Investigating the potential role of CHD1L, a chromatin-remodelling factor involved in the DNA damage response, in childhood neuroblastoma

Neuroblastoma is a very serious cancer, comprising around one tenth of childhood tumours, with around 15 cases in 100 being incurable. Neuroblastoma is unusual as depending on the age of patient diagnosis, cure rates differ greatly due to huge differences in tumour biology. In particular, if children are diagnosed at ages beyond 12 months, the tumour will likely to have spread to other organs, meaning that the disease is likely to resist treatment. The differences between tumours is due to tumours losing large parts, or copying unwanted extra parts, of their DNA by mistake. This causes cells to incorrectly function and become cancerous. Extra copies of one DNA portion, 1q, is found in over one fifth of neuroblastoma patients, associated with poor recovery. We predict that one particular gene (CHD1L) from this 1q DNA region becomes more active in patients with extra 1q DNA, as there are more copies of it. We will measure how much CHD1L is produced in different neuroblastoma cells, to see if in fact more CHD1L is active in cells with extra 1q DNA. This may help lead to simpler diagnostic tests for neuroblastoma patients and to help find the best form of cancer treatment.

Grant Award – Kidscan Pump Priming Grant (2016)
Funding Award – £5,000
Funding Awarded To – Dr Christopher Cooper
Research Location – University of Huddersfield
Lead Researcher – Dr Christopher Cooper