Dr Merino received her PhD from the University of Burgundy, in France, studying the molecular mechanism involved in the extrinsic pathway of apoptosis, in particular TRAIL-mediated cell death. In 2008 she joined the Molecular Genetics of Cancer Division at WEHI as postdoctoral fellow to study the role of the intrinsic pathway of apoptosis in immune homeostasis and cancer progression.
Dr Merino’s work was extended to the study of BH3 mimetics, small molecules that inhibit pro-survival proteins. In collaboration with the pharmaceutical companies Genentech and AbbVie (US), Dr Merino and colleagues showed that the new BH3 mimetic ABT-199 (Venetoclax) was highly toxic in leukemic cells, but not in a large subset of normal hematopoietic cells. In 2012, Dr Merino joined the Stem Cells and Cancer Division (WEHI), to study the effect of ABT-199 on breast cancer. She found that this BH3 mimetic has a great synergistic effect in combination with Tamoxifen and mTOR inhibitors in the treatment of oestrogen positive breast cancer. More recently, in collaboration with Servier (France), she found that the inhibition of MCL-1 using new specific inhibitors might benefit women with triple negative and HER2 amplified breast cancer. Altogether these pre-clinical models have contributed / will contribute to the clinical development of this new class of drugs for the treatment of both leukaemia and breast cancer.
Since April 2017, Dr Merino is a laboratory head at the Olivia Newton John Cancer Research Institute. Her group focuses on breast cancer progression and heterogeneity. She is characterising the ability of PDXs (Patient Derived Xenografts) to metastasise in immunodeficient mice, and performed transcriptomic analysis of circulating tumour cells and metastasis to identify the survival pathways responsible for the survival of disseminated cells. She is also developing new PDX models using cellular barcoding to track the clonal origin of metastases in different organs. These models will be useful not only to understand how the tumour spreads, but also how current therapies influence tumour heterogeneity.
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Olivia Newton John Cancer Research Institute
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