Ralf H. Adams

After studying biochemistry at the University of Bayreuth, Ralf Adams started his research career at the Max-Planck-Institute for Brain Research and the Goethe University Frankfurt in Germany, where he obtained his Ph.D. in 1996. His work involved the cloning of new members of the semaphorin gene family and the characterization of their function in axon guidance.

Next, he moved to Rüdiger Klein's laboratory at the European Molecular Biology Laboratory in Heidelberg and began to work on the role of Eph/ephrin molecules in blood vessel morphogenesis. Together with his collaborator Angel Nebrada, he also investigated the function of the p38alpha mitogen-activated protein kinase.

In 2000, he became head of the Vascular Development Laboratory at the Cancer Research UK London Research Institute (formerly, Imperial Cancer Research Fund), where he and his laboratory made significant achievements by combining genetic approaches in the mouse with a wide range of cell and molecular biology methods. Several of their discoveries are directly relevant for human pathologies. For example, they were the first to show that the Eph receptor ligand ephrin-B1 controls skeletal morphogenesis and that defects in the human gene (EFNB1) lead to Craniofrontonasal Syndrome (CFNS). A different project has connected the cytoplasmic multi-PDZ domain protein GRIP1, an interaction partner of Eph/ephrin proteins and other molecules, with the rare but severe human congenital disease Fraser Syndrome. They also demonstrated that Junctional Adhesion Molecules (JAMs) are critical regulators of cell polarity.

Since he has moved as Director to the Max Planck Institute for Molecular Biomedicine and Professor the University of Münster in 2008, Ralf Adams and his group have continued to provide insight into key processes controlling developmental blood vessel growth and, in particular, its regulation by Notch, VEGF and Eph/ephrin signaling.

Geneviève Almouzni Pettinotti

Geneviève ALMOUZNI, PhD (EMBO member, Member of the French Academy of Sciences, fellow of the American Association for the Advancement of Sciences, Director of the Research Center of the Institut Curie from sept. 2013 to sept. 2018 and honorary director since then) is director of research exceptional class at the CNRS. She is Principal Investigator of the Chromatin dynamics team in the Nuclear dynamics research Unit (UMR3664 CNRS/Institut Curie) since 1999. She is a world leader in understanding genome organization and function during development and disease in particular in cancer. She has combined biochemistry, cell biology and physical approaches with advanced imaging to explore chromatin dynamics. Active in the field of epigenetics and European actions, she coordinated the EpiGeneSys Network of Excellence to move epigenetics towards systems biology. She is highly engaged in promoting young scientist career. She received prestigious grants (ERC Advanced Grants) and awards including Woman in Sciences FEBS / EMBO (2013) and the grand prix FRM (2014). She served on the EMBO Council (Vicechair in 2014), ERC Council (2019), chair of the alliance EU-LIFE and co-chairs European FETFlagship initiative LifeTime.

Julian Downward

Julian Downward obtained his bachelor's degree in Natural Sciences from Cambridge University and then studied for his Ph.D. in the laboratory of Michael Waterfield at the Imperial Cancer Research Fund in London, where he established in 1984 the link between a retroviral oncogene (v-erbB) and a cellular growth regulatory protein, the EGF receptor.

In 1986, he moved to Robert Weinberg's laboratory at the Whitehead Institute at the Massachusetts Institute of Technology in Cambridge, MA, where he began work on the role of Ras proteins in human cancer.

In 1989 he started his own lab at the Imperial Cancer Research Fund, now Cancer Research UK London Research Institute, where his lab has provided insights into the molecular mechanisms of function and regulation of oncogenic proteins of the Ras family and the importance of their mutational activation in human tumours.

In 2005 Julian was made a Fellow of the Royal Society, the UK's national academy of sciences, and became Associate Director of the Cancer Research UK London Research Institute.

Jan Hoeijmakers

Jan Hoeijmakers studied biology in Nijmegen. His PhD work on trypanosomes at the Univ. of Amsterdam resolved the molecular basis for antigenic variation by which trypanosomes switch each time surface coats and thereby escape from immune surveillance causing sleeping sickness.

In 1981 he joined the Dept. of Genetics of the Erasmus Univ. to work on DNA repair. He cloned the first of many subsequent human DNA-repair genes allowing elucidation of the reaction mechanism of nucleotide excision repair, discovered the strong evolutionary conservation of DNA repair, elucidated the basis of several enigmatic human repair syndromes, identified a new class of 'basal transcription disorders', generated a large number of DNA-repair mouse mutants that provided valuable insight into the complex etiology of human repair disorders and discovered a very strong, unanticipated link between DNA damage, repair and aging. Some of the repair mutants exhibit dramatically accelerated but bona fide aging limiting lifespan to only 3 weeks. Conditional mutants allowed targeting of accelerated aging to specific organs/stages of development (e.g. mouse mutants with dramatic aging only in the brain), making aging amenable to manipulation. Expression profiling revealed an unexpected similarity between short- and long-lived mice: both suppress the somatotrophic axis. This work led to the identification of a very important 'survival response' that promotes successful aging and counteracts cancer by redirecting energy from growth to defenses.

