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17 April 2014 12:48 pm ,
Vol. 344 ,
Officials last week revealed that the U.S. contribution to ITER could cost $3.9 billion by 2034—roughly four times the...
An experimental hepatitis B drug that looked safe in animal trials tragically killed five of 15 patients in 1993. Now,...
Using the two high-quality genomes that exist for Neandertals and Denisovans, researchers find clues to gene activity...
A new report from the Intergovernmental Panel on Climate Change (IPCC) concludes that humanity has done little to slow...
Astronomers have discovered an Earth-sized planet in the habitable zone of a red dwarf—a star cooler than the sun—500...
Three years ago, Jennifer Francis of Rutgers University proposed that a warming Arctic was altering the behavior of the...
- 17 April 2014 12:48 pm , Vol. 344 , #6181
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Turning a Tumor's Lights Off
12 June 2006 (All day)
When Olympic sprinters push themselves to the limit, the energy-producing pathways in their cells switch gears, turning to an oxygen-free pathway to keep the juice flowing. Cancer cells also use this pathway--called anaerobic glycolysis--even when there is plenty of oxygen around. Now, researchers have found that blocking a key enzyme involved in anaerobic glycolysis significantly slows the growth of tumors. The findings, say experts, suggest a new way to target cancer with drugs.
In 1924, German biochemist Otto Warburg first described how cells shift to anaerobic glycolysis when they become cancerous, and the "Warburg effect" has intrigued cancer biologists ever since. One possible reason for the shift is that tumors must sometimes cope with a lack of oxygen, or hypoxia--hence the need for anaerobic energy production. Warburg and later scientists postulated that interfering with glycolysis might be a way to treat cancer. In 1997, molecular biologist Chi Dang of Johns Hopkins Medical School in Baltimore, Maryland, found that blocking one enzyme involved in glycolysis, lactate dehydrogenase A (LDH-A), could slow the growth of cancer cells in petri dishes.
Now cancer researchers at Harvard Medical School in Boston, Massachusetts, have shown that blocking LDH-A, using a technique called RNA interference (ScienceNOW, 10 November 2004), lowers the growth rates of cancer cells by about 100 fold. Furthermore, when the team, lead by cell biologist Valeria Fantin, implanted LDH-A-normal cancer cells and LDH-A-deficient cancer cells in mice, LDH-A-deficient tumors grew more slowly and took two-and-a-half times longer, on average, to kill the mice than LDA-A-positive tumors. "We were really amazed at the differential growth rate of these tumors," says Fantin, whose team publishes its findings in this month's issue of Cancer Cell.
Dang agrees, calling the new results "dramatic." Fantin suspects that the risk of toxic side-effects will be low because case studies have shown people without functioning LDH-A are nonetheless healthy. But Dang cautions that any drug will have to hit LDH-A and not LDH-B, which may be important for heart function.