The study which involved scientists from Australia, the U.S., Sweden, the UK, France, Spain and Italy, has found that common genetic variations are responsible for doubling a person's risk of developing the deadly melanoma.
Australian scientist Dr. Stuart MacGregor from the Queensland Institute of Medical Research, says the revelation could lead to a test to identify people who were genetically more susceptible to the disease.
Dr. MacGregor says those identified as vulnerable could then reduce their exposure to the sun and regularly have their skin checked.
Incidents of melanoma have increased and an early diagnosis of the cancer is vital so treatment can begin in order to ensure a better outcome.
Each year as many as 1,000 Australians die from melanoma and it is predicted that by 2011, more than 11,600 new cases will be diagnosed in that year, compared with 8,900 in 2001.
The study which began 20 years ago involved 4,124 Australians of European descent living in New South Wales, Queensland and Victoria.
Lead author Dr. Kevin Brown, also at the Queensland Institute of Biomedical Research in Brisbane, says a variation in the ASIP gene is implicated in the skin cancer and identifying mutations that are common could help explain why most people with melanoma developed the cancer, while others were protected.
Other research carried out by another international team including scientists from Australia, has also found a link between variations in genes that control the colour of skin, hair and eyes and an increased risk of deadly tumours.
Skin cancer is one of the most common malignancies and people with fair skin have a higher chance of getting tumours than those with darker complexions.
Scientists from DeCode Genetics Inc. also suggest gene testing would more precisely identify an individual's risk, and who may need to be targeted for therapy.
DeCode's study looked at DNA from more than 70,000 people with and without cancer to identify the link.
The results of both studies are published in the journal Nature Genetics.
The goal of the vaccine is to prompt the immune system to recognize amyloid beta protein and remove it. To create the vaccine, Bowers and the research group use a herpes virus that is stripped of the viral genes that can cause disease or harm. They then load the virus container with the genetic code for amyloid beta and interleukin-4, a protein that stimulates immune responses involving type 2 T helper cells, which are lymphocytes that play an important role in the immune system.
The research group tested several versions of a vaccine. Mice were given three injections of empty virus alone, a vaccine carrying only the amyloid beta genetic code, or a vaccine encoding both amyloid beta and interlueikin-4, which was found to be the most effective.
"We have learned a great deal from this ongoing project," Bowers said. "Importantly, it has demonstrated the combined strengths of the gene delivery platform and the immune shaping concept for the creation of customized vaccines for Alzheimer's disease, as well as a number of other diseases. We are currently working on strategies we believe can make the vaccine even safer."
Bowers expects the vaccine eventually to be tested in people, but due to the number of studies required to satisfy regulatory requirements, it could be three or more years before human trials testing this type of Alzheimer's vaccine occur.
Grants from the National Institutes of Health supported the study. In addition to Bowers, authors of the Molecular Therapy article include Maria E. Frazer, Jennifer E. Hughes, Michael A. Mastrangelo and Jennifer Tibbens of the Medical Center and Howard J. Federoff of Georgetown University Medical Center.
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