Daniel Aberdam is a biologist, expert in skin physiopathology and stem cells. Director of Research INSERM from 1995 and long term visiting Prof. at the Technion (Haifa) from 2006 to 2013. From 2014, Daniel Aberdam is group leader at the Skin Research Center (Hospital St-Louis, Paris). He completed his first degrees in life sciences at Pierre and Marie Curie University (Paris, France) and his PhD at the Weizmann Institute (Israël) on the oncogenic potential of homeotic genes. During his postdoctoral stage from 1990 to 1995, he discovered the identity of genes responsible for severe human skin diseases that then allowed the first antenatal diagnosis for junctional epidermolysis bullosa syndromes. Then, his scientific interests turned on epidermal gene regulation with the identification of skin specific promoters. Then, his group has focused on the physiopathology of stem cells and designed original cellular models from embryonic stem cells that recapitulate embryonic normal and pathological skin and cornea formation. It allows the characterization of genes and signaling pathways involved in these critical steps and their involvement in skin defects found in patients affected by human congenital disorders, like ectodermal dysplasia syndromes. This team was the first to demonstrate the ability of pluripotent stem cells to produce a full thickness skin. More recently, the group used cell reprogramming of patient samples to modelize in vitro genodermatoses and identified small compounds able to rescue the phenotype. Their studies allow identifying potential therapeutic tools and a new metabolic pathway used by pluripotent stem cells. To date, Dr. Aberdam has published over 87 scientific articles and received several awards, including from the French Académie des Sciences. He serves on the editorial boards of Stem Cells, Cell Death and Differentiation and Cell Death and Disease.
Dr Avi Ashkenazi is Senior Staff Scientist at Genentech Inc. He received his PhD in Biochemistry in 1986 from the Hebrew University of Jerusalem, Israel. He trained as a postdoctoral fellow from 1986 to 1989 at the University of California, San Francisco, and at Genentech. In 1988 Dr Ashkenazi received the first prize of the Boehringer Ingelheim Award for his studies on G protein-coupled muscarinic acetylcholine receptors. In 1989 he joined Genentech as a Research Scientist. There, in the early 1990's, he helped develop the immunoglobulin Fc-fusion protein technology—now widely used in biology laboratories around the world and in certain biotechnology drugs including tumor necrosis factor (TNF) receptor fusion proteins. Later, Dr Ashkenazi's group discovered several novel members of the TNF ligand and receptor superfamilies, most notably, the apoptosis-inducing ligand Apo2L/TRAIL and its "death" and "decoy" receptors.
Basic research in Dr Ashkenazi's laboratory discerned how Apo2L/TRAIL triggers apoptosis via its receptors DR4 and DR5, and translational work by the group led to the development and clinical investigation of a class of molecules called proapoptotic receptor agonists (PARAs) to target this pathway in cancer. Most recently, his team elucidated how different ubiquitination events control activation and inactivation of the apoptosis-initiating protease caspase-8, and established an important role for caspase-8 in apoptosis activation by genotoxic and proteotoxic stress. To date, Dr Ashkenazi has published over 150 scientific articles and has co-edited a book on Antibody Fusion Proteins and two volumes of Methods in Enzymology on Regulated Cell Death. His top 5 publications have been cited over 12,000 times in sum. Dr Ashkenazi has trained over 25 postdoctoral fellows to date. He is an inventor on 69 US issued patents and has served on the editorial boards of Current Biology, Nature Reviews Cancer, Journal of Biological Chemistry, Clinical Cancer Research, Cancer Biology and Therapy, Molecular Cancer Therapeutics and Cell Death and Differentiation.
Nicolas G Bazan
Nicolas Bazan's research is focused on understanding cellular and molecular mechanisms to prevent, ameliorate and eventually contribute to curing neurodegenerative diseases and other neurological conditions. For this purpose, his laboratory uses experimental models of Alzheimer's disease (AD), epileptogenesis, ischemic stroke, traumatic brain injury, pain and of retinal degenerative diseases (age-related macular degeneration and retinitis pigmentosa). His laboratory research has led to the uncovering of new gene regulation and necessary proteins for cell survival in the retinal pigment epithelial cells that are providing unified events amenable to be harnessed to slow down the onset and early progression of neurodegenerations. Most recently his laboratory has uncovered the molecular principles involved in the retention/conservation of docosahexaenoic acid (DHA) necessary for cell survival signalling in retinal pigment epithelial (RPE) cells and photoreceptors. This mechanism uncovered a new function for the Adiponectin Receptor 1. He and his colleagues discovered the cell survival mediator neuroprotectin D1 and coined its name (NPD1). Under conditions of uncompensated oxidative stress, NPD1 is made on demand from DHA when disruptors of homeostasis evolve and the initial inflammatory response needs to be modulated to protect RPE cell integrity. NPD1 is the first biologically active mediator of the novel docosanoid family. Bazan and his colleagues found that neurotrophins are agonists for the synthesis of this mediator in RPE cells, that 15-lipoxygenase-1 (15-LOX-1) is the enzyme that catalyses its synthesis, that it targets protein phosphatase 2A (PP2A) to regulate anti-/pro-apoptotic proteins during RPE oxidative stress, and that it regulates proteostasis in RPE cells. They identified transcription of pro-inflammatory genes as a target of NPD1 and demonstrated that the CA1 hippocampal area from short-post mortem, early-stage AD patients displays a 25-fold loss of NPD1 as well as of the enzyme for the synthesis of this lipid mediator. A central theme of Bazan's laboratory is to understand early responses to oxidative stress, inflammation and conditions that recapitulate neurodegenerations aiming to gain insight into mechanisms. His common thread of concepts has included homeostatic regulation, necessary proteins, epigenetic events, and bioactive lipid mediators. In addition, Bazan and his colleagues has developed molecules for clinical application, including novel, non-narcotic, non-toxic analgesics targeting various forms of pain including neuropathic pain; novel anti-inflammatories; compounds effective for slowing down invasiveness of glioblastoma multiforme; genetically-engineered transdifferentiated fibroblasts for neurons and genetically-engineered adipose tissue cells for neurodegenerative diseases ; stroke and traumatic brain injury.
