CURICULUM VITAE of Patrick Auberger
Date of Birth December 16, 1957, Annecy, Haute-Savoie (74), France
Education
1983: PhD in Cellular and Molecular Pharmacology, UNS
1994: HDR: Enabling for Research Management, UNS
Nationality French
Professional experience
1985: INSERM U145 Chargé de Recherche Second Class
1989: INSERM U364 Chargé de Recherche First Class
1994: INSERM U364 Directeur de Recherche Second Class
1997: Head of the CJF INSERM 96.05
2000-2007 Head of INSERM Unit 526
2001: Directeur de Recherche First Class
2003-2009 Interface Grant with the CHU
2008: Head of Team 2, INSERM U895 (C3M)
2008: Scientific Deputy Director of INSERM U895 (C3M)
2010: Translational Research Hospital Contract
Institutional peer evaluation
2003-2008 Member of the INSERM Scientific Commission 2
2004-2008 Member of the Clinical Research Delegation
2001-2005 Member of the Clinical Research Commission (representing INSERM)
2002-2006 Member of the Scientific Council for Clinical Research CHU Nice
2003-2006 Member of the Scientific Committee of Biointerference (Start-Up)
Since 2005 Deputy President of the Scientific Council of the Nice Medicine Faculty
Since 2005 Member of the INCA Scientific Council
Since 2008 Member of the Scientific Council of the LNCC
Since 2008 President of the Scientific Advisory Board of INSERM U866
Since 2010 Member of the Scientific Council of the Nice Medicine Faculty
Since 2010 Member of the Administrative Council of the Nice Medicine Faculty
Since 1989 Member of the French Society for Immunology
Since 2004 Member of the International Cell Death Society
Peer review EMBO J, Blood, J Biol Chem, Oncogene, Faseb J, Autophagy, Cell Death Diff, Leukemia, Cancer Res, BBRC, Mol Cancer Ther, JID
Edition Senior Editor of the American Journal of Cancer Research
Expert for MRC, Welcome Trust, AERES, LNCC, ARC, ANR, Region
Thesis/HDR Participation in more than 120 PhD and HDR
Distinction Prix Joseph Amalric de la Ligue Nationale Contre le Cancer 1995
Teaching 12h per year (Medical School students and Master 1/2)
Training 18 Thesis and more than 40 Master students
License Production of an antibody directed against legumain. 2007,
DVTT N° 05213
Our project iinclude three main topics. In the first one, we will continue to explore the mechanisms of resistance to TKI in Chronic Myelogenous Leukemia (CML). Several candidate proteins involved in resistance have been identified and the role of Fyn, Axl, Erk1/2, SPARC and Itgb3 will be more specially investigated in cell lines and primary cell from CML patients. In addition, our recent findings strongly suggest that targeting autophagy is an original and novel therapeutic avenue for this disease and other hematopoietic malignancies. In this context, we have identified compounds including Resveratrol, Acadesine and original analogues of Acadesine (ongoing license) that are able to eradicate TKI-resistant CML cells. The molecular mechanisms highlighting the effect of these agents will be determined. Our goal is to propose in a near future, clinical trials in CML using such compounds that are currently tested clinically for other tumoral and non-tumoral pathologies. Interestingly, both molecules behave as metabolic stress-inducing agents and their implication in the AMPK/mTORC pathway will be analyzed (Grant PLBioINCA 2011-2013). In addition, as AMPK is a universal inductor of autophagy we will also investigate the role of autophagy in physiological hematopoietic cell differentiation. Several lines of evidence support a crucial role for autophagy in erythroid differentiation and we reported recently that autophagy is important for megakaryocytic differentiation of the K562 CML cell line. The role of autophagy and cathepsins, a family of cystein proteinase involved in the regulation of autophagy will therefore be analyzed during erythroid and megakaryocytic differentiation of hematopoietic stem cells. The second aspect of our project is devoted to analyze the role of Lyn in keratinocyte biology and psoriasis. The main tasks of this axis will be to i) validate LynDN mice as a new model of psoriasis, ii) characterize Lyn cleavage and caspase activation in keratinocytes in vitro, iii) uncover the molecular mechanisms responsible for psoriasis in LynDN mice, iv) evaluate Lyn expression and cleavage in human psoriasis and v) analyze the immune system of LynDN mice. Finally, the third topic of our poject deciphers the role of Bcl-B in the physiopathology of B cells and plasma cells. The recent production by our Team of an EmBcl-B transgenic mice model that recapitulates the main features of multiple myeloma was a pre-requisite to study the physiological role of this protein. Moreover, the function of Bcl-B as an inhibitor of both apoptosis and autophagy will be also evaluated. Finally the possibility to shift Bcl-B activity from an antiapoptotic to a proapoptotic function with specific small peptides will be used in order to validate new potential therapeutic strategies in MM.