Inactivation of CBP Gene Causes Lymphoma in Mouse Model

Researchers exploring the molecular origins of cancer have used a unique mouse model to link inactivation of the CBP gene in thymocytes to the development of lymphoma.

The investigators, from St. Jude Children's Research Hospital (Memphis, TN, USA) and the Mayo Clinic (Rochester, NY, USA), worked with a "conditional knockout mouse” that lacked the gene for CBP in its thymocytes. The other cells in the bodies of the mice possessed functional copies of the gene.

Results published in the February 2004 issue of Cancer Cell showed that these mice regularly developed lymphomas. Tumor development was not related to functioning of the tumor-suppressing protein p53. However, absence of CBP did correlate with reduction in the levels of a protein named p27Kip1. When mice lacking the CPB gene were engineered to also lack the gene for p27Kip1, lymphoma development was accelerated.

"Overall, our findings suggest that CBP loss leads to lymphoma in cooperation with a mechanism that reduces the amount of p27Kip1,” explained senior author Dr. Jan M. van Deursen, associate professor of biochemistry and molecular biology at the Mayo Clinic College of Medicine. "Moreover, the CBP conditional knockout mice will be a valuable resource for helping unravel the role of CBP in cancer and normal development.”




Related Links:
St. Jude Children's Research Hospital
Mayo Clinic