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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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New Clue to Cancer Protection in Down Syndrome
20 May 2009 (All day)
Down syndrome causes mental retardation and a host of health problems. But it also appears to protect people from cancer. Researchers have now found a potential genetic mechanism for this protective effect. The findings might one day lead to cancer-prevention treatments in the general population.
People with Down syndrome have three copies of chromosome 21 instead of the standard two. That means that they have an extra copy of each of the 231 genes on this chromosome. Because studies have suggested that these individuals also have a lower incidence of colon, breast, and other solid tumor cancers, researchers have long wondered whether one of these extra genes might confer protection. Last year, geneticist Roger Reeves of Johns Hopkins University in Baltimore, Maryland, and colleagues found that the mouse version of one of the triplicated genes--called Ets2--suppresses tumor formation in mice, though the mechanism remains unclear (ScienceNOW, 2 January 2008).
The new findings point to another gene and a clear-cut mechanism. Cancer researcher Sandra Ryeom of Children's Hospital Boston and colleagues took aim at a gene on chromosome 21 called DSCR1 (also known as RCAN1). Previous work suggested that the protein made by this gene interferes with blood vessel formation, or angiogenesis. Inhibiting angiogenesis is one strategy for stopping tumor growth, so Ryeom and her colleagues wondered if this could be happening in Down syndrome.
To investigate, the researchers first looked at tissue from electively aborted human fetuses to see whether the gene was overactive in those with Down syndrome. It was: DSCR1 protein levels were 1.8 times higher than normal. Next, the team created a strain of mice with an extra copy of Dscr1, the mouse version of the gene. One extra copy of just this one gene was enough to suppress angiogenesis and inhibit the growth of transplanted tumors in these mice, the team reports in tomorrow's issue of Nature.
"This is a really interesting addition to what we know about resistance to tumors" in people with Down syndrome, says Reeves. He and Ryeom agree that the protective effects of Dscr1 and Ets2 likely have different mechanisms, with Ets2 acting at an earlier stage before tumors are big enough to initiate angiogenesis. And there are likely to be additional genes involved in the protective effect, Ryeom says.
Ryeom hopes the findings will lead to better strategies for treating cancer in the general population. Drugs that inhibit angiogenesis generated much hope (and media hype) in the late 1990s, but the success so far has been modest. This new work points to components of the angiogenesis signaling pathway that might be more effective drug targets, Ryeom says. Alternatively, she says, blocking angiogenesis might work better as a preventative measure than as a cure. Compounds that block angiogenesis are relatively nontoxic for adults, Ryeom notes, and she thinks it might be possible to develop a low-dose, anticancer drug that people could take like a vitamin. The idea makes good sense biologically, but there would be serious regulatory hurdles for any drug intended to be used before people develop cancer, says David Threadgill, a geneticist at North Carolina State University in Raleigh.