Mikhail V Blagosklonny
Mikhail (Misha) V. Blagosklonny, MD, Ph.D. Professor of Oncology at Roswell Park Cancer Institute, Buffalo, NY, USA. His research interests range from molecular and cellular biology to clinical investigations and specifically include oncogenes and tumor suppressors, signal transduction, cell cycle, mitosis, apoptosis, anticancer therapeutics with emphasis on translation of basic science into new anticancer strategies such as exploiting cancer cell cycling and drug resistance for selective protection of normal cells. He has extended this approach to other age-related diseases and aging itself, thus revealing anti-aging drugs such as rapamycin to be used today (Cell Cycle, 2006, 5 : 2087 - 2102). He is an author of hyper-function theory of aging as well as anti-cancer approaches know as chemotherapeutic engineering and cell cyclotherapy.
Dr. Blagosklonny published 300 research articles, reviews and book chapters. He is the Founding Editor and Editor-in-Chief of Cell Cycle and also Co-editor and co-founder of Aging, Oncotarget and Oncoscience. He serves or has served as an Associate Editor for Cancer Biology & Therapy, Autophagy, Cancer Research, Cell Death and Differentiation, International Journal of Cancer, The American Journal of Pathology and PLOS ONE.
Christoph Borner studied Biology at the University in Basel where he graduated in 1984 with a specialization in biochemistry. He continued his training under the supervision of Prof. Urs Eppenberger and Dr. Doriano Fabbro at the Women’s Hospital of the University of Basel and received his PhD in 1988 on the topic of the immunological and biochemical characterization of protein kinase C (PKC) in human breast cancer cells. He then got a postdoctoral fellowship of the Swiss National Science Foundation (SNF) to join the laboratory of Prof. I. Bernhard Weinstein at the Columbia University in New York City to continue his work on the potential oncogenic function of particular PKC isoforms. In 1991 he returned to Switzerland to perform a second postdoc/maître assistant position in the laboratory of Prof. Jürg Tschopp at the Institute of Biochemistry of the University of Lausanne in Epalinges. Here he completely changed the research topic and started to work on apoptosis, in particular the characterization of the survival factor Bcl-2, the only known member of the protein family at that time. After 2 years, he succeeded to obtain a prestigious SNF START grant (today called Junior Professorship) to become for the first time an independent group leader at the Institute of Biochemistry of the University of Fribourg, Switzerland. He continued to work on the Bcl-2 family (in particular on its binding partners and subcellular localization) and also began studying caspase-independent cell death mechanisms.
In 2000 he was appointed as Associate Professor in Medical Cell Research at the Institute of Molecular Medicine of the Albert Ludwigs University of Freiburg, Germany. He was promoted to Full Professor at the same institution in 2006 and was the first to win the competition to build up a doctoral/graduate school (the Spemann Graduate School of Biology and Medicine, SGBM) in the frame of the German Excellence Initiative in Freiburg. He successfully defended the school for the second funding phase in 2012 and also became an executive board member of the excellence research cluster BIOSS (Centre of Biological Signaling Studies). He also helped building up a new study track in Molecular Medicine from 2000 on and was its study dean from 2009-2010. Recently, he became the director of the International Master Program in Medical and Biological Sciences (IMBS) between the Universities of Buenos Aires and Freiburg and received the Doctor honoris causa of the University of Buenos Aires for his achievement in the program. Since he started to work in Freiburg, Germany, Christoph Borner has made major contributions to the field of interaction partners and posttranslational modifications of Bcl-2 family members, mechanisms of caspase-independent cell death and, more recently, identification of death signaling pathways induced by viruses and fungi as well as by FasL in conjunction with TNFα in primary hepatocytes.
Navdeep Chandel is a professor in the Department of Medicine and Cell Biology at Northwestern University located in Chicago. He received a BA in mathematics and Ph.D. in Cell Physiology at University of Chicago. He also did his post-doctoral work at University of Chicago. In 2000, he established his lab at Northwestern University focusing on the role of mitochondria as signaling organelles. Historically, mitochondria have been primarily viewed as biosynthetic and bioenergetic organelles. His work has elucidated that mitochondria participate in signaling by releasing reactive oxygen species which regulate distinct biological outcomes including differentiation, proliferation, and adaptation to stress.
Aaron Ciechanover was born in Haifa, Israel in 1947. He is a Distinguished Professor in the Technion - Israel Institute of Technology in Haifa. He received his M.Sc. (1971) and M.D. (1975) from the Hebrew University in Jerusalem, and his D.Sc. (1982) from the Technion. There, as a graduate student with Dr. Avram Hershko and in collaboration with Dr. Irwin A. Rose from the Fox Chase Cancer Center in Philadelphia, USA, they discovered that covalent attachment of ubiquitin to a target protein signals it for degradation. They deciphered the mechanism of conjugation, described the general proteolytic functions of the system, and proposed a model according to which this modification serves as a recognition signal for a specific downstream protease.
