Researchers at The University of Nottingham have identified three sets of genetic markers that could potentially pave the way for new diagnostic tools for a deadly type of brain tumour that mainly targets children.
The study, published in the latest edition of the prestigious journal 'Lancet Oncology, was led by Professor Richard Grundy at the University's Children's Brain Tumour Research Centre and Dr Suzanne Miller, a post doctoral research fellow in the Centre.
It focuses on a rare and aggressive cancer called Central Nervous System primitive neuro-ectodermal brain tumours. Patients with CNS PNET have a very poor prognosis and current treatments, including high dose chemotherapy and cranio-spinal radiotherapy are relatively unsuccessful and have severe lifelong side-effects. This is particularly the case in very young children.
Despite the need for new and more effective treatments, little research has been done to examine the underlying causes of CNS PNET, partly due to their rarity. The Nottingham study aimed to identify molecular markers as a first step to improving the treatments and therapies available to fight the cancer.
The Nottingham team collaborated with researchers at the Hospital for Sick Kids in Toronto, Canada, to perform an International study collecting 142 CNS PNET samples from 20 institutions in nine countries.
Professor Richard Grundy said: "Following our earlier research we realised that an international effort was needed to bring sufficient numbers of cases together to make the breakthrough we needed to better understand this disease or indeed diseases identified in our study. The next step is to translate this knowledge into improving treatments."
By studying the genetics of the tumours, they discovered that instead of one cancer, the tumours have three sub-types featuring distinct genetic abnormalities and leading to different outcomes for patients.
They found that each group had its own genetic signature through subtle differences in the way they expressed two genetic markers, LIN28 and OLIG2.