A gene previously shown to be linked to obesity may also increase the risk of a deadly form of skin cancer, say researchers writing in Nature Genetics.
Analysis of data from 73,000 people, led by the University of Leeds, found a specific section of the “fat gene” was associated with malignant melanoma.
It is the first time the gene has been linked with a specific disease independently of weight.
The results suggest a wider role for the gene than originally thought.
Malignant melanoma is the fifth most common cancer in the UK with about 12,800 new cases and about 2,200 deaths each year.
An international team analysed genetic data from the tumours of 13,000 malignant melanoma patients and 60,000 unaffected individuals.
They found that those with particular variations in a stretch of DNA within the “fat gene” or FTO gene, called intron 8, could be at greater risk of developing melanoma.
Previous research linking the FTO gene with obesity found that variants in a section called intron 1 are linked with being overweight and overeating.
Several other diseases have been linked to the gene but also to having a high body mass index.
This is the first time that researchers have found a link between the FTO gene and a disease which is not linked to obesity and BMI.
It opens up a new direction in work looking at how the gene functions as until now the focus has been on its effects on weight gain and factors such as regulating appetite.
Study author, Dr Mark Iles, a senior research fellow at the Leeds Institute of Molecular Medicine, said: “This is the first time to our knowledge that this major obesity gene, already linked to multiple illnesses, has been linked to melanoma.
“This raises the question whether future research will reveal that the gene has a role in even more diseases?”
He added: “When scientists have tried to understand how the FTO gene behaves, so far they’ve only examined its role in metabolism and appetite.
“But it’s now clear we don’t know enough about what this intriguing gene does.”
Dr Julie Sharp, Cancer Research UK’s senior science information manager, said: “These are fascinating early findings that, if confirmed in further research, could potentially provide new targets for the development of drugs to treat melanoma.
“Advances in understanding more about the molecules driving skin cancer have already enabled us to develop important new skin cancer drugs that will make a real difference for patients.”
She added the best way to prevent melanoma was to avoid damage caused by too much sun exposure and sunbeds.
“Getting a painful sunburn just once every two years can triple the risk of melanoma.”
–Courtesy of BBC News
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(CBS News) Childhood obesity for some kids may be triggered by two genetic variations, according to a new study.
Although poor food choices and lack of exercise are often blamed for the country’s burgeoning childhood obesity epidemic, the researchers behind the new study say a genetic component may also share some responsibility.
“This is the largest-ever genome-wide study of common childhood obesity,” study author Dr. Struan F.A. Grant, associate director of the Center for Applied Genomics at The Children’s Hospital of Philadelphia, said in a written statement. “As a consequence, we have definitively identified and characterized a genetic predisposition to common childhood obesity.”
The researchers looked at 14 earlier studies that included 5,500 obese kids and 8,300 healthy control subjects. By genotyping the DNA from children with obesity, the researchers found two novel variations – one near a gene on the 13th chromosome and the other near chromosome 17 – that had never been previously implicated in other studies as related to obesity. The genes might be tied to intestinal function, but the researchers aren’t certain.
The genes are “very common in the population,” Grant told HealthDay. The genes can be identified in adults but express much weaker, suggesting the genes’ biggest impacts are during the first years of life.
The findings are published in the April 8 issue of Nature Genetics.
“This work opens up new avenues to explore the genetics of common childhood obesity,” Grant said in the statement. “Much work remains to be done, but these findings may ultimately be useful in helping to design future preventive interventions and treatments for children, based on their individual genomes.”
According to WebMD, inheriting the genetic marker on chromosome 13 would increase a child’s obesity risk by 22 percent, and inheriting the other market would contribute to a 14 percent raised risk.
More than one-third of all U.S. children and adolescents are overweight or obese, and childhood obesity rates have tripled over the past 30 years.
But the findings don’t suggest that obesity is exclusively caused by genes. Experts commenting on the study said babies born with the genes may not necessarily grow into obese children.
“This does not mean that those who are genetically susceptible are destined to become obese adults, because a healthy lifestyle remains an important factor that can reduce one’s genetic susceptibility,” Dr. Ruth Loos, director of the Genetics of Obesity and Related Metabolic Traits Program at Mount Sinai School of Medicine in New York, told USA Today. “If some of these genes turn out to be drug-able targets, then maybe this could lead to new medication,” Loos said. “But that is indeed years away.”
“We may know more about childhood obesity, but until there’s a magic bullet, the treatment will be the same,” Dr. Keith-Thomas Ayoob, assistant clinical professor of pediatrics at the Albert Einstein College of Medicine in New York City, told MedPage Today. “Kids still need to have better diets and they really need to be more active.”