A new line of research explores the dynamic organization of DNA repair in living cells and intact organisms. His group generated the first mouse mutants with intrinsic defects in the biological clock. He owns several patents and discovered compounds that influence aging. His multi-disciplinary research has received several important awards.

In 2004 he started the 'DNage' whose mission is to provide solutions for medical/health problems associated with aging.

David Ish-Horowicz

Dr Ish-Horowicz gained his PhD at the MRC Laboratory of Molecular Biology in Cambridge on tRNA structure, and conducted postdoctoral work on Drosophila molecular genetics with Walter Gehring at the Biozentrum in Basel, Switzerland. He then established his own lab at the Imperial Cancer Research Fund (now Cancer Research UK), initially at their Mill Hill site, then in Oxford and, finally, at the main ICRF/CR-UK Lincoln's Inn Fields laboratory in London. He is currently a Professor of Cell and Developmental Biology at University College London and a Visiting Scientist in the Biochemistry Department, Oxford University.

Dr Ish-Horowicz's studies has driven major advances in understanding the molecular processes that generate different cell-types in developing animals, in both Drosophila and vertebrate model systems. His work identified the first metazoan corepressor, Groucho/TLE, which regulates transcription in response to many signalling pathways, including Notch and Wnt. He also showed how molecular motors transport selected mRNAs along microtubules to help target asymmetric protein production within cells. In vertebrates, he demonstrated that Notch intercellular signalling acts in the nervous system to maintain neuronal stem cells and, thereby, to generate neuronal diversity. He also provided the first evidence that a cyclic transcriptional oscillator acts during vertebrate segmentation in order to produce regular reiterated body-structures such as the axial skeleton. For these and other findings, he was awarded the 1997 Gulbenkian Science Prize and the 2007 Waddington Medal of the British Society of Developmental Biology, and was elected a Fellow of the Royal Society in 2002.

Maria Jasin

Maria Jasin obtained a Ph.D. from the MIT and performed postdoctoral research at the University of Zürich and Stanford University. Her lab at Memorial Sloan Kettering Cancer Center performed the first gene editing experiment through generation of a DNA double-strand break (DSB) in the mammalian genome, demonstrating both gene correction and mutagenesis, and developed genetic and molecular assays to identify DSB repair events that continue to be widely used. These experiments established a crucial role for homologous recombination, also called homology-directed repair (HDR), as well as nonhomologous end-joining (NHEJ) in DSB repair.
With the approaches thus established, her lab determined that the breast cancer suppressors BRCA1 and BRCA2 are crucial in HDR repair, thus implicating HDR as a tumor suppression mechanism, and, further, that these proteins function at distinct steps in the pathway. Identification of their role in this pathway is being exploited in the treatment of BRCA1/2-deficient cancers. Her lab further established that BRCA1/2 and associated proteins play critical roles in the protection of stalled replication forks, and that BRCA2 is an essential gene for the suppression of replication stress. The lab also has a major effort directed at understanding the generation and repair of programmed DSBs during meiotic progression, which are essential for genome transmission, and in modelling cancer translocations.
Dr. Jasin is a member of the National Academy of Sciences, the National Academy of Medicine, and the American Academy of Arts and Sciences. She was awarded the Basser Global Prize for BRCA Research in 2018 and the Shaw Prize in Life Science and Medicine in 2019.

Klaus Rajewsky

Klaus Rajewsky developed a general method of targeted mutagenesis in mouse embryonic stem cells by introducing bacteriophage- and yeast-derived recombination systems, which opened the way for conditional gene targeting. Using this and other methods in his immunological work, he developed, together with N. A. Mitchison and N. K. Jerne, the antigen-bridge model of T-B cell cooperation, identified germinal centers as the sites of antibody somatic hypermutation, the B cell antigen receptor as a survival determinant of B cells, and the germinal center as a major site of human B cell lymphomagenesis, including Hodgkin lymphoma. Over the last years the work of his group has focused on mechanisms of microRNA control and the development of mouse models of human B cell lymphomas.

After postdoctoral work at the Institut Pasteur in Paris he built an immunology department at the Institute for Genetics at the University of Cologne, where he stayed for 38 years, was the founding Program Coordinator of the EMBL Mouse Biology Program at Monterotondo near Rome, worked for 10 years at Harvard Medical School in Boston, and is since 2012 at the Max-Delbrück-Center for Molecular Medicine in Berlin, Germany.

Klaus Rajewsky won numerous scientific awards and is a member of several learned societies including the National Academy of Sciences of the USA and the American Academy of Arts and Sciences.