癌症起源及应对

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 :癌症或为细胞进入安全模式”?癌症是人体细胞试运转安全模式”所产生的吗，就像受损计算机系统在面临外部威胁时试着保护自己那样？这是美国亚利桑那州立大学宇宙学家Paul Da

24、vies和同事得出的结论，他们提出了一个备受争议的癌症起源新理论。该理论主要基于癌症的进化根源。如果该理论正确，他们的模型提示，氧气治疗和感染病毒或细菌的一些非传统疗法可能尤其有效。乍看之下，Davies似乎不像 癌症战争”中的战士，他是物理学出身，而非生物医学。但是，大约7年前，他被邀请在亚利桑那州建立一个新机构 一一由国立癌症研究所资助的 12所机 构中的1个，以便将物理学家和肿瘤学家联合在一起，发现该疾病的新视角。我们被要求从上到下重新思考癌症。Davies。随后，Davies与澳大利亚国立大学天体生物学家Charley Lineweaver和英国伦敦健康科学中心肿瘤学家Mark Vin

25、cent展开合作，提出了 返祖现象”模式，将癌症定位为古老 预编”特性 的重新表达。在上个月发表于生物学论文集的新研究中，该研究小组指出，因为癌症出 现在许多动物、植物和人类中，那么它必须从亿万年前开始进化，那时生物拥有共同的单细胞祖先。在那时，细胞受益于永生，或无限增殖能力，正如癌症那样。但当复杂的多细胞生物开始出现，“永生被转包给卵子和精子。 Davie就，不涉及繁衍的体细胞不再需要这种机能。该研究小组提出的假设是，当健康细胞面临环境威胁时，例如辐射或生活因素，细胞能够回复到预编的安全模式这样一来，细胞会抛弃更高的机能，并将它们的休眠能力切换至增 殖能力，以便存活下来。癌症是一种自动防障功

26、能， Davie雕到，乙旦这个子程序被触发，就会冷酷地运行该程序。”9月11日，在英国帝国理工学院举办的一个医学工程会议上，Davies描述了一系列基于这种返祖现象的癌症疗法。Davies指出，与简单地攻击癌症复制能力不同，该模型揭示了撞症的阿喀琉斯之踵”。例如，如果该理论正确，那么癌症进化初期地球的环境更酸且氧气更 稀薄。因此，研究人员预测，利用高水平氧气和在饮食中加入还原糖以降低酸性，能够抑制肿瘤并引起肿瘤收缩。比利时布鲁塞尔自由大学生理学家Costantino Balestra表示，利用氧气治疗癌症已经被独立研究了许多年，并且似乎支持Davies的观点。在一份已经递交同行评议但未出版的论文中， Balestra和同事证实，轻微提高氧气水平，能开始诱导白血病细胞死亡，并不损害