As a post doctoral fellow with Dr. Harvey Lodish at the M.I.T., he continued his studies on the ubiquitin system and made additional important discoveries. It is now clear that ubiquitin-mediated proteolysis plays major roles in numerous cellular processes, and aberrations in the system underlie the pathogenesis of many diseases, among them certain malignancies and neurodegenerative disorders. Consequently, the system has become an important platform for drug development. Among the numerous prizes Ciechanover received are the 2000 Albert Lasker Award, the 2003 Israel Prize, and the 2004 Nobel Prize in Chemistry (shared with Hershko and Rose). Among many academies, Ciechanover is a member of the National Academy of Sciences of the USA (Foreign Associate) and the Israeli Academy of Sciences and Humanities.
Ruggero De Maria
Ruggero De Maria graduated in Medicine in 1989 and specialized in Endocrinology in 1994. He has been Scientific Director of the Regina Elena National Cancer Institute (Rome, Italy) since November 2011. He was appointed this position by the Italian Minister of Health for a five year term. His aim is to create a productive synergy between basic and clinical research.
Throughout the years, De Maria has gained international recognition for his research activity on cancer stem cells (CSCs), a rare population of cells responsible for tumour initiation and growth. During his term as Head of the Department of Hematology, Oncology and Molecular Medicine at the National Institute of Health, Rome (Istituto Superiore di Sanità) from 2008 to 2011 his research team was the first to isolate CSCs from colon and lung cancers and develop innovative CSC-based preclinical models of these tumours, thus has published several seminal articles on glioblastoma stem cells.
De Maria's current research programs are centred on the molecular characterization of CSCs with the aim of discovering innovative biomarkers and molecular targets to improve cancer management and develop novel cancer therapies. Other research interests comprise the study of microRNA and the microenvironment in solid tumors.
In 2013, he was appointed President of the Italian ACC Association (Alleanza Contro il Cancro/Alliance against Cancer) until 2018. He currently holds several Editorial Board positions on internationally renowned scientific journals. He has published over 150 original peer-reviewed articles and reviews in the most important journals including Nature, Science, Nat Med, Nat Immunal, J Exp Med. He sits on various prestigious Advisory Board Committees such as the Pezcoller Foundation AACR International Award, AACR INNOVATOR Award, Veronesi Foundation, AIRC, PACRI, ATENA, EuroCSCT Marie Curie Network, and InBev-BAILLET LATOUR Health Prize.
Giannino Del Sal
Giannino Del Sal isa biologist expert in the mechanisms of tumor initiation and progression. Director of the Department of Life Sciences since 2012 and Full Professor in Applied Biology since 2001 at the University of Trieste, Italy, Giannino Del Sal is Chief of the Molecular Oncology Unit at LaboratorioNazionale CIB (LNCIB) in Area Science Park in Trieste since 1996.
Giannino Del Sal graduated in Biology at the University of Trieste, and had his research training at the International Centre for Genetic Engineering and Biotechnology (ICGEB) in Trieste, at the European Molecular Biology Laboratory (EMBL) in Heidelberg, at LNCIB in Trieste and at the University of Trieste. Thereafter, he worked as an associate expert at ICGEB in the Cell and Genome Studies Unit, as a visiting scientist in the Laboratory of Cell Biology of the US biotech company Mitotix Inc. in Cambridge, and as an assistant and associate professor in Applied Biology at the University of Trieste.
Since the beginning of hisscientific career, Del Sal's research has been mainly focused on tumor biology, embracing and integrating the study of the mechanisms of tumor suppression in health and cancer, the investigation of the role of different oncogenic pathways in cancer development and metastasis, and more translational activities devoted to the development of new tools for cancer therapy.
Del Sal wasthe first to clonethe Sonic Hedgehog binding protein GAS1, and to characterize its functions in the context of growth arrest. His team discovered new post-translational modifications and new sub-cellular localizations of the tumor suppressor p53, as well as new regulatory mechanisms of p53 and p53 family proteins. Focused on the role of phospho-dependent protein conformational changes as key signal transduction events in cancer, his group highlighted the role of the prolyl-isomerase Pin1 in Notch pathway control and in the control of proliferation and maintenance of normal and cancer stem cells of the mammary epithelium.His team discovered the contribution of Pin1 to full activation of mutant p53 oncogenic functions and characterized the proteasome machinery as a key target of a common gain-of-function program shared by diverse missense mutants of p53 in cancer. Del Sal's group discovered new hormonal and metabolic mechanisms of control of the Hippo pathway transducers YAP/TAZ, and using drug repositioning approaches identified compounds able to target YAP/TAZ and mutant p53 pathways in triple negative breast cancer.
To date, Giannino Del Salauthored over 120 publications among scientific articles,reviews and book chapters. He is also inventor of two patents. In 2006 he was elected member of EMBO.
Mohanish Deshmukh, Ph.D. is a Professor of Cell Biology & Physiology and the Neuroscience Center at the University of North Carolina, Chapel Hill. Mohanish received his PhD from Carnegie Mellon University. He then went to Dr. Eugene Johnson’s lab in Washington University St. Louis for his postdoctoral research where he pursued his interests in apoptosis, focusing on this pathway in mammalian neurons.
Mohanish's research interests have focused on identifying the unique mechanisms by which the apoptotic pathway is regulated in neurons and embryonic stem cells. In particular, his lab has identified mechanism by which the apoptotic pathway is highly restricted in neurons for their long-term survival – many of these mechanisms are also engaged by cancer cells to evade apoptosis. Additionally, his lab focuses on strategies for preventing neurodegeneration as well as for triggering apoptosis in brain tumors.
