BOSTON, Dec. 15 (UPI) -- U.S. cancer researchers say they've found a link between a common mutation that can lead to cancer and a distant gene regulator that enhances its activity.
The Children's Hospital Boston scientists say their discovery could lead to drugs targeting B-cell lymphomas, including Burkitt's lymphoma, an aggressive cancer in children, as well as multiple myelomas and other blood-related cancers.
Lymphomas often originate in B cells, the scientists said -- the same cells that produce antibodies to help fight infections. B cells can become cancerous if a gene known as c-myc leaps to another section of DNA -- the IgH region, responsible for building antibodies -- fuses with it, and somehow becomes over-activated.
The researchers said scientists have wondered for years how that oncogenic activation occurs, in particular what component in the IgH region activates c-myc. The new study not only identifies the regulatory component, but marks the first time researchers are able to understand how that movement of genes, or "chromosomal translocation," can hijack a B cell's operation badly enough to lead to cancer.
"IgH-to-myc translocation is the classic example of activation of an oncogene in cancer," says Frederick Alt, senior author of the study. "But nobody really understood how it works."
The complex research is reported in the journal Nature.
