Researchers from the University of Leeds, UK, the Charit University Medical School and the Max Delbrck Centre for Molecular Medicine (MDC) in Berlin, Germany, have discovered a new driving force behind cancer growth.
Their studies have identified how 'junk' DNA promotes the growth of cancer cells in patients with Hodgkin's lymphoma. Professor Constanze Bonifer (University of Leeds) and Dr Stephan Mathas (Charit, MDC) who co-led the study suspect that these pieces of 'junk' DNA, called 'long terminal repeats', can play a role in other forms of cancer as well. The work is published in Nature Medicine.*
The researchers uncovered the process by which this 'junk DNA' is made active, promoting cancer growth.
"We have shown this is the case in Hodgkin's lymphoma, but the exact same mechanism could be involved in the development of other forms of blood cancer," said Prof. Bonifer. "This would have implications for diagnosis, prognosis, and therapy of these diseases."
'Long terminal repeats' (LTRs) are a form of 'junk DNA' - genetic material that has accumulated in the human genome over millions of years. Although LTRs originate from viruses and are potentially harmful, they are usually made inactive when embryos are developing in the womb.
If this process of inactivation doesn't work, then the LTRs could activate cancer genes, a possibility that was suggested in previous animal studies. This latest research has now demonstrated for the first time that these 'rogue' active LTRs can drive the growth of cancer in humans.
The work focused on cancerous cells of Hodgkin's lymphoma (the Hodgkin-/Reed Sternberg cells) that originate from white blood cells (antibody-producing B cells). Unusually, this type of lymphoma cell does not contain a so-called 'growth factor receptor' that normally controls the growth of other B-cells.
They found that the lymphoma cells' growth was dependent on a receptor that nor
|Contact: Paula Gould|
University of Leeds