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Hit cancer where it hurts

机译:在痛苦中击中癌症

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It seemed like the perfect target. An enzyme that gives cancer cells their everlasting ability to divide, but which is missing from most normal cells. Could this be the one weak spot common to all cancers, the route to a universal cure with no serious side effects? Discovered in the mid-1980s, this enzyme, called telomerase, generated a great deal of excitement among cancer researchers. Telomerase is largely missing from healthy cells, but 90 per cent of cancers churn it out by the bucketload. It gives them the ability to keep dividing long after they should have aged and died. Telomerase's discovery raised the hope that it could somehow be used to single out cancer cells from normal cells, and perhaps even strip them of their deadly immortality. In the early 1990s, telomerase was the focus of great optimism. But several major setbacks have been enough to scare away drug companies and convince some researchers that telomerase as a cancer therapy was a dead end. One of the biggest blows was the discovery that it takes months for a cancer cell to stop dividing after telomerase activity has ceased. For most cancer patients, that is simply too slow. But now comes a new twist. Researchers delving deeper into basic telomerase biology have uncovered evidence that this enzyme's role in cancer is a great deal more complex -and possibly even more critical - than originally thought. At the same time, there is growing excitement over recent experiments that have uncovered new and more efficient ways of killing cancer cells by exploiting telomerase. One approach, an anti-cancer vaccine that trains immune cells to zero in on cells making telomerase, already looks promising in clinical trials on cancer patients. As a result, some researchers are now quietly optimistic that telomerase may yet emerge as a powerful tool in the fight against cancer. "As our understanding of telomerase has become more sophisticated, its attractiveness as a target has not gone away," says Elizabeth Blackburn, co-discoverer of telomerase. "It's gotten stronger."
机译:这似乎是完美的目标。一种使癌细胞具有持久分裂能力的酶,但大多数正常细胞却缺乏这种酶。这可能是所有癌症都普遍存在的一个薄弱环节,这是一种没有严重副作用的普遍治愈途径吗?在1980年代中期发现的这种酶,称为端粒酶,在癌症研究人员中引起了极大的兴奋。端粒酶在健康细胞中基本缺失,但90%的癌症会因负担而将其淘汰。它使他们有能力在本应衰老和死亡后的很长一段时间内保持分裂。端粒酶的发现使人们希望它可以以某种方式从正常细胞中分离出来,甚至剥夺它们的致命生命。在1990年代初期,端粒酶成为人们高度乐观的焦点。但是,几次重大挫折足以吓to制药公司,并说服一些研究人员将端粒酶作为一种癌症疗法是死胡同。最大的打击之一是发现端粒酶活性停止后癌细胞停止分裂需要几个月的时间。对于大多数癌症患者来说,这太慢了。但是现在有了新的转折。研究人员更深入地研究了端粒酶的基本生物学原理,发现该酶在癌症中的作用比最初认为的要复杂得多,甚至可能更为关键。同时,人们对最近的实验感到越来越兴奋,这些实验发现了利用端粒酶杀死癌细胞的新的,更有效的方法。一种方法是将抗癌疫苗训练成端粒酶的细胞中的免疫细胞归零,这种方法已经在针对癌症患者的临床试验中看起来很有希望。结果,现在一些研究人员对端粒酶仍可能成为抗癌的有力工具感到乐观。端粒酶共同发现者伊丽莎白·布莱克本(Elizabeth Blackburn)说:“随着我们对端粒酶的了解变得越来越复杂,它作为靶标的吸引力还没有消失。” “它变得越来越强大。”

著录项

  • 来源
    《New scientist》 |2004年第2454期|p.40-43|共4页
  • 作者

    Garry Hamilton;

  • 作者单位

    Seattle;

  • 收录信息 美国《科学引文索引》(SCI);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 自然科学总论;
  • 关键词

  • 入库时间 2022-08-18 02:56:47

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