Researchers may have found a previously unknown cause behind the development of pediatric cancer, which they say could enable earlier detection of the disease in young children. A team of scientists at the University of Bergen in Norway, found that children with pediatric cancer were more likely to produce autoantibodies that target several proteins needed for normal DNA repair. They also found that children with pediatric cancer had more of these antibodies even years before their diagnoses.
The study was published in the journal Frontiers in Immunology on October 14. Childhood cancer is rare, but the more common types include blood cancers, like leukemia and lymphoma, as well as tumors of the brain, spinal cord and bone. Adults are more likely to experience cancer of the lungs, breast, colon, prostate and skin, so this means that the cells which the cancers originate from are typically different between childhood and adult cancers.
Where antibodies are used by the immune system to identify and destroy things like viruses and germs, autoantibodies harm your body instead of protecting it, meaning they are a malfunctioning type of antibody. Autoantibodies can mistake healthy tissue for something unwanted in the body and target those rather than the substances that can make you unwell. This can lead to the development of a series of autoimmune diseases like type 1 diabetes, lupus, Graves' disease, multiple sclerosis, rheumatoid arthritis, and many others.
It is not yet clear what causes the immune system to accidentally produce autoantibodies, though some believe it could be down to a certain trigger, like an infection that stresses or damages the immune system, or environmental factors like exposure to certain toxins, or even genetics. The researchers tested tumor and blood samples between 2014 and 2017 from 175 adults and children with sarcoma or acute lymphoblastic leukemia, through the NoSarC Norwegian Sarcoma Study, the Norwegian Childhood Cancer Biobank, and the Oslo University Hospital Cancer Research Biobank. These samples were compared with healthy anonymized people such as blood donors and children participating in the Bergen Growth Study or visiting a clinic in Bergen.
They found that children aged between two and 19 who had pediatric cancer had a significantly higher number of IgG class antibodies—ones which mainly target RAD52, NUMA1, ALKBH7, APBB1, UNG, and MGMT genes, which are heavily involved in DNA repair. Study author Ola Myklebost, who is also a professor of molecular oncology at the University of Bergen, told Newsweek that it is already known that autoantibodies can be "induced by mutated proteins in the cancer," however, their findings "did not fit this picture." Instead, they uncovered something different. "We showed that patient autoantibodies could enter cells and even nuclei, and could bind and tie up these proteins outside the nucleus, thus preventing their repair activity," he said.
He added that through this mechanism, mutation rate was increased, alongside the risk of cancer, which was "substantiated by our detection of such autoantibodies eight-fold more frequent in school children who later got cancer than controls who did not." "This is a very interesting concept as differences in immune response between cancer patients and healthy individuals are very important for immunotherapy application," Dr. Yvonne Saenger, a professor of medicine at Stony Brook University who was not involved in the study, told Newsweek. "More research is needed to determine whether these antibodies impact cellular processes and whether these antibodies develop in response to the tumor or predispose to cancer." Myklebost said "this is an important new hypothesis on how cancer can arise, perhaps not only in childhood cancer, but also in young adults and occasionally in adults too." "More work is required to prove causality, and also the precise patterns of autoantibodies and their specificities that are critical.
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