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Dr Philippe Juin obtained his PhD degree in 1995 for his work on mitochondrial assembly. During his post-doc in the UK, he defined the mitochondrial apoptotic pathway as one major intrinsic tumor suppressor mechanism triggered by oncogene deregulation. As an Associate Researcher at INSERM, he led increasingly ambitious investigations of the regulation of the mitochondrial apoptotic pathway by Bcl-2 family members in human cancer cells and he created in 2012 an INSERM team that specifically focusses on the role of this pathway in stress adaptation and tumor escape. This team gained international recognition for its fundamental and translational research on the regulation of therapeutic response and tumor progression by BCL-2 family members (Nature Rev. Cancer 2013, Cell Rep. 2016, EMBO Rep. 2018 in press). This team contributed to establish that changes in mitochondrial apoptotic priming are at the core of breast cancer cells response to cytotoxic stress and treatments, being influenced by oncogene signaling, tumor suppressor pathways, therapy and tumor context. This team recently established a new function of BCL-2 members, that contributes contributing to the self renewal of breast cancer initiating cells, and defined the molecular events involved (Nature Comm., 2017).
Dr. Ju's major research interest is in the development of miRNA based therapeutics and biomarker in gastrointestinal cancer. The Ju laboratory studies the mechanisms of microRNAs in cancer stem cell resistance, epithelial to mesenchymal transition (EMT), autophagy, and apoptosis. His group made initial discovery of the regulatory relationship between p53 tumor suppressor and microRNA. Dr. Ju and his group discovered the superior stability of microRNA in archival formalin fixed paraffin embedded (FFPE) clinical specimens which serves as the foundation of microRNA based biomarker discovery.