Researchers from the University of Leeds, UK, the Charité University Medical School and the Max Delbrück Centre for Molecular¹ Medicine (MDC) in Berlin, Germany, have discovered a new driving force behind cancer growth. Their studies have identified how 'junk' DNA² promotes the growth of cancer cells in patients with Hodgkin's lymphoma（淋巴瘤） . Professor Constanze Bonifer (University of Leeds) and Dr Stephan Mathas (Charité, 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 mechanism³ could be involved in the development of other forms of blood cancer," said Prof. Bonifer. "This would have implications for diagnosis⁴, prognosis（预知） , and therapy of these diseases."

'Long terminal repeats' (LTRs) are a form of 'junk DNA' - genetic⁵ 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 embryos⁶（胚胎，晶胚） are developing in the womb（子宫） .

If this process of inactivation⁷ doesn't work, then the LTRs could activate⁹ cancer genes¹⁰, a possibility that was suggested in previous animal studies. This latest research has now demonstrated for the first time that these 'rogue¹¹' 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 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 'hijacked¹²' this receptor for their own purposes by activating¹³ some of the 'junk DNA'. In fact the lymphoma cells activated¹⁴ hundreds, if not thousands, of LTRs all over the genome, not just one.

Hodgkin-/Reed Sternberg cells may not be the only cells that use this method to subvert¹⁵（推翻，颠覆） normal controls of cell growth. The researchers found evidence of the same LTRs activating the same growth receptor in anaplastic（还原成形术的） large cell lymphoma, another blood cancer.

The consequences of such widespread LTR activation⁸ are currently still unclear, according to the study's authors. Such processes could potentially activate other genes involved in tumour¹⁶ development. It could also affect the stability of chromosomes¹⁷ of lymphoma cells, a factor that may explain why Hodgkin-/Reed Sternberg cells gain many chromosomal¹⁸（染色体的） abnormalities over time and become more and more malignant¹⁹（恶性的，有害的） .