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The Kids Research Institute Australia researcher, Dr Raelene Endersby, will work to develop less toxic treatments for children with brain cancer, thanks to support from Cancer Council WA.
A new combination of drugs could help to increase survival rates with fewer side effects for some children with one of the most aggressive forms of childhood brain cancer.
While profound treatment responses have been realised using immunotherapy for some cancer types, this is yet to be seen for paediatric brain cancer patients.
Neuroblastoma is a complex childhood cancer of the nerve cells and the most common solid tumour in children outside of the brain. The average age of diagnosis is 1-2 years and tragically 50% of children with high-risk neuroblastoma lose their battle within five years.
Radiation therapy is an essential component of brain cancer treatment. However, the high doses currently required are extremely damaging to the growing brains and bodies of children.
Tissue resident memory T cells are cancer killing immune cells that have emerged as key players in immune-mediated control of solid cancers, as well as being markers of prognosis and predictors of response to immunotherapy.
Co-Head, Brain Tumour Research
Head of Paediatric and Adolescent Oncology and Haematology, Perth Children’s Hospital; Co-head, Brain Tumour Research Program, The Kids Research Institute Australia
DNA methylation-based classification is now central to contemporary neuro-oncology, as highlighted by the World Health Organization classification of central nervous system tumors. This expansion is a result of newly identified tumor types discovered through our large online repository and global collaborations, underscoring CNS tumor heterogeneity.
Chemotherapy often kills a large fraction of cancer cells but leaves behind a small population of drug-tolerant persister cells. These persister cells survive drug treatments through reversible, non-genetic mechanisms and cause tumour recurrence upon cessation of therapy. Here, we report a drug tolerance mechanism regulated by the germ-cell-specific H3K4 methyltransferase PRDM9.