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Characterizing synthetic lethal targets for genome-informed precision cancer medicine

School of Biomedical Sciences

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Dr L Cheung Applications accepted all year round Funded PhD Project (Students Worldwide)

About the Project

Ovarian cancer is a leading cause of cancer death in women. Identification of novel, actionable and effective strategies to treat the disease could significantly contribute to the improvement of patient survival. Genomic aberrations in cancer may represent synthetic lethal targets because cancer cells harboring particular aberrations are contextually more vulnerable to therapeutics than normal cells.

This PhD project will focus on characterizing genomic mutations that cause synthetic lethality by enhancing the responses of ovarian cancer cells to chemotherapy. The project involves genetic screens, function and pathway analyses as well as anti-cancer drug assays. This research will reveal critical mechanisms determining chemotherapy responses in ovarian cancer, with potential to have a major translational impact on patient survival.

This is an exciting opportunity to identify new approach to treat cancer. We are looking for candidates who are highly motivated, fluent in English with wet lab experience in biological or biomedical science. Students will become proficient in cell culture, tumor biology, a wide range of cellular and molecular techniques, and omics analyses.
Dr. Lydia Cheung has a major interest in genomic characterization and the associated signaling of cancer, through which we will understand the biology of treatment response and drug resistance. We have identified a number of genomic alterations that may inform therapeutic responses.
Further details about our work are available at

Faculty information, funding opportunities and application deadlines:


Selected references:
(1) Li X et al. Deregulated Gab2 phosphorylation mediates aberrant AKT and STAT3 signaling upon PIK3R1 loss in ovarian cancer. 2019. Nature Communications 10 (1), 716

(2) Cheung LW et al. Naturally occurring neomorphic PIK3R1 mutations activate the MAPK pathway, dictating therapeutic response to MAPK pathway inhibitors. 2014 Cancer Cell 26 (4), 479-494
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