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A Clue for Tumor Survival Lies in How Sweet It Is 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领 May 7, 2008, 4:19 pm
A Clue for Tumor Survival Lies in How Sweet It Is
Posted by Ron Winslow
Researchers have long been puzzled by the fact that some of medicine’s most touted new cancer drugs work only 10% to 20% of the time against many common tumors. Now scientists at University of Texas M.D. Anderson Cancer Center in Houston have come up with a possible explanation that could reshape thinking about one of oncology’s major treatment targets.
长久以来，研究者们一直困惑于一个谜题：为什么一些备受推崇的抗肿瘤新药对许多常见肿瘤的治疗效果只能达到10%到20%？日前，休斯敦市德克萨斯大学下属的安德森博士肿瘤中心的科学家们对这一谜题进行了解答。而他们的解答可能使人们对肿瘤的一个主要治疗靶点重新审视。
Many of the drugs home in on a receptor that is abundant on the surface of cancer cells. But it turns out that the receptor, despite interference from the drugs, also helps the cancer cells thrive by helping to assure their food supply.
许多药物是通过干扰肿瘤细胞表面大量表达的受体来发挥作用。但研究表明，尽管受药物干扰，受体仍然可以给肿瘤细胞提供营养支持，从而促进肿瘤细胞生长繁殖。
For more than two decades, pharmaceutical and biotech companies have made the epidermal growth factor receptor, or EGFR, a key target of new cancer therapies, based on evidence that blocking this receptor disrupts cellular signals that cause tumor cells to grow and proliferate. The payoff has been impressive: Erbitux from ImClone Systems and Bristol-Myers Squibb; Tarceva from Genentech and OSI Pharmaceuticals; Iressa from AstraZeneca and Vectibix from Amgen are among EGFR blockers now available to treat colorectal, lung, breast and other cancers.
在过去的二十多年里，制药公司跟生化公司一直将表皮生长因子受体（EGFR）做为新肿瘤治疗方案的主要靶点，因为有研究表明阻断EGFR，就可以使细胞信号传递中断，从而遏制细胞的生长繁殖。这一方面所取得的成就也令人注目：其中ImClone Systems and Bristol-Myers Squibb公司的Erbitux；Genentech and OSI Pharmaceuticals的Tarceva；阿斯利康公司的Iressa和Amgen公司的Vectibix是目前用于临床治疗结直肠肿瘤、肺癌、乳腺癌和其他肿瘤的EGFR拮抗剂。
The drugs work by preventing an enzyme called tyrosine kinase from launching a signaling cascade that fuels tumor cell growth. But the generally limited response to these treatments has caused cancer experts to wonder if EGFR’s role in the disease is limited as well.
这些药物的作用机制是阻断酪氨酸激酶启动信号级联反应，后者可以促进肿瘤细胞生长。但肿瘤对这种治疗方案的反应总体上是有限的，这使得肿瘤学家们开始怀疑EGFR在疾病发展过程中的作用是否也是有限的。
In a paper being published this week in the journal Cancer Cell, Isaiah Fidler and Mien-Chie Hung and their colleagues at M.D. Anderson report on in a series of laboratory experiments in which they discovered that EGFR plays a second role in promoting the survival of cancer cells: it helps tumor cells get a constant and plentiful supply of the sugar glucose, a critical nutrient.
在本周发表于《Cancer Cell》杂志上的一篇文章中，安德森肿瘤中心的Isaiah Fidler 、 Mien-Chie Hung及其同事们报道说，通过一系列的实验，他们发现EGFR在促进肿瘤细胞生存方面只是起一个次要作用，即它可以帮助肿瘤细胞持续获得大量的重要营养物质---葡萄糖。
EGFR does this by binding to and stabilizing another protein on the cell surface called SGLT1 (for sodium/glucose co-transporter). Without this mechanism, Fidler tells the Health Blog, “the cell will undergo glucose starvation.” In the process, the cell essentially devours itself and dies.
EGFR是通过与细胞表面一种称为SGLT1的蛋白（一种钠-糖共转运通道）结合并使之稳定来发挥上述作用的。Fidler告诉Health Blog工作人员说，如果没有这一机制，“肿瘤细胞将会缺乏葡萄糖。”在这一过程中，肿瘤细胞只能依靠自身的营养来生存，并最终死亡。
The glucose role is independent and thus unaffected by turning off the kinase-activated growth signals, the researchers found. Even in face of drugs that block the kinase activity, “the tumor cell that expresses very high levels of EGFR and very high levels of SGLT will remain viable,” Fidler says.
研究者们发现，葡萄糖的作用是独立的，因此关闭酪氨酸激酶激活的生长信号通路并不会对葡萄糖产生影响。即使使用能阻断激酶活性的药物，“那些高表达EGFR、SGLT的肿瘤细胞仍能存活。”
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作者:admin@医学,生命科学 2010-11-27 05:11
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