Kay Kendall Leukaemia Fund Intermediate Research Fellow
I completed my DPhil in the lab of Louis Mahadevan, Department of Biochemistry, where I studied the role of dynamic histone acetylation in the control of gene expression. I joined the Milne lab in 2016, where my research is directed towards understanding the role of enhancers in leukaemia, focusing on MLL-AF4 ALL. I am interested in using this knowledge to identify novel targets to disrupt epigenetic regulation as a therapeutic intervention.
I use a variety of high-throughput techniques to understand the regulation of chromatin and gene expression, including ChIP-seq (and small cell number techniques such as ChIPmentation), ATAC-seq and RNA-seq. In addition, I use the 3C technology Next Generation Capture-C to investigate the physical association of enhancers and promoters, and how this is regulated. I also have an interest in the role of the immune system in cancer targeting, in collaboration with the Multi-dimensional Innate and Adaptive Immune Responses lab (HIU), particularly how cancer cells can manipulate the extracellular environment to suppress immune activity.
In addition to my research activities, I teach topics in molecular cell biology for Biochemistry undergraduates at Oxford. I was a stipendiary lecturer at Worcester College from 2014-2019, and I continue to be involved in tutorials and admissions at Worcester and a number of other colleges.
Potent, p53-independent induction of NOXA sensitizes MLL-rearranged B-cell acute lymphoblastic leukemia cells to venetoclax.
Fidyt K. et al, (2022), Oncogene
A human fetal liver-derived infant MLL-AF4 acute lymphoblastic leukemia model reveals a distinct fetal gene expression program.
Rice S. et al, (2021), Nat Commun, 12
Defining genome architecture at base-pair resolution.
Hua P. et al, (2021), Nature, 595, 125 - 129
A KMT2A-AFF1 gene regulatory network highlights the role of core transcription factors and reveals the regulatory logic of key downstream target genes.
Harman JR. et al, (2021), Genome Res
BET inhibition disrupts transcription but retains enhancer-promoter contact.
Crump NT. et al, (2021), Nat Commun, 12