Scientists have found three new gene variations linked to the development of Hodgkin lymphoma, one of the most common cancers in young adults, and say the findings should help in the development of better treatments.
Around a quarter to half of all cases of Hodgkin lymphoma, a type of cancer originating from white blood cells called lymphocytes, are thought to be triggered by infection with Epstein-Barr virus (EBV), but the disease can also develop in patients who have never been exposed to the virus.
Scientists had suspected genetic factors might be involved, since having a family history of the disease increases risk, but until now they had not been able to identify any specific genetic risk factors.
In a study published in the journal Nature Genetics on Sunday, an international team of scientists found three new variations in the letters of the DNA code that give an increased risk of developing Hodgkin lymphoma. Two of the variants are more common in people not exposed to EBV, they said.
Hodgkin lymphoma
Epstein-Barr virus is a very infectious type of herpes virus that can cause a number of diseases ranging from mild cold-like symptoms to glandular fever and potentially other autoimmune disorders.
“Many cases of Hodgkin lymphoma are linked to Epstein-Barr virus, but we have found the first evidence of genes that could be involved in promoting this cancer’s development in people not exposed to the virus,” said Professor Richard Houlston of the Institute of Cancer Research (ICR), who led the study.
“Understanding the biological triggers for Hodgkin lymphoma is crucial as it opens the door to creating new targeted therapies for this disease.”
Latest data from the International Agency for Research on Cancer show almost 68,000 people worldwide were diagnosed with Hodgkin lymphoma in 2008. The global death rate from this cancer is around 21,700 a year.
Hodgkin lymphoma
Houlston’s team used a technique called a genome wide association study to scan the whole genomes of 589 Hodgkin lymphoma patients and compare the results to 5,199 people without the disease. They then confirmed the results by analyzing another 5,400 people.
They found genetic variants on chromosomes 2, 8 and 10 were significantly more common among Hodgkin lymphoma sufferers than in those without the disease.
They also found that a region on chromosome 6 — which contains a family of genes involved in the immune system — is linked to a higher risk of disease, a finding the scientists said had previously been suspected but not confirmed until now.
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Scientists at the Duke Cancer Institute have decoded secrets of a very common virus that can cause cancer.
About 90 percent of people are infected at some time in their lives with Epstein-Barr virus (EBV), usually with no ill effects.
But individuals with compromised immune systems, such as people with organ transplants or HIV infection, have a greater risk of cancer occurring because of this virus.
Now, scientists have discovered a pathway that infected cells use to root out EBV infections, a finding that has implications for understanding the human response to cancer-causing viruses in general.
“Using cell culture studies, we have uncovered a major pathway that the infected host cell activates to prevent an oncogenic virus from causing cancer,” said senior author Micah Luftig, Assistant Professor of Molecular Genetics and Microbiology.
“We proposed that the cell was sensing that the virus is trying to take over. When this oncogenic stress response is activated, it keeps the virus in check, and now we know why,” Luftig said.
The Luftig group also learned how the Epstein-Barr virus overcomes the cell”s response.
Luftig and his team, including lead authors Pavel Nikitin and Chris Yan, found two enzymes, called kinases, which were critical in mediating this oncogenic stress response and preventing unchecked B-cell cell growth, called immortalization.
When the scientists blocked the ATM and Chk2 kinases, unchecked growth resulted in 10 times more infected cells.
The study appeared in the Dec. 15 online issue of Cell Host and Microbe.