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© Jacob SEELER & Anne DEJEAN, Institut Pasteur
Immunostaining of PML nuclear bodies involved in acute promyelocytic leukemia

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CV

Anne Dejean is Research Director at INSERM, Professor at the Institut Pasteur and Head of the Laboratory of Nuclear Organization and Oncogenesis/INSERM U993. She graduated from Pierre et Marie Curie University in Paris and earned her PhD in Pierre Tiollais’ lab at the Institut Pasteur in 1983. Member of EMBO and of the French Academy of Sciences, she has received the Gagna and Van Heck Prize in 2003, the L’Oréal-UNESCO for Women in Science Awards in 2010, the Grand Prix INSERM in 2014 and the Sjöberg Prize in 2018. She was awarded two ERC Advanced Grants, in 2011 and 2018.

A molecular biologist, Anne Dejean investigates the molecular and cellular mechanisms involved in the development of human cancers. She discovered that HBV may act as an insertional mutagen in liver cancer. Since then, Dejean’s team has contributed several pioneering concepts in the areas of nuclear receptors and tumorigenesis with their discovery that retinoic acid receptors (RAR) genes are mutated in human cancers.  They first found such a mutation in HBV-associated liver cancer and cloned the RARb gene. They then discovered the PML-RARa oncogenic fusion protein as the causative genetic event in acute promyelocytic leukemia (APL), dissected its molecular components, and provided a rationale for the retinoic acid and arsenic dual treatment for APL, the first described and so far most efficient example of oncogene-targeted therapy. Dejean’s team then demonstrated that a particular sub-nuclear structure, which they named the PML Nuclear Body, is disrupted in APL and showed that both retinoic acid and arsenic are able to correct this cellular defect.

In the last twenty years, A. Dejean’s lab contributed to the emergence of the SUMO field by deciphering important biological and pathophysiological activities of this process in regulating nuclear events.  Notably, A. Dejean and colleagues demonstrated that arsenic induces the polysumoylation of PML-RARa as well as its degradation in APL, they generated the first mouse models for the graded ablation of sumoylation and unveiled an epigenetic role for SUMO that, in marking chromatin-associated proteins by a unique modifier, represses innate immunity and safeguards cell identity. Recent projects in her lab aim at understanding how SUMO on chromatin regulates cell fate decisions in normal and cancer states.

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