Faulty DNA may put people with autism spectrum disorder at a higher risk of cancer, according to a new study.
Researchers at the UC Davis MIND Institute recently discovered that autistic children, particularly those with severe autism spectrum disorder, are significantly more likely to have deficits in a cancer-fighting gene that suppresses cellular damage from environmental stressors.
The study also revealed that their gene deficit was also seen in the fathers of autistic children exhibiting the faulty gene.
"In the presence of some type of environmental stressor, the tumor suppressor p53 stops cell division to allow the repair of damaged DNA ," said Cecilia Giulivi, the senior author of the current paper and director of the Redox Biology Lab at UC Davis, and an affiliate of the MIND Institute.
Giulivi and her team compared blood samples of children with autism to those collected from normally developing children. Researchers also compared the blood samples of parents from both groups of children.
Blood sample analysis revealed that autistic children and their fathers were significantly more likely to have deficits in the p53 gene, which helps protect against environmental stressors.
"Mitochondrial DNA deletions and higher p53 gene copy ratios were more common in children with AU and their fathers. The incidence of Mitochondrial DNA deletions in fathers of children with autism was increased 1.9-fold over fathers of typically neurodeveloping children, suggesting a role for deficient DNA repair capacity not driven by paternal age. Deletions in Mitochondrial DNA and altered p53 gene copy ratios seem to result from genetics (children with severity scores ≥8) and/or act in concert with environmental factors (children with 6-7 severity scores)," wrote researchers, according to the study.
"Deletions in mtDNA and altered p53 gene copy ratios appear to result mainly from genetics, particularly in children with more severe autism, whereas the gene x environment interaction seems to play a greater role in children with autism with less severe symptoms," Giulivi said.
"Altered p53 and mitochondrial DNA gene-copy ratios segregate with autism," Giulivi concluded "These outcomes seem to originate from a deficient paternal DNA repair capacity, particularly in children with more severe versions of the disorder."
The latest findings were published in the journal Pediatrics.
