This year's Nobel Prize in medicine went to a trio of scientists who discovered the enzyme telomerase, which allows cells to divide without any limits, making them effectively immortal.

    It may be nature's greatest double-edged sword. Coax cells into producing telomerase, and they will survive indefinitely, but they will also become cancerous.

    To safeguard against cancer, adult cells keep track of how many times that they have multiplied, and once they have reached a pre-set limit - often around 80 divisions - they die. Telomerase interferes with this record keeping.

    If you can find a drug or gene therapy that interferes with telomerase, it could fight the unchecked growth of cancer cells, said Mark Muller, a cancer researcher who studies telomeres at the University of Central Florida.

    "Ninety percent of all cancer cells are telomerase rich," Muller said.

    Several companies, including Geron, have started testing drugs that gum up the telomerase enzyme, so that it can't extend the lives of cancer cells.

    Telomerase lengthens telomeres, repetitive DNA sequences that sit at the ends of chromosomes. Each segment of a telomere is like a ticket that gives it permission to divide. When cells run out of those credits, they cease dividing.

    Geron is developing a modified DNA molecule that gets stuck inside of telomerase, so that it can't build up the ends of telomeres in cancer cells. The company is also working with a vaccine that trains cancer patients' immune systems to attack cells that produce telomerase. In adults, almost all of the cells that produce telomerase are cancerous.

    Those cancer treatments took shape almost 20 years after academics made a breakthrough discovery.

    In the early 1980's Elizabeth Blackburn, Carol Greider and Jack Szostak identified telomerase and learned how it works. Some scientists speculated people could live longer by using the enzyme to buy extra time for their aging cells, but that idea remains risky and unproven.

    "By itself, lengthening telomeres would probably just increase the rate of tumor formation," said Chris Patil, a researcher at the Buck Institute for Age Research in Novato, California. "Experiments with mice have shown that lengthening telomeres extends lifespan, but only if you introduce multiple other mutations to block cancer."

    Considering the risks of telomere-extension therapy, he thinks that scientists have bigger fish to fry.

    "In the absence of a comprehensive understanding, it's very dangerous," Muller said. "We have to figure out how to do maintenance on our telomeres."

    Muller thinks humans could live for 90 to 210 years once scientists know more about the molecular basis of aging.

    "If we could figure out how to do maintenance, we could extend our lives," he said. "But it has to be done very carefully, and we'd have to have a comprehensive understanding of the mechanism. "

    本年度诺贝尔医学奖被发现端粒酶酵素的三位科学家共同夺得，端粒酶酵素使细胞无限分裂，也就是使细胞长生不老。

    对细胞进行诱导，使之产生端粒酶，这些细胞会无限期的生存下去，但也会癌变。这也许是大自然最大的双刃剑。

    为预防癌症，成人细胞记录细胞分裂的次数，一但达到八十次左右的预定极限，细胞就会死亡。端粒酶干扰这一记录过程。

    在佛罗里达大学进行端粒酶研究的癌症研究者，马克*穆勒说，如果你能找到一种药物或基因疗法，那么就能抵制癌细胞的过度增长。

    "百分之九十的癌细胞都富含端粒酶，"穆勒说。

    包括杰龙公司在内的几家公司已开始进行抑制端粒酶酵素的药物试验，使之不能延长癌细胞的生命。

    端粒是位于染色体末端的DNA重复序列，而端粒酶使端粒变长。一个端粒的每一个片段就象一张细胞分裂的通行证。细胞分裂到预定的次数时，就停止分裂。

    杰龙公司正在研发一种经修饰的DNA分子，它可附着在端粒酶内部，使之不能在癌细胞内延长端粒末端。该公司还在研发一种疫苗，这种疫苗训练患者的免疫系统去攻击产生端粒酶的细胞。在成年人中，几乎所有产生端粒酶的细胞都是癌细胞。

    在学术上突破性发现二十年之后，才形成这些癌症疗法。

    上世纪八十年代初，伊利莎白*布拉克本、卡洛*格雷德及杰克*绍斯塔克三人识别出端粒酶，并了解其作用原理。有些科学家推测，用这种酶为正在老化的细胞赢得多余的时间，这样可以延长人的寿命。但这种想法是危险的，也未被证实。

    "仅仅延长端粒可能只会增加肿瘤形成率，"在位于美国加利福尼亚州的巴克老年研究所工作的研究员，克丽丝* 帕蒂尔说，"白鼠试验已表明，只有在导入成倍的其它突变阻止癌症的情况下，延长端粒才会延长寿命。"

    因为延长端粒疗法具有危险，他认为还有更大的问题需要科学家去解决。

    "在缺乏全面了解的情况下，用延长染色体端粒的方法来延长寿命是极其危险的，"穆勒说，"我们必须知道如何保养我们的端粒。"

    穆勒认为，科学家进一步了解了衰老的分子基础之后，人类就能活到九十到二百一十岁。

    "如果明白如何保养，我们就能延长寿命。但这样做必须慎之又慎，还必须对其机理有全面的了解。"穆勒说。