Mohanish has received the Burroughs-Wellcome New Investigator Award, and at UNC, has been recognized with Teaching Excellence and Mentor of the Year Awards. He is currently the Co-Director for the MD/PhD program at UNC. Mohanish has also served on multiple study sections including the NIH, American Heart Association, American Cancer Society, and the DOD Breast Cancer Research Program.
Vishva Dixit has conducted pioneering studies defining key components of the cell death pathway. His laboratory was among the first to:
- show that caspases are components of the death receptor-induced apoptotic pathway;
- demonstrate that death receptors signal by an entirely novel mechanism of recruiting and activating a death protease (FLICE/caspase-8) by an induced proximity mechanism;
- identify the mammalian death protease equivalent to the CED3 protein in worms (YAMA/caspase-3) as well as other pro-apoptotic caspases including caspase-6, -7 and -9.
- show that the death domain-containing molecule MyD88 is a key signaling adaptor;
- discover paracaspases and metacaspases: two ancient families of caspase-related proteins, one of which plays a key role in MALT lymphoma;
- discover the non-canonical inflammasome pathway.
Vishva is currently Vice President of Research, runs an active research laboratory, and has published well over a hundred scientific articles. He also has a significant number of patents to his name. He is a Foreign Member, European Molecular Biology Organization, a member of the Institute of Medicine, the American Academy of Arts and Sciences and the National Academy of Sciences.
Brian D Dynlacht
Brian D Dynlacht is a Professor of Pathology at the New York University School of Medicine. For the past two decades, his laboratory has studied the role of RB and E2F in growth regulation and differentiation. More recently, his laboratory has focused on epigenetic and transcriptional control of myogenic differentiation. Another area of interest concerns the mechanistic basis of centriole and ciliary biogenesis. He serves on multiple grant review panels and is a reviewer or editorial board member for many peer-reviewed journals.
Marc Freeman started his laboratory at The University of Massachusetts Medical School in 2004 (Worcester, MA). The Freeman laboratory studies a number of topics relevant to neuron-glia signaling in the healthy and diseased brain, including: glial engulfment of neuronal cell corpses and axonal debris, molecular mechanisms of axon auto-destruction, and mechanisms by which glia control of neural circuit assembly such as glial pruning of axons, dendrites and synapses. The model systems they employ for their studies include Drosophila, mice, and human cell lines. Freeman is a Professor and Vice Chairman of the Department of Neurobiology, and in 2013 was appointed an Investigator of the Howard Hughes Medical Institute.
Simone Fulda, MD, is Full Professor of Experimental Cancer Research and the Director of the Institute for Experimental Cancer Research in Pediatrics at the Goethe-University Frankfurt, Germany. She trained as both pediatric oncologist and molecular/cell biologist in Germany, Harvard Medical School Boston, San Francisco, Phoenix and in the U.K. Her research focusses on the elucidation and exploitation of cell death signaling pathways in cancers and during cancer therapy.
Douglas R Green
Doug Green is the Peter C. Doherty Endowed Chair of Immunology at St Jude Children’s Research Hospital. Prior to this he was Head of the Division of Cellular Immunology at the La Jolla Institute for Allergy and Immunology. Professor Green received his PhD from Yale University. His research has focused on the process of active cell death and cell survival. His research extends from the role of cell death in the regulation of cancer and immune responses in the whole organism to the fundamental molecular events directing the death of the cell. He has published over 450 papers, chapters, and books, and is an ISI "highly cited" investigator. His recent book is “Means to an End: Apoptosis and Other Cell Death Mechanisms,” published in 2011 by Cold Spring Harbor Laboratory Press and available at Amazon.
Mads Gyrd-Hansen is at the Ludwig Institute of Cancer Research and is an Associate Professor at the University of Oxford. His research focuses on understanding how pro-inflammatory signalling is regulated in the context of innate immune responses, tumorigenesis and cancer. His main interests are in the function and regulation of the ubiquitin system in these processes, with emphasis on delineating the non-degradative functions of polyubiquitin chains. He studied Biochemistry at the University of Copenhagen and carried out his PhD at the Danish Cancer Society Research Centre. This was followed by postdoctoral work at the Institute of Cancer Research in London, where he became interested in ubiquitin. He has led a research group since 2011, initially at the University of Copenhagen and at the Ludwig Cancer Research Oxford Branch since 2013. His recent work has investigated how ubiquitin controls signalling downstream the bacteria sensor NOD2 - a pattern recognition receptor central for maintaining an efficient immunological barrier in the gastrointestinal tract, and for which loss-of-function mutations predisposes to inflammatory bowel disease (IBD). Notably, his group identified the ubiquitin ligases X-linked IAP (XIAP) and LUBAC, and the deubiquitinases OTULIN and CYLD, as central signal integrators of ubiquitin-mediated pro-inflammatory NOD2 signalling. Mads has received several accolades, including the EMBO Young Investigator award.
J Marie Hardwick
Dr. Hardwick is a Professor at Johns Hopkins University. She holds appointments in the Schools of Public Health and Medicine, Departments of Molecular Microbiology & Immunology, Pharmacology and Molecular Sciences, Neurology, Biochemistry & Molecular Biology, and Oncology. She earned a PhD in microbiology from the University of Kansas and was a postdoctoral fellow in virology at the University of Alabama, Birmingham. Her lab uses mouse, Drosophila and yeast genetic model systems to understand the molecular determinants of cell death, particularly in the brain. The overall strategy is to determine the normal cellular function of cell death factors.
