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新研究发现,富含抗氧化剂的食物(如红茶,巧克力和浆果)可能会增加某些癌症的风险

   2020-07-30 medicalxpress240
核心提示:某些细菌和富含抗氧化剂的食物(如红茶和热可可)中发现的代谢物,则它对突变的基因特别好客,并会加速肠癌的生长

长期以来困扰着医生的事实是:小肠癌非常罕见,而邻近的,虽然小得多的器官大肠癌却是男女癌症死亡的主要原因之一。结肠似乎吸引了癌症呢?

为了回答这个问题,耶路撒冷希伯来大学(La)劳滕贝格免疫学和癌症研究中心的Yion Ben-Neriah教授及其以Eliran Kadosh博士为首的团队发现,癌症突变本身并不一定是不良行为者。实际上,在肠道等某些微环境中,这些突变实际上可以帮助机体抵抗癌症,而不是传播癌症。但是,如果肠道微生物组产生高水平的代谢物,例如某些细菌和富含抗氧化剂的食物(如红茶和热可可)中发现的代谢物,则它对突变的基因特别好客,并会加速肠癌的生长。他们的突破性发现今天发表在《自然》上。

Ben-Neriah和他的团队在仔细研究胃肠道癌症时牢记肠道微生物群,也许发现了为什么只有2%的癌症在小肠生根,而高达98%的癌症在小肠生根的原因。在结肠。这两个器官之间的一个主要区别是它们的肠道细菌水平:小肠几乎没有,而结肠则很多。Ben-Neriah解释说:“科学家开始越来越重视肠道微生物群在我们健康中的作用:它们的积极作用,在这种情况下,还包括它们在辅助和教be疾病方面的有害作用。”

一点背景:TP53是在每个细胞中发现的基因。它产生一种称为p53的蛋白质,该蛋白质可作为细胞的屏障,抑制细胞中的基因突变。但是,当p53受损时,它将不再保护细胞;反之,恰恰相反:它驱动癌症,帮助肿瘤扩散和生长

为了检验他们的肠道菌群发挥作用的理论,研究人员将突变的p53(“驱动癌”)蛋白引入了肠道。令人惊讶的是,小肠通过将突变的p53癌症驱动因子转换回正常的p53而反应,变成了比健康的p53蛋白更能抑制癌症生长的“超级抑制剂”。但是,当将突变的p53导入结肠时,它们并没有发生任何变形,而是忠于其驱动癌的性质,并促进了癌的扩散。本尼里亚回忆说:“我们为所见所闻所吸引。” “肠道细菌对突变的p53蛋白具有Jekyll和Hyde效应。在小肠中,它们完全改变了方向并攻击癌细胞,而在结肠中,它们促进了癌细胞的生长。

为了进一步检验他们的理论,即肠道菌群是为什么突变的p53在小肠中起着肿瘤阻断剂的作用,但在结肠中却起着肿瘤促进剂的作用,科学家们施用了抗生素杀死结肠的肠道菌群。一旦他们做到了,突变的p53将无法继续进行其癌症狂潮。

这种菌群中有什么能使结肠癌如此迅速地扩散?仔细的分析确定了罪魁祸首:肠道菌群会产生代谢产物,又称“抗氧化剂”,在诸如红茶,热巧克力,坚果和浆果等食物中含量很高。显然,当科学家给小鼠喂食富含抗氧化剂的饮食时,它们的肠道菌群会加速p53的癌症驱动模式。对于有大肠癌家族病史的患者,这一发现特别令人担忧。

“从科学上讲,这是一个新领域。我们惊讶地看到微生物组在多大程度上影响了癌症突变,在某些情况下完全改变了它们的性质,” Ben-Neriah说道。展望未来,那些患有大肠癌高危人群的人可能希望更频繁地筛查肠道菌群,并对他们消化的食物,抗氧化剂和其他方面三思而行。

英文原文

Antioxidant-rich foods like black tea, chocolate, and berries may increase risk for certain cancers, new study finds


It is a fact that has long baffled doctors: Cancer in the small intestine is quite rare, whereas colorectal cancer, a neighboring though much smaller organ, is one of the leading causes of cancer death for men and women. What is it about the colon that seems to attract cancer?

To answer this question, Professor Yinon Ben-Neriah at Hebrew University of Jerusalem (HU)'s Lautenberg Center for Immunology and Cancer Research and his team led by Dr. Eliran Kadosh, found that cancer mutations are not necessarily bad actors in and of themselves. In fact, in certain micro-environments like the gut, these mutations can actually help the body to fight cancer, not spread it. However, if the gut microbiome produces high levels of metabolites, like those found in certain bacteria and antioxidant-rich foods like black tea and hot cocoa, then it acts as a particularly hospitable environment to mutated genes and will accelerate the growth of bowel cancers. Their breakthrough findings were published today in Nature.

Ben-Neriah and his team kept gut microbiomes in mind as they took a closer look at gastrointestinal cancers, and may have found the reason why only 2% of cancers take root in the small intestine, whereas a whopping 98% of cancers take place in the colon. One major difference between these two organs is their levels of gut bacteria: the small intestine contains few, whereas the colon contains multitudes. "Scientists are beginning to pay more and more attention to the role gut microbiomes play in our health: both their positive effects and, in this case, their sometimes pernicious role in aiding and abetting disease," explained Ben-Neriah.

A little background: TP53 is a gene found in every cell. It produces a protein called p53 which acts as the cell's barrier, suppressing genetic mutations in the cell. However, when p53 becomes damaged, it no longer protects the cell; quite the opposite: It drives the cancer, helping tumors spread and grow.

To test their theory that gut flora was at play, the researchers introduced mutated p53 ("cancer-driving") proteins into the gut. Amazingly, the small intestine reacted by converting the mutated p53 cancer driver back to normal p53, turning into "super-suppressors" that were better at suppressing cancer growth than healthy p53 proteins. However, when mutated p53 was introduced into the colon, they did no switcheroo but stayed true to their driving-cancer nature and promoted the cancerous spread. "We were riveted by what we saw," recalls Ben-Neriah. "The gut bacteria had a Jekyll and Hyde effect on the mutated p53 proteins. In the small bowel they totally switched course and attacked the cancerous cells, whereas in the colon they promoted the cancerous growth."

To further test their theory that gut flora was a major factor as to why mutated p53 were acting as tumor blockers in the small bowel but tumor accelerants in the colon, the scientists administered antibiotics to kill off the colon's gut flora. once they did, the mutated p53 was not able to go on its cancer spree.

What's in this flora that makes colon cancer spread so quickly? A close analysis identified the culprit: gut flora that produces metabolites, aka "antioxidants", which are found in high concentrations in foods such as black tea, hot chocolate, nuts and berries. Tellingly, when the scientists fed mice an antioxidant-rich diet, their gut flora accelerated p53's cancer-driver mode. This finding is of particular concern to those patients with a family history of colorectal cancer.

"Scientifically speaking, this is new territory. We were astonished to see the extent to which microbiomes affect cancer mutations—in some cases, entirely changing their nature," shared Ben-Neriah. Looking towards the future, those at high-risk of colorectal cancer may want to screen their gut-flora more frequently and think twice about the foods they digest, antioxidant and otherwise.

 
标签: 肿瘤 癌症 p53
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