Freya graduated from Lancaster University in 2018 with a First Class MSci degree in Natural Sciences. During her degree, Freya developed an interest in biochemistry and cell biology, and their application in cancer biology.
During her research project, Freya turned her focus towards understanding how genomic stability affects cancer risk. Her research project analysed the role of long wavelength ultra violet light (UVA) in increasing risk for the development of skin cancer. In this project, Freya analysed the role of DNA repair signalling networks that repair mutations that occur during UVA exposure.
In her current project, Freya aims to understand how cells regulate DNA replication to maintain genomic stability.
Accurate duplicagtion of the genome during DNA replication is essential for maintaining a healthy genome. Despite its high-fidelity, DNA replication can introduce mutations, particularly at times of replication stress, that are drive tumourigenesis in 10-30% of cancers.
Mutations introduced as a result of replication stress are recognised via ATR signalling pathways, leading to their removal. We have found a novel dinucleotide (diadenosine tetraphosphate, Ap4A) that potentially contributes to maintenance of genomic stability via regulation of DNA replication.
Ap4A is an alarmone that is produced in response to genotoxic, thermal and environmental stress. In breast carcinoma, reduced Ap4A levels correlate with poor prognosis, suggesting that Ap4A may be clinically significant.
Our data suggest that Ap4A can inhibit cellular proliferation by preventing the G1/S transition via inhibition of DNA replication.
Freya’s project aims to determine how Ap4A prevents cellular proliferation, which will potentially aid the design of rational approaches to increase Ap4A levels for use in cancer therapy.