Group Leader PI3K isoforms, Signalling & Cancerogenesis SigDYN - Team 17
CRCT UMR1037, Toulouse, France. Dir: Dr. Jean-Jacques Fournié
Program financed by INSERM, ARC, LNCC, ERG-EU Framework 7 program, RITC, UPS, Horizon 2020, Fondation de France, Ligue régonale contre le Cancer, Canceropole GSO
currently 3 PhD Students funded by LNCC, ITN Horizon2020- 1 Master student funded by Inca
group composed of 12 persons: 1 INSERM Ingeneer, 2 Clinicians, 4 Teaching clinicians or researchers, 1 post-doc
Junior Group leader CR2 - Equipe 6 CRCT - C Susini puis S Pyronnet
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)
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
PI 3-kinases (PI3Ks) are key signal transduction enzymes which are generally considered to be excellent new targets for therapeutic interference. Mammals have multiple PI3K isoforms.
We study the isoform-specific role of the signalling enzymes PI3Ks using new unique mouse models in which each isoform of PI3K is genetically inactivated.
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 in this clinical context.
We focus our attention on two lethal pathologies with no treatment, pancreatic and ovarian cancers.
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