CV Science

Paulo De Sepulveda PhD

Course and current status

• Head of the Signaling, Hematopoiesis Laboratory at CRCM (Centre de Recherche en Cancerologie de Marseille). The group is composed of 2 Inserm scientists, 2 Technicians, 1 postdoctoral fellow, 4 PhD students. Our reserach is financed by Fondation ARC, Cancéropole PACA, Fondation Leucémi Espoir.

• INSERM Scientist since 2000, Centre de Recherche en Cancérologie de Marseille

            Signaling downstream of activated RTK receptors/ Fes and Fer kinases

• 1999-2000 Postdoc at INSERM U199 in Marseille, France

            Socs proteins and KIT signaling

• 1996-1999 Postdoc at Ontario Cancer Institute, Toronto, Canada

            Cloning and characterization of Socs1, a negative regulator of signaling

• 1991-1996 PhD thesis University Paris 7.

            Genetics and developmental biology

• 1990-91 Master in Developmental Biology, U. of Paris, Institut Pasteur.

            Nobel price, François Jacob Laboratory

Expertise

Member of the committee Ligue Contre le Cancer Ile-de-France 2014-now

Member of the committee -Plan Cancer “Formation à la recherche translationnelle” 2014-now

Member of the LIF panel, Marie Sklodowska-Curie Individual Fellowships

Master committee “Développement et Immunologie”, Aix-Marseille University

Scientific summary

Characterization of kinases involved in cell transformation

Protein Kinases are promising therapeutic targets in cancer. While a lot of attention is focused on few well characterized oncogenes/oncoproteins, we postulate that pathologic signalling is still largely unknown and as a consequence a number of essential targets are currently ignored.

Over the last few years, we have performed  screens aiming at identify original novel essential effectors of signalling pathways downstream of the oncogenic c-Kit receptor.

Our current project is split into two axes: a continuation of our search for original targets, and a study of two related kinases FES and FER, previously identified as essential signalling effectors in some leukaemia cells, and their implication in oncogenic mechanisms.