Transgenic mice developed different lymphomas depending on presence or absence of antigen, according to PLos Biology paper.
The B-cell receptor on the surface of B cells cooperates with the MYC oncogene to accelerate the development of B-cell lymphomas, according to a group of scientists. The team from the National Jewish Medical and Research Center also report that disrupting B-cell receptor signals inhibited the growth of the tumors.

To evaluate the role of the B-cell receptor in B-cell lymphomas, the research team developed a series of transgenic mice. They found that the presence of a functional B-cell receptor increased the development of tumors in mice with a translocated MYC oncogene.

The investigators were then able to demonstrate that the B-cell receptor worked with MYC in the development of tumors in the presence as well as the absence of an antigen. When no antigen was present, the mice developed a lymphoma similar to human B-cell lymphocytic leukemia.

When there was an antigen, the mice developed a lymphoma that closely resembled Burkitt’s lymphoma, the scientists state. The researchers explain that they used an autoantigen in a situation resembling autoimmune disease, which in humans reportedly increases the risk of developing B-cell lymphoma 50 to 200 times.

The investigators also say that they were able to prevent and eliminate tumors by treating the mice with immunosuppressants.

“Research into B-cell lymphomas has been hampered by the lack of a good mouse model,” according to leader of the study, Yosef Refaeli, Ph.D., assistant professor of pediatrics at National Jewish. “The mouse we created gives us a very good predictive model of B-cell lymphomas, which can be used to explore not only these and related cancers but also autoimmune disease and basic immunology.”

Researchers from University of California, San Francisco were also involved in the study. The results are published in the June 24 issue of PLos Biology.

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