CV Science

Julie Guillermet-Guibert PhD Cell Biology, Pharmacology

Course and current status

2021-now             Research Director, DR (Inserm)

Group Leader “SigDYN: Integrated Cell Signalling & PI3K isoforms”, CRCT Inserm / CNRS / Université Paul Sabatier

2014-2021           Appointed Researcher, “CRCN” (Inserm)

Group Leader “SigDYN: Cancerogenesis & PI3K Isoforms”, CRCT Inserm / Université Paul Sabatier

2010-2014           Appointed Researcher, “CRCN” (Inserm)

Team “Translation and signaling in pancreatic disease”, I2MC, then CRCT Inserm / Université Paul Sabatier

Scientific summary

SigDYN - DYNAMIC SIGNALLING

I have been working in the field of cell signalling since the beginning of my PhD training. I focused particularly on phosphoinositide signalling starting from my postdoctoral training at the Ludwig Institute for Cancer Research in London. At the time in 2005, the first mutations on the PI3KCA encoding gene were discovered and functions of the various members of this lipid kinase family were unknown. The Ludwig Institute supported my post-doctoral laboratory to create unique genetically modified mouse models that inactivate PI3Ks. Since then, my group and myself actively participate to pioneer and develop novel concept in PI3K signaling and we continue to contribute to the dissemination of the related research tools in France and in Europe. These models are also stored at the EMMA European Mouse Mutant Archive, an EU-funded organization.

In 2010, I was recruited permanent Researcher in Inserm and pursued my activity in France, expanding on translational research. I have been leading a research group since 2014. I mentored 3 post-doctoral fellows, 3 MD/PharmD residents, of whom 3 are faculty member in France (Inserm or Hospitals) and trained/is training 8 PhD students. I currently head the “SigDYN: Integrated Cell Signalling & PI3K isoforms” team at The Cancer Research Center of Toulouse (CRCT).

My group actively contributed to the renewed appraisal of PI3K importance in health and disease. Within European consortia, we identified regulations of and by PI3Ks in cancer and inflammation. Our major basic studies led to the identification of KRAS-PI3K signaling being necessary for pancreatic cancerogenesis.

Currently,

- we think it is important to understand the context-dependent mechanisms limiting the efficacy of PI3K inhibitors (tumor-microenvironment interactions);

- we study the contribution of mechanical cues to cancer cell signaling (PI3K and beyond);

- we translate our findings into clinical research.

Keywords genetically modified mouse models, PI3Ks, cell signalling, GPCR, isoform specificity, pancreas, inflammation, metabolism, ovary, ascite, primary samples, oncogene-induced cancerogenesis, kinase, lipid signalling, Akt, mTOR, mechanobiology, bioprinting, biotechnologies