Julie Guillermet-Guibert
  • E-mail :[email]
  • Phone : +33 5 31 22 41 11
  • Location : Toulouse, France
Last update 2018-05-03 22:35:58.692

Julie Guillermet-Guibert PhD Cell Biology, Pharmacology

Course and current status

CRCN INSERM, PhD, HDR, Team leader

Member of European Consortium Phd "PI3K in health & disease"

Member of COST action BM1204 

 

Current situation

since 2014

Group Leader PI3K isoforms, Signalling & Cancerogenesis SigDYN - Team 17

Oncopole de Toulouse, CRCT UMR1037, Toulouse, France. Dir: Prof. Gilles Favre

Program financed by INSERM, ARC, LNCC, ERG-EU Framework 7 program, RITC, UPS, Horizon 2020, Fondation de France, Ligue régionale contre le Cancer, Canceropole GSO

Group composed of 10 persons: 1 INSERM researcher, 1 INSERM Ingeneer, 2 Teaching clinician-researcher, 1 post-doc, 2 PhD Students funded by ITN Horizon2020, 2 Master students, 1 undergraduate

Previous experience:

2010-2014

Junior Group leader CR2 - Equipe 6 CRCT

2005-2010

Post-doctoral Fellow, Ludwig Institute for Cancer Research, London, UK, Then Institute of Cancer, Bart and the London, UK. Lab of Bart Vanhaesebroeck, PhD.

Grants: FRM Fellowship / EMBO Post-doctoral Fellowship (LTF) /Marie Curie Intra-European Fellowships for Career Development (IEF-EU Framework 6 program)

2001-2005

 Ph.D. in the laboratory of Christiane Susini, PhD. INSERM Unit 531, Toulouse, France. Apoptotic effect of the GPCR somatostatin receptor sst2 in pancreatic cancer cells

Grants: Allocation couplée pour Normalien-ENS Lyon

Scientific summary

Why do we call ourselves SigDYN?

Our group studies in vivo dynamic signalling. Pathological cells communicate with environing cells in the organ where they malfunction: this communication create a favorable environment towards the development of the pathology. This heterotypic communication “network” in a pathological organ, called signal network, is thus the result of their interaction but also an Achille’s heel that could be annihilated by targeted therapies.

We accumulated data demonstrating that a family of molecules at the cross bridge of signaling networks, PI3Ks, regulates major physiological and pathological conditions, such as angiogenesis, immune cell proliferation, platelet function, appetite, fertility, cancer, tumoral vasculature. PI3Ks are present in 8 forms, so called “isoforms”. We and others demonstrated that each of class I isoform have different actions. The roles of class II and class III PI3Ks are underexplored.

We study this class of enzyme as paradigm signalling nodes or signalling platforms to understand intercellular communication in physiopathological contexts. We aim in particular to better understand the initiation of the incurable pancreatic inflammatory condition, pancreatitis, or the biology of two lethal pathologies, pancreatic cancer and ovarian cancer.

For this we have access to state-of-the art integrative biology technologies ranging from transcriptomics, phosphoproteomics and physiopathological modeling. We indeed use innovative unique mouse models in which each isoform of PI3K is genetically inactivated, and have access to patient-derived primary cultures of cancer cells but also environning cells prior treatment.

While global PI3K inhibitors are already tested in clinical trials for cancer applications, the implication of the different isoforms of PI3K in cancer is still unclear and intensely debated. This project targets to increase the understanding of the complex relationship within the different isoforms of PI3K in cancer cell signalling in vivo, in order to better target and prevent secondary effects and resistance in this clinical context.

Application of PI3K targeting drugs are also foreseen in other pathologies than cancer.

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

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