The Hardwick lab identified non-apoptotic "day-job" functions of anti- and pro-apoptotic regulators of cell death including cellular and viral BCL-2 family proteins. They found that BCL-2 family proteins and caspases regulate viral pathogenesis in the brain, that BCL-2 family proteins can be cleaved by caspases to convert them from anti- to pro-death functions, and that BCL-2 proteins regulate neuronal activity and alter seizure behaviors in mice. BCL-xL regulates membrane structure, mitochondrial membrane dynamics and energetics. She developed yeast (Saccharomyces cerevisiae) as a model to identify novel factors that mediate gene-dependent cell death. These approaches also revealed the pressures of cell death on genome evolution. Knocking out any individual gene in the yeast genome leads to two mutations, the engineered gene knockout and a specific second evolved mutation in another gene that dramatically alters cell death and/or growth rates. These evolved yeast mutations have led to the identification of new human disease genes that cause neurodegeneration. She is the inaugural David Bodian Professor and is a fellow of the American Association for the Advancement of Science.
H Robert Horvitz
Dr. H Robert Horvitz received the Nobel Prize in Physiology or Medicine in 2002. He is the David H. Koch Professor of Biology at the Massachusetts Institute of Technology (MIT); an Investigator of the Howard Hughes Medical Institute; Neurobiologist (Neurology) at the Massachusetts General Hospital; a Member of the MIT McGovern Institute for Brain Research; and a Member of the MIT Koch Institute for Integrative Cancer Research. Dr. Horvitz received S.B. degrees in Mathematics and in Economics from MIT in 1968. He performed his graduate studies at Harvard University in the laboratories of Drs. James Watson and Walter Gilbert and received his PhD in Biology in 1974. Dr. Horvitz then joined Dr. Sydney Brenner as a postdoctoral fellow at the Medical Research Council Laboratory of Molecular Biology in Cambridge, England. Since 1978, Dr. Horvitz has been an Assistant, Associate and Full Professor in the Department of Biology at the Massachusetts Institute of Technology. His research involving C. elegans has helped define evolutionarily conserved molecular genetic pathways important in human biology and human disease, including the pathway responsible for programmed cell death, or apoptosis. Dr. Horvitz is a member of the Board of Trustees of the Massachusetts General Hospital and is Chairman of the Board of Trustees of the Society for Science and the Public. He was President of the Genetics Society of America. He has served on many editorial boards, visiting committees and advisory committees and has received numerous honors. Dr. Horvitz has been a consultant to pharmaceutical, biotechnology and venture capital companies.
Ichijo's research group is based at The University of Tokyo (http://www.f.u-tokyo.ac.jp/~toxicol/html/member/ichijo.html), Japan. Hidenori Ichijo performed his PhD at the Tokyo Medical and Dental University. In 1998, he became professor and PI at the Tokyo Medical and Dental University. His research activities focus on molecular mechanisms of stress signalling pathways, including ASK family MAP kinases, PGAM5 mitochondrial protein phosphatase, and SOD1-Derlin-1-dependent ER stress.
These phenomena are studied in an integrated way at the level of biochemistry, cell biology and various diseases models. His research increasingly uses genome-wide siRNA library screening, chemical biology, high content screening and development of conditional transgenic models. Hidenori Ichijo's work has been published in more than 227 articles and has been cited over 21,000 times, with an h index of 75.Hidenori Ichijo has been vice president of The Japanese Biochemical Society (2007-2008, 2011-2013) and is a president elect of 39th annual meeting of The Molecular Biology Society of Japan (MBSJ) (http://www.mbsj.jp/en/meetings/annual/index.html) (2016). He received Academic Award of the Mochida Memorial foundation in 2013.
Ricky Johnstone is based at Peter MacCallum Cancer Center, Melbourne, Australia where he established the Gene Regulation Laboratory and heads the Cancer Therapeutics Program aimed at bringing together a critical mass of researchers with the aim to translate fundamental research findings into clinical outcomes that will benefit cancer patients. In 2008 Dr Johnstone was appointed as an Assistant Director of Research at the Peter MacCallum Cancer Centre and will play a key role in defining the strategic direction of the research division over the coming years. Using knockout mice, the Johnstone Laboratory is involved in the following research areas: collaborative basic, translational and clinical research into the anti-cancer activities of histone deacetylase inhibitors; basic and pre-clinical characterization of novel apoptosis-inducing therapeutic agents used alone and in combination; use of functional genomics-based screens to identify novel tumor suppressor genes and genes that regulate the apoptotic response to new anti-cancer agents; and characterization of novel signal transduction pathways stimulated by type I and II interferons.
Scott H Kaufmann
Dr. Kaufmann received his M.D. and Ph.D. degrees from the Johns Hopkins University School of Medicine, where he also completed clinical training and a postdoctoral fellowship in experimental oncology. His early career independent work provided the first biochemical demonstration that widely used anticancer drugs induce apoptosis in susceptible cells (PMID: 2790800) and the first demonstrations of caspase-mediated proteolysis during apoptosis (PMID: 2790800, 8358726, and 8090205). He is currently Professor and Chair of the Department of Molecular Pharmacology at the Mayo Clinic, where his translational efforts involve the preclinical and early clinical development of new antineoplastic agents. Current studies in the Kaufmann laboratory also continue to investigate the regulation of apoptosis, in particular modulation of the death receptor pathway for therapeutic benefit in ovarian cancer and hematological malignancies (PMID: 24895135) as well as mechanisms of stress-induced Bax/Bak activation at the molecular level (PMID: 21727192 and 25246614).
