Invited Speakers





















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:
- Geneviève Almouzni, Institut Curie, FR (The EMBO Keynote Lecture)
- Jonathan Chubb, University College London, MRC, GB
- Martin Fussenegger, ETH Zürich, CH
- Pamela Munster, University of California, San Francisco, US
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
- Anne-Lise Børresen-Dale, Oslo University Hospital The Norwegian Radiumhospital. NO
- 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
- Stefan Lewegie, Institute of Molecular Biology, DE
- 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
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Geneviève AlmouzniBuilding chromatin: histone variants and chaperones at work Chromatin organization in the nucleus provides a large repertoire of information in addition to that encoded genetically. A major goal for my group involves understanding how histones, the major protein components of chromatin, the bricks, can mark functional regions of the genome through their variants or post-translational modifications, along with non-coding RNA and other chromatin regulators. Errors in the establishment and propagation of these chromatin components, possibly involving imbalance in their deposition pathways, can lead to mis-regulation of genome functions and pathological outcomes, such as cancer. The propagation of centromeric identity represents a model of choice for the study of epigenetic mechanisms. Our work has focused on histone chaperones, as architects of chromatin organisation and key chromatin determinants of centromere identity. We will present our latest findings on this topic in the context of deregulation in cancer. |
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Lucia AltucciBRD9 is critical in acute myeloid leukemia 1 Department of Precision Medicine, University of Campania "Luigi Vanvitelli", Vico L. De Crecchio 7, 80138, Napoli, Italy 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. |
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Pilar BlancafortEpigenetic editing as an innovative strategy of tumour targeting in pre-clinical studies Dr. Pilar Blancafort is currently an associate professor of Cancer Epigenetics at The University of Western Australia. Her academic background involved undergraduate (Universitat de Barcelona, Spain) and graduate (Universite de Montreal, Canada) degrees in Biochemistry and Molecular Biology, followed by a post-doctoral fellowship with the Barbas laboratory at the Scripps Research Institute (La Jolla, USA). In 2005, she established her own laboratory at the University of North Carolina at Chapel Hill, as Assistant Professor and later as tenured Associate Professor in 2011. In 2012, Professor Blancafort moved her laboratory at the University of Western Australia, School of Human Sciences. Her laboratory focuses on the intersection between cancer genomics and molecular cancer therapeutics. The Blancafort lab has pioneered the development of (epi)genome editing and nanotechnology approaches to target cancers that are currently refractory to treatment and associated with poor outcomes, such as triple negative basal-like breast cancers. She joined the Harry Perkins Institute of Medical Research in 2014. She hold’s a Cancer Council of Western Australia (CCWA) and Australian Research Council (ARC) Future Fellowship. Pilar Blancafort 1,2, Charlene Waryah1,2, Joseph Cursons3,4, Melissa J Davis3,4,5, Greg J Goodall6,7, Cameron Bracken,6,7, Erik Thompson8, Andrew Redfern9,10 |
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Tiziana BonaldiMS- based Chromatin Proteomics to dissect the code of histone post –translational modifications
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Anne-Lise Børresen-DaleEpigenetics of breast cancer: Implications on progression and clinical outcome PhD, MD (h.c), Professor Emerita,Department of Cancer Genetics, Institute for Cancer Research, Oslo University Hospital The Norwegian Radiumhospital, and Institute for Clinical Medicine, Faculty of Medicine at University of Oslo.
