Day 2 :
Keynote Forum
Vojin Rakić
Center for the Study of Bioethics-University of Belgrade, Serbia
Keynote: What is involuntary moral enhancement?
Biography:
Vojin Rakić is a Full Professor and is Director of the Center for the Study of Bioethics and Head of the European Division of the UNESCO Chair in Bioethics. He is also Chair of the Cambridge Working Group for Bioethics Education in Serbia. He is also Head of the Serbian Unit of the UNESCO Chair in Bioethics. He has a PhD in Political Science from Rutgers University in the United States (1998). He has graduated in Philosophy in Serbia and has MA degrees in European Studies from the Central European University in Prague and from the Department of Political Science of Rutgers University. He has worked as a Senior Research Fellow at the Center for Higher Education Policy Studies at the University of Twente in the Netherlands (1999-2001). Between 2001 and 2003, he was a U.N. Special Adviser to the Government of Serbia. Since 2003 he works as a university Professor in Belgrade. His publications include various books and edited collections, as well as numerous articles from the domain of (bio-)ethics and political philosophy.
Abstract:
During the previous years, voluntary moral bioenhancement (VMBE) has been contrasted to Compulsory Moral Bioenhancement (CMBE), promoted primarily by Persson and Savulescu. In this presentation a third possible type of MBE will be discussed: Genome editing for moral enhancement of the unborn that is neither voluntary nor compulsory, but involuntary. The focus of the presentation will therefore be on genome editing that is aimed at moral enhancement of human offspring. It will be argued that genome editing might have the potential to engineer human offspring in three domains: To be more empathetic, less violently aggressive and with a higher potential for complex moral reflection. Genome editing will be discussed in these three domains. It will be argued that a combination of VMBE and IMBE might be the best option humans have to enhance themselves morally.
Keynote Forum
Meena Upadhyaya
Cardiff University, UK
Keynote: Recent developments in neurofibromatosis type 1 and RASopathies: Novel therapeutic targets
Time : 11:00-12:00
Biography:
Professor Meena Upadhyaya OBE, is a distinguished professor in the Division of Cancer and Genetics, Cardiff university, UK. She obtained her PhD in Medical Genetics from Cardiff University and gained FRCPath from Royal College of Pathologists, London. She has made substantial contributions to the molecular understanding of a number of genetic conditions including neurofibromatosis type 1, facioscapulohumeral muscular dystrophy, Legius syndrome, Charcot Marie Tooth disease, Duchenne Muscular Dystrophy, Sotos syndrome, Hunters syndrome inter alia and also supervised numerous PhD, MD, MSc and undergraduate students. Prof. Upadhyaya has published well over 200 papers in peer reviewed journals and co-edited three books and sits on a number of Committees. She is also passionate about women’s equality in all spheres of life.
Abstract:
Neurofibromatosis type 1 (NF1) is a common autosomal dominantly inherited tumor predisposition syndrome affecting 1/3000-4000 individuals worldwide. Neurofibromin, the protein encoded by NF1 gene down-regulates Ras. The Ras/MAPK pathway plays an essential role in regulating the cell cycle and cellular growth, differentiation and senescence, all of which are critical to normal development. In NF1 patients, benign plexiform neurofibromas can transform into aggressive malignant tumors called Malignant Peripheral Nerve Sheath Tumors (MPNSTs), currently, there are no effective treatments for MPNSTs. The RASopathies are a clinically defined group of medical genetic syndromes caused by germline mutations in genes that encode components or regulators of the Ras/MAPK pathway. These disorders include neurofibromatosis type 1, Legius syndrome, Noonan syndrome, Noonan syndrome with multiple lentigines (LEOPARD), capillary arteriovenous malformation syndrome, Costello syndrome cardiofaciocutaneous syndrome and SYNGAP1 autism. Because of the common underlying Ras/MAPK pathway dysregulation, they have overlapping phenotypic features, including cancer, facial dysmorphia, neurocognitive impairment, pain and cardiovascular, musculoskeletal, gastrointestinal and cutaneous abnormalities. NF1 was the first Rasopathy syndrome reported in the RAS pathway. Several ongoing clinical trials exist for RASopathies including NF1 and effective treatments for certain clinical features are on horizon. NF1 also has great importance and significance in a number of sporadic cancers and functions as a central tumor suppressor gene in these cancers. With the recent advances in sequencing technologies, high-throughput drug discovery platforms, increasing availability of more sophisticated animal models and application of the state-of-art tumor imaging techniques, diagnosis and treatment of patients with RASopathies is improving.