“Junk” DNA promotes the growth of cancer cells in patients with Hodgkin’s lymphoma, and possibly other forms of blood cancer, researchers from the University of Leeds, the Charite University Medical School and the Max Delbruck Centre for Molecular Medicine have found.

“Long terminal repeats” (LTRs), a form of “junk DNA,” are usually made inactive when embryos are developing in the womb. If this process of inactivation doesn’t work, these “rogue” active LTRs can drive the growth of cancer in humans, the research demonstrated.

They found that the lymphoma cells’ growth was dependent on a receptor that normally regulates the growth of other immune cells, but it is not usually found in B-cells. However in this case, the Hodgkin-/Reed Sternberg cells “hijacked” this receptor for their own purposes by activating hundreds, if not thousands, of LTRs all over the genome, not just one.

More info: University of Leeds news