Sharad Kumar is the co-Director of the Centre for Cancer Biology, a Research Professor and Chair of Cancer Biology at the University of South Australia, and an affiliate Professor at the University of Adelaide. His laboratory discovered a number of key genes/proteins, including the developmentally regulated Nedd genes, such as Nedd1, a key centrosomal protein required for y-tubulin recruitment; Nedd2 (caspase-2), one of the first mammalian caspases; Nedd4, the first and the founding member of the WW-HECT type of ubiquitin-protein ligase family; Nedd5 (Sept2), the first characterised mammalian septin; and Nedd8, a ubiquitin-like protein involved in a protein modification pathway, now widely known as neddylation. The laboratory also discovered a large part of the Drosophila cell death machinery, including four caspases and both Bcl-2-like proteins, and defined a caspase-independent, autophagy-depended cell death process. Other discoveries from his group include Ndfips as regulators of the Nedd4 family of ubiquitin ligases, the functions of Nedd4 family of ubiquitin ligases and Ndfips in regulating ion channels and transporters, and an unexpected role of caspase-2 as a tumour suppressor. His group continues to study caspase biology and functions, mechanisms of developmentally programmed cell death, and the physiological functions and regulation of the Nedd4 family members. He is a Fellow of the Australian Academy of Science and 2013 ASBMB Lemberg Medallist. His work has also been recognised through the 2003 ASBMB Amersham Biosciences Award, the 2009 Ranbaxy Research Award and the 2013 FAOBMB Research Excellence Award.
Professor Xin Lu studied Biochemistry at Sichuan University and then Cancer Research at Peking Union Medical School in Beijing. She was awarded an IARC WHO fellowship to come to the Imperial Cancer Research Fund in London in 1986 and studied for her PhD under Birgit Lane. In 1993 she joined the Ludwig Institute for Cancer Research (LICR), St. Mary's Branch, Imperial College as an Assistant Member and was progressively promoted to LICR Full Member and Professor at Imperial College in 2000. In 2004, she was appointed as the Director of the LICR’s UCL Branch but moved the unit to Oxford in 2007. She is an elected Member of EMBO and Fellow of the Academy of Medical Sciences.
Professor Lu's research is focused on understanding tumour suppression and to identify molecular switches that selectively kill cancer cells. Cancer is a disease where cells grow in the wrong place at the wrong time. Regenerative medicine involves growing cells to replace the ones that were lost or damaged. Therefore, understanding molecular mechanisms that control cell growth is vital, both to stop cancer cell growth and to grow normal cells to replace the damaged ones. Professor Lu's research team has been one of the major research groups in the world to study the regulation of the tumour suppressor function of the p53 protein whose function is lost in most human cancers. The majority of nuclear import pathways are mediated by importin-cargo interactions. Yet around 50% of all nuclear proteins do not use this pathway. Through a detailed understanding of the regulation of the ASPP proteins, Professor Lu's group has identified identified a code that defines RaDAR as a novel nuclear import pathway of ankyrin repeats (AR) containing proteins. AR is a structural motif found in over 250 human proteins with diverse functions. The RaDAR (RanGDP/AR) pathway is acquired by the most common familial melanoma-associated CDKN2A mutation, leading to nuclear accumulation of mutant p16ink4a. It is frequently used by AR-containing transcriptional regulators, especially those regulating NF-ĸB/p53. All these suggest the existence of an Ankyrin repeats signaling and its role in infection and cancer.
Jan Paul Medema
Jan Paul Medema studied Chemistry in Leiden graduating in 1991 with a specialisation in biochemistry and medical biochemistry. He continued his training under the guidance of professor Hans Bos at the University of Utrecht and received his PhD in 1996 on the topic of the oncoprotein p21Ras. He then decided to study the role of programmed cell death in tumor biology and immunology in order to understand the basic concepts of cell death signalling and the way these are perturbed in cancer. He unravelled several modes of cell death escape, specifically in the face of a cytotoxic immune response. Later on his work moved into the direction of cancer heterogeneity and its role in cell death resistance, tumor growth and therapy response. His work centers around the role of cancer stem cells in these processes as well as the role of inter-patient heterogeneity in the aggressiveness of tumors.
Dr. Nagata obtained a Ph.D. in 1977 from University of Tokyo for the thesis "Purification and characterization of polypeptide chain elongation factor from pig liver". From 1977 to 1981, he did post-doctoral research in laboratory of Prof. Charles Weissmann (Institute of Molecular Biology, University of Zürich), where human interferon-α cDNA was identified. In 1982, Dr. Nagata returned to Institute of Medical Science, University of Tokyo as an assistant professor, and identified cDNA for granulocyte colony-stimulating factor (G-CSF). In 1987, Dr. Nagata was appointed as a Head of Molecular Biology Department of Osaka Bioscience Institute, where he characterized G-CSF receptor, and started to work on apoptosis. From 1995-2007, he was a professor in Department of Genetics, Osaka University Medical School. In 2007, he moved to Kyoto University as a professor in Department of Medical Chemistry, Graduate School of Medicine. Dr. Nagata was the president of Japanese Biochemical Society (2005-2006), and Japanese Society of Molecular Biology (2007-2008). He was a councilor for Human Frontier Science Program in Strasbourg from 2006 to 2009, and a member of Science Council of Japan since 2008. Dr. Nagata serves or served as an editorial member of various journals including Science, Immunity, Cancer Cell, and Cell Death Differ. The awards include Emil von Behring Prize (Germany), Robert Koch Award (Germany), Prix Lacassagne (France), Debrecen Award (Hungary), Japan Academy Prize and Imperial Prize from the Japan Academy, and Keio Medical Science Prize from Keio University. Dr. Nagata is recognized as a Person of Cultural Merit from the Japanese Government in 2001 and nominated to an associate of The Japan Academy in 2010. He obtained a Honorary Doctorate from University of Zürich in 2012.
