"Cancer gene" twice as likely to be defective in children with autism 

Researchers at the UC Davis MIND Institute have found that a gene whose role is to suppress cellular damage is twice as likely to be defective in children with autism spectrum disorder (ASD) and that the deficit is also present in their fathers. This is more common among children with a more severe case of ASD. ASD is a developmental disability characterized by difficulties in social interaction and communication and by restricted or repetivite patterns of thought and behavior. The tumor suppressor p53 stops cell division to allow the repair of damaged DNA. In a study conducted on mice, a p53 deficient mice and altered p53 and p53-dependant mice it has been reported in autism via interaction between p53 and another tumor suppressor gene known as Pten. The study suggests there is a link between DNA repair capacity and genomic instability influenced by environmental triggers. The research was conducted on children with autism from ages 2-5 and also their parents. The research examine the mtDNA copy number and deletions and p53 gene copy ratios. The mtDNA deletions and high p53 gene copy ratios were more common in children with autism and their fathers. Deletions of mtDNA and altered p53 gene copy ratios result mainly from genetics. Altered p53 originate from a deficient parental DNA repair capacity, particularly in children with more severe versions of the disorder. 

The article was both interesting and informative. It demonstrated how a cancer gene is defective in a child with autism. Its interesting how the article states that this is due to the childs father and how they were able to find this information out. I think this article was overall a good read and i learned something new from it. 

 

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