Research
Monoallelic deletion of the short arm of chromosome 17p (del17p) is a common feature of many cancers, including haematological, pancreatic and colorectal. This chromosomal abnormality has been predominantly studied in haematological malignancies, and the clinical features (rapid disease progression, resistance to therapy, short survival) have to date been primarily linked to loss and/or dysfunction of the tumour suppressor TP53 which is located at 17p13.1. However, chromosome 17p also contains over 300 other protein coding genes as well as over 300 non-coding RNAs (miRNA and lncRNA), and the impact of the deletion of these is poorly understood.
In our group, we are interested in how the loss of heterozygosity and resulting haploinsufficiency of these genes may influence cell behaviour. We are particularly interested in the role del17p plays in the development of Richters transformation, whereby chronic lymphocytic leukaemia (CLL) transforms into an aggressive form of diffuse large B cell lymphoma. Using CRISPR/Cas9, our lab was the first to generate an isogenic CLL cell line that contains a deletion of chromosome 17p. I work closely with Professor Joseph Slupsky, who is an expert in CLL biology, and Professor Nagesh Kalakonda, a clinician scientist.
Research grants
Understanding the role of SNHG32 as a regulator of adaptive resistance in lymphoid cancers.
NORTH WEST CANCER RESEARCH INCORPORATING CLATTERBRIDGE CANCER RESEARCH (UK)
January 2027 - July 2030