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St. Jude/Mayo Clinic study finds direct link between CBP gene and lymphoma

. p53 is critical to the ability of the cell to undergo self-destruction when it sustains serious damage to its DNA--a process called apoptosis. This prevents the cell from becoming cancerous. But even though CBP is known to help activate p53, the loss of CBP in these white blood cells, called thymocytes, triggered cancer even though p53 activity appeared normal.

"Given the large body of scientific literature on the subject, it would be natural to think that if CBP loss triggered cancer, p53 activity would need to be greatly reduced, but that's not what we found," Brindle said. "So it is unclear what role CBP has with regard to p53 function."

The St. Jude-Mayo team also found an increase in the activity of cyclin E and Skp2, two proteins known to be part of a signaling pathway in cells that leads to cancer. Cyclin E and Skp2 break down a protein called p27Kip1. The researchers showed that such reduction of p27Kip1 activity in the CBP knockout mice accelerates the development of lymphoma.

"Overall, our findings suggest that CBP loss leads to lymphoma in cooperation with a mechanism that reduces the amount of p27Kip1, van Deursen said. "Moreover, the CBP conditional knockout mice will be a valuable resource for helping unravel the role of CBP in cancer and normal development."
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Contact: Bonnie Cameron
bonnie.cameron@stjude.org
901-495-4815
St. Jude Children's Research Hospital
24-Feb-2004


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