Team members
 

Normal and pathological angiogenesis

Gilles PAGÈS, Research Director, DR1 Inserm
 

Leader

Research Director, DR1 Inserm
Tel: +33 (0)4 92 03 12 32
GP_XXX
 

Current members

PhD student
Tel: +33 (0)4 92 03 12 32
Je prépare mon doctorat sous la direction du Dr Gilles Pagès et du Dr Maeva Dufies. Je travaille sur un nouvel inhibiteur ciblant la kinase Plk1, impliquée dans le cycle cellulaire et surexprimée dans les cancers de la tête et du cou.
Assistant Professor, MCU UCA
Tel: +33 (0)4 92 03 12 28
Research Director, DRCE CNRS
Tel: +33 (0)4 92 03 12 22
The “Tumour Hypoxia and Metabolism" team studies the physiology of the tumour cell under conditions of acidic, nutritional and oxidative stresses. Through a genetic approach, the team seeks to identify new targets with anticancer potential for pre-clinical developments.
Technician, CAL
Tel: +33 (0)4 92 03 12 32
Engineer, Non permanent CNRS
Tel: +33 (0)4 92 03 12 30
PHD in Combined Developmental Exposure to Estrogenic Endocrine Disruptor and Nutritional Imbalance Induces Adult Prostate Lesions: Mechanisms of Action in team of Dr. Benahamed mohamed at C3M in Nice. Actually I am interested to understand the role of CD44 and CD98, the chaperones of the major import carriers of amino acids, and in particular the XCT.
Researcher, CRCN Inserm
Tel: +33 (0)4 92 03 12 27
Since 1991, I work on ERK signaling pathway in the team of Jacques Pouysségur. Recently I have been trying to unravel the specific roles of ERK1 and ERK2 isoforms. By combining sequence comparison with protein expression in all clades of vertebrates, we propose that both isoforms are functionally redundant. Currently we focus on comparing and understanding the mechanisms regulating ERK1 and ERK2 expression.
Researcher, CRCN CNRS
Tel: +33 (0)4 92 03 12 28
Researcher, CRCN Inserm
Tel: +33 (0)4 92 03 12 30
Researcher, CRCN CNRS
Tel: +33 (0)4 92 03 12 29
 

Alumni

Researcher, Non permanent CNRS
Tel: +33 (0)4 92 03 12 29
I work on the unexpected role of the lymphatic marker VEGFC in brain cancer medulloblastoma after irradiation treatment. I try to understand why different medulloblastoma subtypes do not equally respond to the same treatments. We have discovered that tumoral VEGFC expression determines the cancer fate after treatment by changing the cell phenotype.
Research teams