Moshe Oren received his Ph.D. in 1978. Upon completing post-doctoral training in Princeton University and SUNY-StonyBrook, he joined Weizmann Institute in 1981. His main area of research is cancer biology, with particular focus on the p53 tumor suppressor gene. Moshe Oren is married to Rachel, and is father to Yossi, Yael, Yaara and Yonathan and grandfather to Yair, Renana, Arbel, Dvir and Ayelet.
Dr Piacentini is a Full Professor at University of Rome "Tor Vergata", Rome, Italy. He is also President of the Biotechnology Program at the university, is on the Board of Directors for the European Cell Death Organization and is Basic Research Director at the National Institute for Infectious Diseases in Rome. Since 1993, he has been the Founder and an Editor of the journal Cell Death & Differentiation. He is a journal reviewer for other journals including Brain Research, Cancer Research, Cancer Cell, and Nature. Furthermore, Dr Piacentini has organized several international meetings including the 14th Euroconference on "Apoptosis or Programmed Cell Death". He has co-edited a book entitled "Methods in Enzymology: Programmed Cell Death". His research interest is to understand the molecular mechanisms regulating apoptosis and autophagy under both physiological and pathological conditions. In particular, he is interested in the pathogenesis of Huntington's disease with particular regard to the role of TG2 and mitochondria. He is also studying infectious diseases such as HIV and HCV. With autophagy, he is characterizing the role of Ambra1, a key component of the Beclin1 complex.
David C Rubinsztein
David Rubinsztein did his medical training, BSc(Hons) and PhD at the University of Cape Town. He came to Cambridge in 1993 as the first Senior Registrar in the UK in Genetic Pathology and obtained his MRCPath and Certificate of Completion of Specialist Training in 1997 and FRCPath in 2005. When he came to Cambridge, he became interested in the biology of neurodegenerative diseases, particularly Huntington's disease and established a research group to investigate this area. In 1998, he was the first awardee of a Glaxo Wellcome Research Fellow, and subsequently was awarded a Wellcome Trust Senior Research Fellowship from 2002-2011. Since 2012, he has held a Wellcome Trust Principal Research Fellowship, the most senior of their personal research awards. He is Professor of Molecular Neurogenetics, an Honorary Consultant in Medical Genetics, and Deputy Director of the Cambridge Institute for Medical Research at the University of Cambridge.
David Rubinsztein has made important contributions to the understanding of the pathogenesis of Huntington's disease and related conditions, and towards developing rational therapeutic strategies for these conditions. He has identified FDA-approved drugs that may have benefit in these diseases, since he has demonstrated their efficacies and protective mechanisms in a range of cell and animal models. He has helped to illuminate the relevance of autophagy defects as a disease mechanism and autophagy upregulation as a possible therapeutic approach in various neurodegenerative diseases, and has contributed to the basic cell biology of this important catabolic process. He is a frequent speaker at international conferences and has published more than 300 papers, including recent studies in leading journals like Cell, Nature Cell Biology, and Molecular Cell.
His work has been recognised by various honors including:
- 2004: Fellow of the Academy of Medical Sciences
- 2007: Graham Bull Prize in Clinical Science (from Royal College of Physicians)
- 2009: Spinoza Visiting Professorship (University of Amsterdam)
- 2011: Elected member of EMBO (European Molecular Biology Organisation)
- 2014: Selected as one of Thomson Reuters' Highly Cited Researchers 2014 in the categories Biology and Biochemistry and Molecular Biology and Genetics (http://highlycited.com/).
Paolo Salomoni is at Samantha Dickson Brain Cancer Unit, UCL Cancer Institute, London, UK. Paolo Salomoni was appointed Brian Cross Professorial Research Associate at the UCL-Cancer Institute, Department of Cancer Biology in October 2009. He leads the Samantha Dickson Brain Cancer Unit, the first UK research centre fully dedicated to brain cancer research, funded by The Brain Tumour Charity (formerly known as Samantha Dickson Brain Tumour Trust). He is also part of the UCL Centre for Stem Cells and Regenerative Medicine and of UCL Neuroscience. Paolo started his PhD training at the Kimmel Cancer Center, Philadelphia, under the supervision of Bruno Calabretta. In 1999, he moved to the Memorial Sloan-Kettering Cancer Center, New York, in the laboratory led by Pier Paolo Pandolfi. After finishing his postdoctoral training at MSKCC in 2003, he moved to the Medical Research Council Unit in Leicester, where he was programme leader track and then programme leader.
His main focus is on molecular mechanisms underlying cell fate control in normal and neoplastic stem cells, and how alterations of these mechanisms contribute to cancer. In particular, we have investigated two main processes involved in tumourigenesis:
- alteration of chromatin function and the interchromatin space;
- metabolic deregulation. His work has several translational ramifications, as studies conducted in his laboratory have led to a number of Phase II clinical trials for the use of an metabolic drugs in cancer therapy.
