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Leukemia stem cells identified by Stanford researchers

em cells - such as the blood-forming stem cells in the bone marrow that produce both red blood cells and immune cells. Instead, Jamieson found that the cancer started when a normal adult cell mutated and gained the ability to self-renew.

Another surprise has to do with how chronic myelogenous leukemia develops. Most people with the disease have a mutation in which chromosomes 9 and 22 swap ends. This trade fuses genes coding for two different proteins into a single unit that makes a cancer-causing protein called BCR-ABL. All blood cells in these people carry the swapped chromosome, but only macrophage/granulocyte progenitor cells become cancerous.

Although the cancer stem cells still bore some resemblance to macrophage/granulocyte progenitor cells, they also stood apart. One difference was a protein called beta-catenin, found in abundance in the nucleus of the cancer stem cells. This protein is commonly found in embryonic cells where it keeps them in a dividing state. "What's novel is that you have this gene turned on in a mature cell," Jamieson said. The protein was particularly abundant in people whose cancers were resistant to the chemotherapy drug Gleevec.

Beta-catenin is part of a pathway kicked off by a protein called Wnt (pronounced "wint"), which has only recently been found to play a role in helping stem cells continue dividing. Wnt is normally only active in cells that must continually divide, such as stem cells and embryonic cells. Most adult cells don't make Wnt and can only divide a limited number of times. In collaboration with Roeland Nusse, PhD, professor of developmental biology, and Laurie Ailles, PhD, a postdoctoral scholar in Weissman's lab, the group found that blocking beta-catenin's Wnt-activating role in the cancer stem cells also blocked their ability to self-renew.

Weissman said that proteins activating the Wnt pathway are commonly mutated in several types of cancer. What's more, a strain of mice in which Wnt
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