CV Science

Michaela Fontenay MD, PhD, Professor of Hematology

Course and current status

1 - Titles and diplomas

1989            Medical Doctor of University Paris 7

1995            Ph. D. of University Paris 7

1997            Assistant Professor, Faculty of Medicine Cochin, University Paris Descartes.

2006            Professor of Hematology, University Paris Descartes.

2011            Professor of Hematology class I, University Paris Descartes

2 – Current functions

         2.1. Teaching at University Paris Descartes

Since 1997    Faculty of Medicine Cochin Port –Royal

Since 2005    Faculty of Medicine Paris Descartes: Hemostasis

                   University diploma of perinatal medicine

                   Master of Onco-hematology University Paris 11

Since 2007    University diploma of infertility

Since 2008    Diploma of specialized medicine in Hematology, and Anesthesiology

         European School of Hematology

Since 2009    Diploma of specialized medicine in Medical Biology

         2.2. Hospital

2012            Head of the laboratory of Hematology, Assistance Publique-Hôpitaux de Paris Cochin-Hôtel-Dieu, Paris

3 – Scientist societies and committees

1994            . Member of the Groupe d'Etudes Hémostase et Thrombose

1995            . Member of the French Society of Hematology and of the International Society of Thrombosis & Hemostasis

2000            . Member of the Groupe Francophone des Myélodysplasies (GFM)

2002-2006     . Member of the Conseil National des Universités (CNU 47-01)

2005             . Member of the scientific board of the European Hematology Association

2006             . Member of scientific board of the GFM

2011             . Expert at the Agence Nationale de la Recherche (ANR)

Scientific summary

Myelodysplastic syndromes (MDS) are clonal disorders of the hematopoietic stem cell characterized by dysplasia on all myeloid lineages and blood cytopenia including anemia in most cases. At early stages, cytological aspects of dyserythropoiesis and a massive apoptosis could be observed. In half of cases, MDS transform in secondary acute myeloblastic leukemia (sAML) with resistance to apoptosis. Comprehensive studies of the pathophysiology of MDS have been conducted to investigate the mechanisms of apoptosis and dyserythropoiesis. Regarding MDS phenotype, the contribution of my team was the demonstration of (i) a Fas-dependent apoptosis due to an overexpression of the Fas receptor and its cognate ligand FasL in early MDS, (ii) the epigenetic extinction of Fas gene during the progression to sAML, (iii) and the evidence for a caspase-dependent cleavage of the erythroid transcription factor GATA-1 in MDS erythroblasts with dyserythropoiesis. Regarding the genotype, the team contributed to the first description of TET2 gene mutation in MDS and sAML, the extensive genotyping of MDS and the studies of relationship between genomic alterations and clinical presentation or prognosis.