Invited Speakers

Geneviève Almouzni

Geneviève Almouzni

Lucia Altucci

Lucia Altucci

Pilar Blancafort

Pilar Blancafort

Tiziana Bonaldi

Tiziana Bonaldi

Maria Carmo-Fonseca

Maria Carmo-Fonseca

Toni Cathomen

Toni Cathomen

Jonathan Chubb

Jonathan Chubb

Luciano de Croce

Luciano de Croce

Martin Fussenegger

Martin Fussenegger

Wouter de Laat

Wouter de Laat

Massimo Loda

Massimo Loda

Luca Magnani

Luca Magnani

Pamela Munster

Pamela Munster

Christoph Plass

Christoph Plass

Maria Rodriguez Martinez

Maria Rodriguez Martinez

Paola Scaffidi

Paola Scaffidi

Vahid Shahrezaei

Vahid Shahrezaei

Henk Stunnenberg

Henk Stunnenberg

Lodewyk Wessels

Lodewyk Wessels

We have invited a core of 20 mainly established investigators and speakers with demonstrated excellent speaker capacities providing an attractive advertisement for our conference. We have carefully selected these invited/keynote speakers to cover the full spectrum of relevant topics in the field taking speaker’s gender into account.

The following speakers have accepted to speak at the meeting:

Keynote speakers:

Invited speakers:

  • Lucia Altucci, Institute of Genetics and Biophysics, IT
  • Pilar Blancafort, University of Western Australia, AU
  • Tiziana Bonaldi, European Institute of Oncology, SRSI, IT
  • Maria Carmo-Fonseca, Instituto de Medicina Molecular Lisbon, PT
  • Toni Cathomen, University Medical Center Freiburg, DE
  • Luciano Di Croce, Centre for Genomic Regulation, ES
  • Wouter de Laat, Hubrecht Institute, NL
  • Massimo Loda, Harvard Cancer Center, US
  • Luca Magnani, Imperial College London, GB
  • Christoph Plass, German Cancer Research Center, DE
  • Maria Rodriguez Martinez, IBM Research, CH
  • Paola Scaffidi, Francis Crick institute London, GB
  • Vahid Shahrezaei, Imperial College London, GB
  • Henk Stunnenberg, Radboud University Nijmegen, NL
  • Lodewyk Wessels, Netherlands Cancer Institute, NL
  • Stefan Legewie, Institute of Molecular Biology (IMB), DE

Geneviève Almouzni

Structure and function of dynamic chromatin organization


Lucia Altucci

Università della Campania Luigi Vanvitelli, Dept. Biochimica Biofisica e Patologia Generale, MD, PhD; Specialisation in medical Oncology Full Professor of General Pathology &Rector’s delegate for Research & Innovation University of Campania Luigi Vanvitelli, Naples, IT.

 


Pilar Blancafort


Tiziana Bonaldi


Maria Carmo-Fonseca

Promoter-proximal convergent antisense transcripts: new targets for rejuvenation and anti-cancer interventions

Maria Carmo-Fonseca
Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Portugal

Aging imposes a barrier to somatic cell reprogramming through poorly understood mechanisms. We found that fibroblasts from old mice express higher levels of Zeb2, a transcription factor that activates epithelial-to-mesenchymal transition. Synthesis of Zeb2 protein is controlled by a natural antisense transcript named Zeb2-NAT. We showed that transfection of adult fibroblasts with specific LNA Gapmers induces a robust downregulation of Zeb2-NAT transcripts and Zeb2 protein and enhances the reprogramming of old fibroblasts into pluripotent cells (Jesus et al. Nat. Commun. 2018). We further identified at genome-wide level additional sense (protein-coding) and antisense (non-coding) transcriptional paired units with closely spaced convergent promoters. We coined the term promoter-proximal convergent antisense transcripts (PCATs) to refer to the non-coding component of these pairs. Native elongating transcript sequencing (NET-seq) revealed consistent polymerase pausing at the TSS of PCATs, which typically initiate within the first intron of the corresponding protein-coding gene. Our results suggest that PCATs represent a novel class of regulatory non-coding RNAs with great potential as targets for rejuvenation and anti-cancer interventions.


Toni Cathomen

Molecular mechanisms governing cell differentiation and cancer processes

Toni Cathomen is Professor of Cell and Gene Therapy and Director of the Institute for Transfusion Medicine and Gene Therapy at the Medical Center of the University of Freiburg, Germany. His research activities focus on the development of disease models and cell therapies based on induced pluripotent stem cells (iPSCs), the improvement of the effectiveness and safety of designer nucleases (CRISPR-Cas and TALEN) for targeted genome editing in clinically relevant human cells, and the development of immune cell therapies (CAR-T cells) for the treatment of various types of tumors.

 


Jonathan Chubb

Implications of transcriptional mechanism for cell decision-making

Prof. Jonathan Chubb is a Welcome Senior Fellow at the MRC Laboratory for Molecular Cell Biology, University College London. His group would like to understand how cells make choices about their fates. To achieve this, they take the view that one needs to observe the gene expression of individual cells before and during the decision-making process, to test how initial cell "state" maps onto final cell fate. In particular, his group develop and use approaches to image the transcription of genes in living cells.

