝基礎(chǔ)可能潛在地導(dǎo)致科學(xué)家們開(kāi)發(fā)出新的治療方法來(lái)阻止癌癥生長(zhǎng),。相關(guān)研究結(jié)果于2012年3月19日發(fā)表在AIP Advances期刊上,。(生物谷：towersimper編譯)
doi:10.1063/1.3697850
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PMID:
Implications of quantum metabolism and natural selection for the origin of cancer cells and tumor progression
Paul Davies, Lloyd A. Demetrius, and Jack A. Tuszynski
Empirical studies give increased support for the hypothesis that the sporadic form of cancer is an age-related metabolic disease characterized by: (a) metabolic dysregulation with random abnormalities in mitochondrial DNA, and (b) metabolic alteration – the compensatory upregulation of glycolysis to offset mitochondrial impairments. This paper appeals to the theory of Quantum Metabolism and the principles of natural selection to formulate a conceptual framework for a quantitative analysis of the origin and proliferation of the disease. Quantum Metabolism, an analytical theory of energy transduction in cells inspired by the methodology of the quantum theory of solids, elucidates the molecular basis for differences in metabolic rate between normal cells, utilizing predominantly oxidative phosphorylation, and cancer cells utilizing predominantly glycolysis. The principles of natural selection account for the outcome of competition between the two classes of cells. Quantum Metabolism and the principles of natural selection give an ontogenic and evolutionary rationale for cancer proliferation and furnish a framework for effective therapeutic strategies to impede the spread of the disease.
