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. "

    本年度諾貝爾醫(yī)學獎被發(fā)現(xiàn)端粒酶酵素的三位科學家共同奪得，端粒酶酵素使細胞無限分裂，也就是使細胞長生不老。

    對細胞進行誘導，使之產(chǎn)生端粒酶，這些細胞會無限期的生存下去，但也會癌變。這也許是大自然最大的雙刃劍。

    為預防癌癥，成人細胞記錄細胞分裂的次數(shù)，一但達到八十次左右的預定極限，細胞就會死亡。端粒酶干擾這一記錄過程。

    在佛羅里達大學進行端粒酶研究的癌癥研究者，馬克*穆勒說，如果你能找到一種藥物或基因療法，那么就能抵制癌細胞的過度增長。

    "百分之九十的癌細胞都富含端粒酶，"穆勒說。

    包括杰龍公司在內(nèi)的幾家公司已開始進行抑制端粒酶酵素的藥物試驗，使之不能延長癌細胞的生命。

    端粒是位于染色體末端的DNA重復序列，而端粒酶使端粒變長。一個端粒的每一個片段就象一張細胞分裂的通行證。細胞分裂到預定的次數(shù)時，就停止分裂。

    杰龍公司正在研發(fā)一種經(jīng)修飾的DNA分子，它可附著在端粒酶內(nèi)部，使之不能在癌細胞內(nèi)延長端粒末端。該公司還在研發(fā)一種疫苗，這種疫苗訓練患者的免疫系統(tǒng)去攻擊產(chǎn)生端粒酶的細胞。在成年人中，幾乎所有產(chǎn)生端粒酶的細胞都是癌細胞。

    在學術(shù)上突破性發(fā)現(xiàn)二十年之后，才形成這些癌癥療法。

    上世紀八十年代初，伊利莎白*布拉克本、卡洛*格雷德及杰克*紹斯塔克三人識別出端粒酶，并了解其作用原理。有些科學家推測，用這種酶為正在老化的細胞贏得多余的時間，這樣可以延長人的壽命。但這種想法是危險的，也未被證實。

    "僅僅延長端�？赡苤粫�增加腫瘤形成率，"在位于美國加利福尼亞州的巴克老年研究所工作的研究員，克麗絲* 帕蒂爾說，"白鼠試驗已表明，只有在導入成倍的其它突變阻止癌癥的情況下，延長端粒才會延長壽命。"

    因為延長端粒療法具有危險，他認為還有更大的問題需要科學家去解決。

    "在缺乏全面了解的情況下，用延長染色體端粒的方法來延長壽命是極其危險的，"穆勒說，"我們必須知道如何保養(yǎng)我們的端粒。"

    穆勒認為，科學家進一步了解了衰老的分子基礎之后，人類就能活到九十到二百一十歲。

    "如果明白如何保養(yǎng)，我們就能延長壽命。但這樣做必須慎之又慎，還必須對其機理有全面的了解。"穆勒說。