 


Luciano di Croce

Molecular mechanisms governing cell differentiation and cancer processes

Since its formation, Di Croce’s group has focused its research efforts on understanding how epigenetic modifications and chromatin changes are established and, once in place, how they affect gene expression, cell differentiation and transformation.

Polycomb and MLL/Trithorax complexes are evolutionarily conserved chromatin-modifying factors originally identified as part of an epigenetic cellular memory system that maintains repressed or active gene expression states. Recent data indicate that they regulate a plethora of cellular processes, including X chromosome inactivation, genomic imprinting, cell cycle control, stem cell biology, and cancer. Polycomb proteins form at least two distinct complexes: the Polycomb-repressive complexes 1 and 2 (PRC1 and PRC2), both possessing histone-modifying enzymatic activities resulting in monoubiquitination at lysine 119 of histone H2A and methylation at lysine 27 of histone H3, respectively. The catalytic activity and the binding of Polycomb to its genomic sites can be modulated by associated factors. The antagonistic function is performed by MLL complexes that trough deposition of methyl marks on lysine 4 of histone H3 positively regulate transcription, thus counteracting the activity of Polycomb complexes. I will discuss how Polycomb and MLL proteins (including novel associated factors) impact on transcription, genome architecture, and their role in stem cell biology.

 


Martin Fussenegger

Synthetic Biology-Inspired Cell-BasedTreatment Strategies of the Future

Since Paracelsus’ (1493-1541) definition that the dose makes the drug, the basic treatment strategies have largely remained unchanged. Following diagnosis of a disease the doctor prescribes specific doses of small-molecule drugs or protein pharmaceuticals which interfere with disease-associated molecular targets. However, this treatment concept lacks any diagnostic feedback, prophylactic impact and dynamic dosage regimen. We have pioneered the concept of metabolic prostheses which, akin to mechanical prosthesis replacing defective body parts, interface with host metabolism to detect and correct metabolic disorders. Metabolic prostheses consist of designer cells containing synthetic sensor-effector gene networks which detect critical levels of disease metabolites, processes pathological input with Boolean logic and fine-tune in-situ production and release of protein therapeutics in a seamless, self-sufficient and closed-loop manner. When implanted inside insulated, immunoprotective and autovascularizing microcontainers the metabolic prostheses connect to the bloodstream, constantly monitor the levels of disease-associated metabolites and trigger an immediate therapeutic response to prevent, attenuate or correct the disease. With their unique characteristic to dynamically link diagnosis to dose-specific in-situ production and delivery of protein pharmaceuticals, metabolic protheses will enable new treatment strategies in the future. To highlight the impact of synthetic biology on future biomedical applications, we will present our latest generation of remote-controlled gene switches, biosensor circuits and metabolic prostheses tailored to diagnose, prevent and cure high-prevalence medical conditions including diabetes, cancer, pain, parkinson’s disease and multidrug-resistant pathogenic bacterica.

 


Wouter de Laat

Single allele chromatin topologies and the discovery of new chromatin loops

Genomic organization in space and time (4D genome) has regulatory impact on gene expression and the epigenetic landscape. We develop new methods to understand chromatin topology in high detail, from the single allele to the cell population level, to assign function to the non-coding genome in health and disease. 

Wouter de Laat (Hubrecht Institute) did his PhD (1998) in the Jan Hoeijmakers lab and was a postdoc in the Frank Grosveld lab at the Erasmus University. Since 2000, his research group works on long-range gene activation and pioneers the use and development of 3C technologies for 3D genome studies. Research highlights include their first demonstration of chromatin loops between genes and enhancers, their discovery that CTCF is a chromatin looping factor, their development of 4C technology and Multi-Contact 4C for detailed DNA contact profiles and their introduction of ‘C’ methods in genetic diagnostics. Wouter de Laat is founder of the biotech company Cergentis, received national and European career grants and is an elected EMBO member.


Massimo Loda

 

 

 

 

 

 

 

 

 


 Luca Magnani

Diving into the dark matter of the breast cancer genome

Recent years have seen an increasing effort to decode the cancer genome. Most of the studies have focused on the coding genome to identify cancer driver genes. My group is interested in the role of the non-coding genome and its potential contribution in driving the transcriptional aberrations common to breast cancer patients. To do so we use a wide-spectrum of techniques including genomic and epigenomics assays in patient-derived samples. I will present the results of a couple of studies  in which mapping the non-coding genome using epigenomic yielded novel insights on cancer progression in luminal breast cancer patients. 

Luca Magnani has trained in Italy and the US before starting his laboratory at Imperial College London. His background is in epigenetics. He has a strong interest in translational science, with a strong focus and breast cancer. He is currently supported by a CRUK career development fellowship and EU grants. His laboratory studies how tumors evolve in response to therapy using genomics and epigenomics. His multi-disciplinary team consist of a medics, biologists and computational biologists and uses and develops cutting-edge approaches to study breast cancer evolution.

