In Ireland Tríona Ní Chonghaile joined the Physiology and Medical Physics Department in the Royal College of Surgeons in Ireland, in 2015. She was recruited under the Strategic Academic Recruitment program (StAR), as a Research Lecturer and became a tenured Lecturer in 2018.

She completed her PhD in Biochemistry in 2008, with Prof. Afshin Samali, at the National University of Ireland, Galway. She had an interest in translational science and moved to the Dana-Farber Cancer Institute/Harvard Medical School to do a postdoc with Prof. Anthony Letai, which was funded in part by a Multiple Myeloma Research Foundation Fellowship. In 2014, she moved back to Ireland and joined Prof. William Gallagher’s group as a Research Fellow working on identifying novel therapeutics for triple negative breast cancer.

Dr. Ní Chonghaile’s lab is interested in understanding why certain cancers are sensitive to chemotherapy induced cell death while others are resistant and how best to treat resistant cancers. She has a particular interest in the BCL-2 family of proteins that regulate the mitochondrial cell death pathway. She uses an innovative technology called “BH3 profiling” to functionally interrogate the cell death signalling in both leukaemia and breast cancers to identify novel effective combinations of treatments.

Based on her work, she received the European Association of Cancer Research (senior) young scientist of the year award (2014), along with receiving the prestigious L’Oréal-UNESCO For Women in Science UK&I Fellowship (2015). Her research is funded by grants from SFI-HRB-Wellcome Trust, H2020 and Breast Cancer Now. She has published in high-impact journals including first author papers Science and Cancer Discovery.

Abstract:
Cytotoxic chemotherapy is the standard of care for patients with triple negative breast cancer (TNBC).

Most patients with advanced TNBC progress after chemotherapy and die from metastatic disease. Currently, no established targeted therapeutics or biomarkers of outcome/response have been clinically approved in the context of TNBC. To identify novel therapeutics for the treatment of chemoresistant TNBC, we performed a high-throughput screen to identify small molecules that are cancer selective but can kill drug-resistant TNBC cells.

We screened a total of 30,000 compounds. To identify the mechanism of action of the lead compound we used a genetic approach to generate an RNAi signature for the compound, which indicated the lead compound was most likely that of histone deacetylase inhibitor (HDAC). Using an in vitro HDAC inhibitor screen, we identified that the compound specifically inhibited HDAC6. We are currently studying the role of HDAC6 in TNBC cells.