Our research seeks to understand why brain tumour stem cells make the decision to make more copies of themselves and what can be done to control this.
Brain cancers, as the name suggests, occur inside the skull, and arise because of abnormal cell division. Cells stop behaving the way they should and start making unlimited copies of themselves which the body stops being able to control.
Brain tumours are now responsible for more deaths in the under 40 age group than any other form of human cancer. One particular subgroup of brain tumours is termed glioblastoma, which is the most lethal and also the most common.
Glioblastoma is classified as a rare disease, which means that it affects less than 1 person in 2,000. It is the most aggressive form of brain tumour and spreads very quickly to other brain regions. Because of this infiltration into surrounding tissues, it is impossible to remove surgically, and many cancer cells are left behind resulting in the reappearance of the tumour.
Chemotherapy, radiation and surgery are the classical treatments, but the disease is most often fatal with a typical life expectancy of only one or two years after diagnosis.
Work at CRM
Professor Steve Pollard and his group work on neural stem cells (cells that play a role during normal brain development). In brain tumours the molecular apparatus that controls the ability of the cancer cells to divide is similar to that used by neural stem cells. Therefore, a full understanding of the molecular and cellular events that control neural stem cell fate may reveal new ways to treat this devastating disease.
His team are particularly interested in how to control the balance between stem cell self-renewal (making more copies of themselves) and differentiation (becoming specialised mature cells that no longer divide). They study the molecular “switches” that control genes important for these transitions.
Once particular “switches” are identified, the team hope to identify new drugs that can specifically block self-renewal of brain tumour stem cells.
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