Immune system link to cancer risk identified
3 October 2007
Genetic variations that predispose some people to glandular fever have been identified by Medical Research Council funded scientists at the University of Edinburgh. The discovery furthers our understanding of how a lymph node cancer called Hodgkin’s lymphoma develops.
These variations known as genetic markers, are sequences of DNA that are involved in maintaining and regulating the immune system and so can influence an individual’s ability to respond to viral infection. The Edinburgh team have discovered genetic markers that leave some people more vulnerable to glandular fever which is caused by infection with Epstein-Barr virus (EBV). The presence of the same genetic markers has also been linked to an increased risk of developing Hodgkin’s lymphoma.
EBV is carried by 90 per cent of adults, the majority of whom never experience any symptoms as a result of infection. However, in some cases, the virus can cause some forms of Hodgkin's lymphoma, one of the most common tumours found in young adults.
Karen McAulay, lead researcher on the project said: "Until now, we haven't understood why Epstein-Barr virus affects people so differently. Now, we have identified a link between glandular fever and specific DNA markers that are involved in immune system regulation. Armed with this knowledge, we can start working on ways to unravel the mechanisms involved and hopefully provide better and more personalised treatments to stop the infection developing into something more serious.’’
The research team analysed 300 blood samples provided by University students. They looked for the presence or absence of specific sequences of DNA known to be linked to the immune system response to viral infection. In doing so they identified so called ‘genetic markers’, sequences of DNA that were more common in people who developed glandular fever than those who didn’t.
The findings suggest that these DNA sequences influence the way the immune system responds to infection by EBV. This genetic variation means that some people are more likely than others to develop glandular fever and have a higher risk of developing Hodgkin’s lymphoma.
The genetic markers involved are linked to T cells, an integral part of the immune system’s response to viral infection. The results suggest that the T cells of people with the genetic variation and who develop glandular fever are less able to control the virus. The research team has suggested that these T cells could be the key to future therapy for diseases caused by EBV.
The research results are published in the Journal of Clinical Investigation,
Dr McAulay concludes: ‘‘T cells found in blood donated by healthy volunteers can be primed in the lab to attack the EBV. We could then give it to people who have glandular fever to destroy the virus perhaps reducing their risk of developing associated cancers like Hodgkin’s lymphoma.’’
Press contact
Phone: 020 7637 6011
press.office@headoffice.mrc.ac.uk
