癌癥起源及應(yīng)對(duì)

1、Physicists model proposes evolutionary role for cancerStressed cells could become cancerous as a safe mode, pointing to oxygen and immunotherapy are the best ways to beat the disease.? Zeeya Merali02 October 2014Article toolsRights & PermissionsAn article by Scientific American.US National Cancer In

2、stituteCould cancer be our cells way of running in safe mode , like a damaged computer operating system trying to preserve itself, when faced with an external threat? That the conclusion reached by cosmologist Paul Davies at Arizona State University in Tempe and his colleagues, who have devised a co

3、ntroversial new theory for cancer origins, based on its evolutionary roots. If correct, their model suggests that a number of alternative therapies, including treatment with oxygen and infection with viral or bacterial agents, could be particularly effective.At first glance, Davies, who is trained i

4、n physics rather than biomedical science, seems an unlikely soldier in the war on cancer . But about seven years ago he was invited to set up a new institute at Arizona State one of 12 funded by the USNational Cancer Institute to bring together physical scientists and oncologists to find a new persp

5、ective on the disease.“We were asked to rethink cancer from thebottom up, Davies says.Davies teamed up with Charley Lineweaver, an astrobiologist at The AustralianNational University in Canberra, and Mark Vincent, an oncologist at the LondonHealth Sciences Center in Ontario. Together they have come

6、up with an atavisticmodel positing cancer is the reexpression of an ancient “ preprogrammed “ trait that 1 has been lying dormant. In a new paper, which appeared iBioEssaysin September, they argue that because cancer appears in many animals and plants, as well as humans, then it must have evolved hu

7、ndreds of millions of years ago when we shared a common single-celled ancestor.At that time, cells benefited from immortality, or the ability to proliferate unchecked, as cancer does. When complex multicellular organisms developed, however, “immortality was outsourced to the eggs and sperm, Davies s

8、ays, and somatic cells(those not involved in reproduction) no longer needed this function.The team s hypothesis is that when faced with an environmental threat to the health of a cell radiation, say, or a lifestyle factor cells can revert to a“ preprogrammedsafe mode ” . In so doing, the cells jetti

9、son higher functionality anditch their dormant ability to proliferate back on in a misguided attempt to survive.Can(fail-safe, “ Davies remarks. Once the subroutine is triggered, it implements its program ruthlessly. ”Speaking at a medical engineering conference held at Imperial College London, on 1

10、1 September, Davies outlined a set of therapies for cancer based on this atavistic model.Rather than simply attacking cancer s ability to reproduce, or“cancer s strencDavies terms it, the model exposes“cancer s Achilles heel. For instance, if thetheory is correct, then cancer evolved at a time when

11、Earth s environment was moreacidic and contained less oxygen. So the team predicts that treating patients with high levels of oxygen and reducing sugar in their diet, to lower acidity, will strain the cancer and cause tumors to shrink.The effects of oxygen level on cancer have been independently inv

12、estigated for many years and appear to support Davies2T sayseCostantino Balestra, a physiologistat Paul Henri Spaak School and the Free University of Brussels, both in Belgium. In unpublished work that has been submitted for peer review, for instance, Balestra and his colleagues have recently demons

13、trated that slightly elevated oxygen levels can begin to induce leukemia cell death without harming healthy cells.“It almost looks too easy, “ Balestra says. Our preliminary results seem to show that supplying a little extra oxygen for one or two hours a day, in combination with other traditional ca

14、ncer therapies, would benefit patients without any harsh side effects.Balestra emphasizes, however, that tlaiwork was not carried out to test Davies hypothesis and cannot be taken as proof that the atavistic model is correct.Davies and his colleagues also advocate immunotherapy specifically, selecti

15、vely infecting patients with bacterial or viral agents. Medical researchers are already investigating the promising effects of such an approach for artificially boosting patients immune systems to aid in their recovery. Immunotherapy has already performed well in treating melanomas, for instance, an

16、d its effects on other cancers are being studied. According to the atavistic model, however, in addition to invigorating the immune system, cancer cells should also be more vulnerable than healthy cells to being killed by infectious agents because they lose higher protective functionality when they

17、“reboot into safe mode, Davies says. Recent studies injecting clostridium spores in rats, dogs and a human patient also appear to support this interpretation, he says.Some scientists, such as David Gorski, a surgical oncologist at Wayne State University in Detroit, Michigan, remain skeptical.The ( p

18、redictions of atavismnothing that scientists haven t come to by other paths, he says.Davies and his colleagues have already begun a more direct test of their theory, in answer to such criticisms.“ The key to our theory is looking at the ages of the genesresponsible for cancer, Davies explains. The a

19、tavistic model claims that with the onset of cancer, cells revert to a more primitive mode and more recently evolved functions are switched off. The team therefore predicts that as cancer progresses, more recently evolved genes should lose function, whereas ancient genes become active.To check if th

