Contact
Biography
Dr Kellaway received her PhD from the University of Manchester in 2016, investigating stem cells from patients with Congenital Hyperinsulinism as a model system. Following this Sophie moved to University of Birmingham to work in the lab of Professor Constanze Bonifer, firstly utilising mouse embryonic stem cells to study the molecular roles of four different RUNX1-associated Acute Myeloid Leukaemia driver mutations including RUNX1-ETO, and subsequently dissecting the pathways which make RUNX1-ETO expressing stem cells grow. Sophie joined the University of Nottingham as Assistant Professor in Cancer Sciences in October 2023.
Expertise Summary
Dr Kellaway's research is focused on blood cancers - specifically Acute Myeloid Leukaemia. She studies gene regulation using integrative genome-wide methods including RNA-seq, ATAC-seq, ChIP-seq, combining laboratory studies with bioinformatic methodology, with a view to identifying novel therapeutic targets to improve treatment outcomes.
Research Summary
Current research is focussed on two main strands:
1. Dissecting functional heterogeneity in RUNX1-driven Acute Myeloid Leukaemia
This project combines CRISPR-Cas9 gene editing and genome-wide gene regulation studies to understand the biochemical basis of different RUNX1 mutations and how this impacts upon varied disease presentation and response to treatment. Research funded by a Leukaemia UK John Goldman Fellowship.
2. Understanding the signals which make leukaemic stem cells grow
We recently showed that leukaemic stem cells in t(8;21) Acute Myeloid Leukaemia respond to specific, lineage-inappropriate signals to promote their growth. This discovery is now being progressed in several directions.
(i) We are seeking to understand precisely how leukaemic stem cells exit quiescence, grow and mature.
(ii) By repurposing approved therapeutics targeting the identified signalling pathways, we are seeking to determine if these could be used to prevent relapse in leukaemia patients.
(iii) We are investigating how conserved this mechanism is across leukaemias with different driver mutations.