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´Master Switch´ Turns Off Cancer
Protein Cuts Off Cells´ Cancer-Growth Machinery


By Daniel DeNoon

WebMD Medical News Reviewed By Brunilda Nazario

January 17, 2003



Researchers say they´ve found a "master switch" for cancer. The switch -- a protein with the tongue-tying nickname CUGBP2 -- makes cancer cells self-destruct.

So far the findings, reported in the Jan. 17 issue of the journal Molecular Cell, apply only to cancer cells grown in a test tube. Human studies aren´t yet on the drawing board. But the Washington University scientists who made the discovery are plenty excited. Heading the research team is Shrikant Anant, PhD.

"We may have found a master switch, a protein that can inhibit many of those genes involved in cancer," Anant tells WebMD. "This may be a great tool for cancer therapy. And it works across the board for many cancers. We would love to see this as a therapy."

Anant´s colleague Brian K. Dieckgraefe (pronounced de-GRAF) agrees. "It looks like this is a master switch that controls a variety of cancers," he tells WebMD.

CUGBP2 is cytidine-uridine-guanosine binding protein. How does it work? It has multiple effects, but one stands out. Normal cells are full of CUGBP2. When their time comes, the protein helps them die off by activating their built-in self-destruct program. But when cells start down the path toward becoming cancers, they somehow lose CUGBP2. This lets them build up lots of an enzyme known as Cox-2.

You may have heard of Cox-2. It´s a major culprit in arthritis and headache. Aspirin-like drugs block its action. So do newer drugs such as Celebrex and Vioxx, which are known as Cox-2-selective inhibitors. Cox-2 plays an even darker role in human disease. When overexpressed by precancer cells, it helps them grow the new blood vessels they need to become tumors.

Aspirins and the new Cox-2 inhibitors seem to help slow cancer growth, but they have a limited effect. Not so with CUGBP2. When Anant´s team put CUGBP2 into cancer cells, more than 70% of them died. Why? The protein shuts off the Cox-2 gene.

"The major advance here is that this might be a single step that keeps tumor cells from dying," Dieckgraefe says. "This may be an important therapeutic advance. I´m also excited because this will lead to a considerable amount of new research into a pathway that may have dramatic anticancer effects."

That´s very likely, says Fadlo Khuri, MD, associate director for clinical and translational research at Emory´s Winship Cancer Institute in Atlanta.

"This paper does make a great deal of sense," Khuri tells WebMD. "What is known about Cox-2 in cancer is quite interesting. In head/neck cancers, lung cancers, colon cancers, they all [produce] more Cox-2 than precancerous cells. The sense among experts is that the Cox-2 inhibitors now available are unlikely to be effective anticancer agents all by themselves. But they may be very potent preventive agents -- and they may be very important in combination with chemotherapy."

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