20、is hypothesis is correct, Davies and his colleagues are currently cross-referencing data from thecancer genome atlaswhich identifies the genes that are involved in cancer, with various databases that classify the genes that we have in common with other species. The latter data set enabs biologists t

21、o trace back genesages. Any correlation that exists between the gene age and cancer will be a boost to the atavistic model. Combining the two data sets hasn t been done before, D says. “ But it s essentiaHminohgtaexercise that doesn t take much money and it s something we re working on now. ”Brendon

22、 Coventry, a surgical oncologist and immunotherapist at the University of Adelaide in Australia, sees value in physicists working with oncologists to piece together existing medica evidence to try to understand cancer s origins. “ Enormousamounts of money and the brightest minds in biological and me

23、dical science have failed to make a big impact in the war on cancer, so maybe it s time for a newparadigm, Coventry says, adding:A cosmologist can look at the cell as anuniverse to be explored in a new way. ”Nature :癌癥或?yàn)榧?xì)胞進(jìn)入安全模式”?癌癥是人體細(xì)胞試運(yùn)轉(zhuǎn)安全模式”所產(chǎn)生的嗎，就像受損計(jì)算機(jī)系統(tǒng)在面臨外部威脅時(shí)試著保護(hù)自己那樣？這是美國(guó)亞利桑那州立大學(xué)宇宙學(xué)家Paul Da

24、vies和同事得出的結(jié)論，他們提出了一個(gè)備受爭(zhēng)議的癌癥起源新理論。該理論主要基于癌癥的進(jìn)化根源。如果該理論正確，他們的模型提示，氧氣治療和感染病毒或細(xì)菌的一些非傳統(tǒng)療法可能尤其有效。乍看之下，Davies似乎不像 癌癥戰(zhàn)爭(zhēng)”中的戰(zhàn)士，他是物理學(xué)出身，而非生物醫(yī)學(xué)。但是，大約7年前，他被邀請(qǐng)?jiān)趤喞Ｄ侵萁⒁粋€(gè)新機(jī)構(gòu) 一一由國(guó)立癌癥研究所資助的 12所機(jī) 構(gòu)中的1個(gè)，以便將物理學(xué)家和腫瘤學(xué)家聯(lián)合在一起，發(fā)現(xiàn)該疾病的新視角。我們被要求從上到下重新思考癌癥。Davies。隨后，Davies與澳大利亞國(guó)立大學(xué)天體生物學(xué)家Charley Lineweaver和英國(guó)倫敦健康科學(xué)中心腫瘤學(xué)家Mark Vin

25、cent展開合作，提出了 返祖現(xiàn)象”模式，將癌癥定位為古老 預(yù)編”特性 的重新表達(dá)。在上個(gè)月發(fā)表于生物學(xué)論文集的新研究中，該研究小組指出，因?yàn)榘┌Y出 現(xiàn)在許多動(dòng)物、植物和人類中，那么它必須從億萬(wàn)年前開始進(jìn)化，那時(shí)生物擁有共同的單細(xì)胞祖先。在那時(shí)，細(xì)胞受益于永生，或無(wú)限增殖能力，正如癌癥那樣。但當(dāng)復(fù)雜的多細(xì)胞生物開始出現(xiàn)，“永生被轉(zhuǎn)包給卵子和精子。 Davie就，不涉及繁衍的體細(xì)胞不再需要這種機(jī)能。該研究小組提出的假設(shè)是，當(dāng)健康細(xì)胞面臨環(huán)境威脅時(shí)，例如輻射或生活因素，細(xì)胞能夠回復(fù)到預(yù)編的安全模式這樣一來(lái)，細(xì)胞會(huì)拋棄更高的機(jī)能，并將它們的休眠能力切換至增 殖能力，以便存活下來(lái)。癌癥是一種自動(dòng)防障功

26、能， Davie雕到，乙旦這個(gè)子程序被觸發(fā)，就會(huì)冷酷地運(yùn)行該程序。”9月11日，在英國(guó)帝國(guó)理工學(xué)院舉辦的一個(gè)醫(yī)學(xué)工程會(huì)議上，Davies描述了一系列基于這種返祖現(xiàn)象的癌癥療法。Davies指出，與簡(jiǎn)單地攻擊癌癥復(fù)制能力不同，該模型揭示了撞癥的阿喀琉斯之踵”。例如，如果該理論正確，那么癌癥進(jìn)化初期地球的環(huán)境更酸且氧氣更 稀薄。因此，研究人員預(yù)測(cè)，利用高水平氧氣和在飲食中加入還原糖以降低酸性，能夠抑制腫瘤并引起腫瘤收縮。比利時(shí)布魯塞爾自由大學(xué)生理學(xué)家Costantino Balestra表示，利用氧氣治療癌癥已經(jīng)被獨(dú)立研究了許多年，并且似乎支持Davies的觀點(diǎn)。在一份已經(jīng)遞交同行評(píng)議但未出版的論文中， Balestra和同事證實(shí)，輕微提高氧氣水平，能開始誘導(dǎo)白血病細(xì)胞死亡，并不損害