ct this," he says. "We thought the mice would develop B-cell tumors like B-cell lymphomas, not one specific disease such as B-cell CLL." Dr. Croce and his co-workers at Fox Chase Cancer Center in Philadelphia and the Istituto Dermatopatico dell'Immacolata in Rome report their findings May 14 in the Proceedings of the National Academy of Sciences.
"We really don't know much about the genetic mechanism involved in the pathogenesis of CLL," Dr. Croce says. "What this tells us is that either the TCL-1 gene or another gene (s) in the TCL-1 pathway are involved in the initiation and maintenance of B-cell CLL. Now we can target drugs at TCL-1 or molecules that interact with TCL-1. Eventually, we'll discover other targets in the future now that we know this pathway is important."
According to Dr. Croce, because the mouse disease is nearly identical to human CLL, the model will enable scientists to investigate all of the steps involved in the development of the disease. It will also tell researchers whether - and which - drugs work best early or late in the development of the disease.
B-cell CLL is a disease of apoptosis, or programmed cell death, gone awry, he explains. Leukemia cells are not dividing or dying; instead they continue to live a very long time. The study results should "provide important clues about the regulation of programmed cell death - why leukemic cells don't die," Dr. Croce notes, "and help us understand genetic mechanisms involved."
There are as many as 10,000 new cases of B-cell CLL in the United States each year. The disease often strikes the elderly, and while incurable, is slow growing, often lasting as long as 10 to 20 years.
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Contact: Steve Benowitz
Thomas Jefferson University
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