 

 


Pamela Munster

Pamela Munster is Co-Director of the Center for BRCA Research, a BRCA-focused clinical and research program at the Helen Diller Family Comprehensive Cancer Center at UCSF. Dr. Munster received her medical degree from the University of Bern, Switzerland; completed her residency in Internal Medicine at Indiana University Medical Center, then moved to Memorial Sloan-Kettering Cancer Center, New York for her oncology and hematology fellowship. She served at Memorial Sloan Kettering as a faculty member in the breast cancer program before joining the Division of Breast Oncology and Experimental Therapeutics Program at Moffitt Cancer Center and Research Institute, Tampa, Florida. Currently Dr. Munster is Professor in Residence at the University of California, San Francisco, where she is also the Director of Early Phase Clinical Trials Program at the Helen Diller Family Comprehensive Cancer Center and Program Leader of Experimental Therapeutics.


Christoph Plass

Prof. Dr. Christoph Plass , studied in Berlin and Lübeck and obtained postdoctoral training in Molecular Biology at the Roswell Park Cancer Institute (RPCI) in Buffalo, NY. He became a full Professor at the Ohio State University in 2005 and accepted the position as head of the Division Epigenomics and Cancer Risk Factors at the German Cancer Research Center in Heidelberg in October 2007. His main interest is in global genome-wide epigenetic patterns.

Maria Rodriguez Martinez

Dr. María Rodríguez Martínez is the technical lead of the group of Systems Biology at IBM Research - Zürich. A physicist by training, she did her PhD and a first postdoc in High Energy Physics at the Institut d’Astrophysique de Paris and Hebrew University respectively. In 2006, she transitioned into Systems Biology as a postdoc at the Weizmann Institute of Science and later at Columbia University. Since 2013 she is a member of the Systems Biology group at IBM Research – Zürich, and an associated member of the Department of Biology at ETH since 2014. Her current research focuses on the development of computational and statistical approaches to unravel cancer molecular mechanisms using high-throughput multi-omics datasets and single-cell molecular data.

 


Paola Scaffidi

Epigenetics mechanisms of tumour maintenance

Paola Scaffidi obtained her PhD from the Open University of London, working at the San Raffaele Institute in Milan, Italy. She then moved to the US National Cancer Institute to work in Tom Misteli's laboratory, first as a postdoctoral fellow and then as a staff scientist. She joined the Cancer Research UK London Research Institute (LRI) in 2014 to lead the Cancer Epigenetics Laboratory. In 2015, the LRI became part of the Francis Crick Institute.

Continuous cancer growth is driven by malignant cells endowed with long-term proliferative capacity, which self-renew indefinitely in an uncontrolled manner. In many cancers, only subsets of cells preserve unlimited proliferative potential during tumor growth, whereas others lose self-renewal ability, either through a differentiation process or as consequence of deleterious genetic alterations. Regardless of their abundance within a cancer, self-renewing cells are essential both for sustaining disease maintenance and for reconstituting the cancer when cytotoxic treatments are not fully effective. Targeting cancer cell self-renewal may therefore be a generally-applicable strategy to prevent disease progression and potential relapse. We have recently characterized an epigenetic mechanism that regulates cancer cell self-renewal in multiple cancer types and involves the linker histone H1.0, and found a pharmacological means to interfere with this mechanism. The implications of these findings will be discussed.


Vahid Shahrezaei

Vahid Shahrezaei has done his PhD in Physics at Simon Fraser University, postdoc at McGill University and is a reader in biomathematics at Imperial college London. He is also Mathematician in residence at MRC London Institute in Medical Sciences. He uses mathematical and statistical approaches to study temporal, spatial and stochastic dynamics of biochemical networks inside cells using single cell and global biological data. His work on modelling intrinsic and extrinsic noise in gene expression is highly cited.


Henk Stunnenberg

Henk Stunnenberg is full professor and head of the Department of Molecular Biology of the Radboud University and the Radboud Medical Centre.
He obtained his PhD in Genetics at the University of Wageningen (NL) and after a post-doc at the University of Zürich (CH), he fulfilled positions as group leader at Hoffmann-LaRoche (CH) and at the Gene Expression Program at EMBL (Heidelberg, DE). He is a member of EMBO since 1994.
Professor Stunnenberg is coordinator of the EU FP7 High Impact Project BLUEPRINT (the BLUEPRINT of Haematopoietic Epigenomes) that runs from 2011-2016 and currently he is Chair of the International Scientific Steering Committee of the International Human Epigenome Consortium (IHEC). In 2013 he received an ERC Advanced Grant of € 2.5 million for his project ‘SysStemCell’.


L.F.A. Wessels

Integrative modeling for precision medicine

Lodewyk Wessels is the head of the Computational Cancer Biology group at the Netherlands Cancer Institute. His group focuses on quantifying and understanding treatment response in model systems and patients. To end they develop besproke and novel computational methods focusing on data integration and tailored to new technologies. Lodewyk Wessels holds a chair in Computational Cancer Biology at the Delft University of Technology and serves as Deputy Director Research of the Nehters Cancer Institute.