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Maria Carmo-FonsecaPromoter-proximal convergent antisense transcripts: new targets for rejuvenation and anti-cancer interventions Maria Carmo-Fonseca 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. |
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Toni CathomenTherapeutic genome editing – opportunities and pitfalls 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. Therapeutic genome editing – opportunities and pitfalls Therapeutic genome editing in hematopoietic cells empower new therapeutic interventions, including novel approaches to treat immunological disorders, infectious diseases, and cancer. We have developed GMP-compliant protocols to manufacture gene edited CD34+ hematopoietic stem cells as well as chimeric antigen receptor (CAR) T cells, with the final goal to establish novel cell therapies for patients suffering from primary immunodeficiencies, chronic infection with human immunodeficiency virus type 1 (HIV-1), and solid tumors. Despite the considerable success in improving their specificity, engineered designer nucleases still induce genotoxic side effects. We established a novel unbiased and genome-wide assay to detect chromosomal aberration induced by off-target activity as well as on-target activity, such as micro-aberrations and translocations, with unparalleled sensitivity. These novel insights in CRISPR-Cas and TALEN-induced genotoxicity in clinically relevant cell types authorize a thorough risk stratification and hence a means to identify the best-suited designer nuclease in combination with the best-suited target site. In conclusion, our developed protocols enable us to achieve genome editing in clinically relevant human cells with high efficiency and to assess the genotoxic risk associated with the expression of CRISPR-Cas9 nucleases and TALENs in those cells, so forming a solid basis for the planned phase I/II clinical studies. |
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Jonathan ChubbImplications of transcriptional mechanism for cell decision-makingProf. 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. |
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Luciano di CroceMolecular mechanisms governing cell differentiation and cancer processesSince 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. |
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Martin FusseneggerSynthetic Biology-Inspired Cell-BasedTreatment Strategies of the Futureis Professor of Biotechnology and Bioengineering at the Department of Biosystems Science and Engineering (D-BSSE) of the ETH Zurich in Basel as well as at the University of Basel. His research focuses on mammalian cell engineering, in particular on the assembly of synthetic gene circuits that process complex control and closed-loop expression logic as well as on the production of theranostic designer cell implants that interface with host metabolism to correct prominent metabolic disorders. 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. |
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Wouter de Laat
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Stefan LegewieDynamics of estrogen-dependent transcription at the single-cell level Stefan Legewie holds a PhD in Biophysics (2008) and is a group leader at the Institute of Molecular Biology, Mainz (Germany). His group develops mechanistic and predictive mathematical models of biological processes in collaboration with experimental partners to better understand cellular heterogeneity, with a focus on the dynamics of signaling and gene regulation. Even genetically identical cells frequently respond in different ways to the same external stimulus, leading to differences in differentiation programs and drug resistance. One important source of cellular heterogeneity is gene expression, as genes randomly switch between transcriptionally active and inactive states, resulting in bursts of RNA synthesis. Furthermore, the cellular state influences the competency of transcription, thereby affecting gene expression in a cell-specific manner. Estrogen signalling promotes breast cancer growth and serves as a paradigm for multi-step epigenetic gene regulation. To gain insights into the heterogeneity of estrogen signaling, we studied the stochastic transcription of the GREB1 gene which is a key regulator of estrogen-induced cell proliferation. We labeled the endogenous GREB1 locus using CRISPR/Cas9 genome engineering and monitored nascent transcription by live-cell imaging. Quantitative stochastic modeling implicated a two-state (ON/OFF) promoter model in which the estrogen stimulus modulates the frequency of transcriptional bursting. The cellular state affects transcriptional dynamics by altering initiation and elongation kinetics and acts globally, as GREB1 alleles in the same cell correlate in their transcriptional output. Our results provide insights into non-genetic heterogeneity arising at the level of transcription and reveal how inhibitors of epigenetic regulation uncouple transcription noise and mean expression level. |
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Massimo LodaMetabolic dependencies in prostate cancer: regulation and targeting of lipogenesis Dr. Loda received his MD in 1980 from the University of Milan, Italy, and his training in pathology at Harvard. He is currently the Chair of the Department of Oncologic Pathology at Dana-Farber Cancer Institute, Associate Member of the Broad Institute of Harvard and MIT. The Loda laboratory studies the role of metabolic alterations in prostate tumorigenesis. We study the mechanisms whereby enhanced lipogenesis affects prostate tumor growth. We do this utilizing biochemical and genomic approaches in cell lines, orthotopic tumor xenograft, genetically engineered murine models and human tumors. Cancer cells hijack metabolic pathways to support bioenergetics and biosynthetic requirements for their uncontrolled growth. Thus, cancer can be considered as a metabolic disease. The link between oncogene-directed cancer metabolic regulation and metabolic rewiring leads to novel diagnostic, imaging and therapeutic approaches. A hallmark of prostate cancer progression is dysregulation of lipid metabolism via overexpression of fatty acid synthase (FASN), a key enzyme in the de-novo fatty acids synthesis. Metastatic castration-resistant prostate cancer (mCRPC) develops resistance to inhibitors of androgen receptor (AR) signaling through a variety of mechanisms, including the emergence of the constitutively active AR variant V7 (AR-V7). Selective FASN inhibition antagonizes CRPC growth through metabolic reprogramming and results in reduced protein expression and transcriptional activity of both full-length AR (AR-FL) and AR-V7, mediated at least in part by the endoplasmic reticulum (ER) stress response. In vivo, FASN inhibition reduced growth of AR-V7-driven CRPC xenografts and human mCRPC-derived organoids, and enhanced the efficacy of enzalutamide in CRPC cells. These findings provide a compelling rationale for the use of FASN inhibitors in mCRPCs, including those overexpressing AR-V7. |
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Luca MagnaniDiving 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. |