The AVIL gene associated with the development of aggressive brain tumours also plays a key role in two rare, but fatal, types of childhood cancer, new research shows.
Scientists from the University of Virginia have described the process whereby malfunctions in the AVIL oncogene (a cancer-causing gene) play an essential role in the development of the two main subtypes of rhabdomyosarcoma.
'These findings, plus our previous work in brain tumour, suggest that AVIL is an oncogene that, when overactivated, may trigger the development of multiple cancer types,' said study lead Professor Hui Li.
Rhabdomyosarcoma is a common paediatric soft-tissue cancer that primarily affects young children, with a survival rate of less than 20 percent. The two main subtypes are driven by distinct mechanisms.
Professor Li and his team initially discovered that AVIL is crucial to the development of glioblastomas, the most lethal form of brain cancer, in 2020. Publishing their findings in Nature Communications.
In this latest study, the team build on that research and propose that AVIL is even more important than previously realised, as researchers were able to demonstrate that AVIL is abnormally upregulated in rhabdomyosarcoma. They were also able to show (using mice and cells in culture) that silencing the gene prevents tumour formation.
'We accumulated multiple lines of evidence supporting [the gene] AVIL as [a] powerful driver for both major types of rhabdomyosarcoma,' said Professor Li. 'The tumours are oncogene-addicted to AVIL, which supports the rationale to design therapeutic interventions to target AVIL in this childhood cancer.'
There is currently no targeted therapy for rhabdomyosarcoma. However, the results of this study suggest that targeting AVIL may be a viable approach in the treatment of both types of this cancer. Small molecule incubators could potentially be used to suppress the AVIL gene, but more research is needed before patient trials can take place.
Professor Li and his team published their latest findings in the journal PNAS.
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