Fox Chase Cancer Center scientists found the gene, called Dlx5, works with a known oncogene, Akt2, to drive cancer in mice by causing white blood cells to spontaneously become cancerous.

The scientists said their findings might lead to the protein that Dlx5 encodes to become a target for drugs to slow the growth of lymphomas and other cancers in humans.

"A chromosomal inversion essentially flips a segment of DNA, placing the Dlx5 gene next to an enhancer in a neighboring gene, which in turn activates a number of other nearby genes," said lead investigator Joseph Testa, "The result is like placing a V8 engine on a Flexible Flyer -- something is going to go fast and without much control."

The study appears in the March 1 issue of the journal Cancer Research.