Guy Salvesen earned his Ph.D. in biochemistry from Cambridge University. He conducted postdoctoral research at the University of Georgia, Strangeways Laboratory and MRC Laboratory of Molecular Biology in Cambridge. In 1987 he was appointed Assistant Medical Research Professor at Duke University. Dr. Salvesen was recruited to Sanford-Burnham Medical Research Institute in 1996. He is Professor in the Program in Cell Death and Survival Networks, Dean of the Graduate Program in Biomedical Sciences at Sanford-Burnham, and Director of Scientific Training at Sanford-Burnham, and holds an Adjunct Professorship in Molecular Pathology at the University of California, San Diego. He is on the editorial board of several journals including Cell Death and Differentiation, Vice Chair for the Americas and Reviews Editor of the Biochemical Journal, and Co-founder of the International Proteolysis Society.
Yufang Shi is Director and Professor of the Institute of Health Sciences, Shanghai Institutes for Biological Sciences of Chinese Academy of Sciences, and Shanghai Jiao Tong University School of Medicine. He received his Ph.D. in Immunology from University of Alberta in 1992. He worked under the supervision of Dr. Douglas Green. There he established the concept of activation-induced cell death (AICD) and found the critical role of c-myc in the regulation of T cell apoptosis. His early investigation provided the foundation of using rapamycin as an adjuvant for chemotherapy. In recent studies, his team has been investigating the mechanism of immunosuppression mediated by mesenchymal stem cells, a key research area for proper application of stem cells in clinical settings. Dr. Shi's group is currently working on the following aspects:
- Understanding how immunosuppression is mediated by mesenchymal stem cells;
- Tumor stroma and tumor immunology;
- Molecular mechanisms of activation-induced cell death in T cell subpopulations.
Dr. Shi has authored over 150 scientific papers including those in Nature, Science, Nature Medicine, Nature Immunology, Immunity, Journal of Experimental Medicine and Cell Stem Cell. Dr. Shi was an Associate Editor of The Journal of Immunology from 1999 to 2003 and is currently an Editor-in-Chief of Cell Death & Disease, a Receiving Editor of Oncogene, and Editorial Board Members on several other journals including Journal of Biological Chemistry, Journal of Molecular and Cell Biology, Stem Cells and Translational Medicine, Cellular and Molecular Immunology, and Cell Death & Differentiation.
John Silke completed a law degree in King's College London, before seeing the error of his ways and completing a second degree in Biochemistry at Churchill College, Cambridge (1992). He completed a PhD in Zürich (1997), Switzerland under Prof. Walter Schaffner, looking at the role of DNA methylation in the regulation of transcription. A Swiss fellowship allowed John to go to Australia to work on cell death mechanisms as a post-doc for Dr. David Vaux in the WEHI (1997-2005). After a five year stint running a lab in La Trobe University, he returned to the WEHI (2011) where his lab focuses on the programmed cell death pathways; apoptosis and necroptosis. He has collaborated with several pharmaceutical companies and is a strong advocate and proponent of using small drug like molecules to complement genetic analyses to investigate cell death pathways involved in regulating inflammation. In particular he is interested in the Inhibitor of APoptosis proteins and their ability to regulate signalling cascades involving RIP Kinases.
Simon Hans-Uwe, M.D., Ph.D., is Professor of Pharmacology and since 2000, has been Director of the Department of Pharmacology, University of Bern in Switzerland. After obtaining a doctoral thesis, he specialized in Clinical Immunology, at the University of Jena, Germany. His Postdoc (1990-92) was completed at the Mount Sinai and General Hospitals, University of Toronto, Canada. Professor Hans-Uwe became a Principal Investigator and Deputy Director (1992-2000) at the Swiss Institute of Allergy and Asthma Research, University of Zurich, Davos, Switzerland, with "Habilitation" in Experimental Immunology (1996). He also obtained a Doctoral thesis (Ph.D. 1996-2001) at the Department of Pharmacology, Hebrew University of Jerusalem, Israel. Research interests include:
- Role of apoptosis and autophagy in inflammatory diseases and cancer.
Among other academic and administrative services, he served as President of the Swiss Society of Pharmacology and Toxicology (SSPT; 2004-2007), President of the Swiss Society of Experimental Pharmacology (SSEP; 2005-2008), President of the European Cell Death Society (ECDO; 2007-2009), and President of the Union of the Swiss Societies for Experimental Biology (USSBE; 2007-2010). He is the Editor-in-Chief of Allergy, the European Journal of Allergy and Clinical Immunology.
Joint Head of the Molecular Genetics of Cancer Division at The Walter and Eliza Hall Institute of Medical Research in Melbourne, Australia. His research is focused on programmed cell death and how defects in this process cause cancer or autoimmune disease and affect the response of tumour cells to anti-cancer therapy. Key discoveries have been that abnormalities in cell death control can cause cancer or autoimmune disease; that Bcl-2 antagonizes multiple pathways to cell death; that Bcl-2 collaborates with c-mycin tumorigenesis; that Bcl-2 inhibits the death of lymphocytes that fail to receive a signal through cytokine or antigen receptors; that Bcl-2 and death receptors regulate distinct pathways to apoptosis; that DNA damage can induce apoptosis in lymphocytes via a pathway that is independent of p53 but can be blocked by Bcl-2; the discovery of pro-apoptotic BH3-only proteins Bim and Bmf; that BH3-only proteins are essential for initiation of programmed cell death and stress-induced apoptosis; that Bim is required for negative selection of autoreactive thymocytes and mature T cells; that the BH3-only proteins Puma and Noxa are essential for DNA damage-induced apoptosis mediated by the tumour suppressor p53. Current efforts include determination of which anti-apoptotic proteins are essential for the development and, more important for clinical translation, the sustained growth of different cancer types. This includes efforts to develop antagonists of pro-survival proteins for cancer therapy.
David Vaux is currently at The Walter and Eliza Hall Institute (WEHI), in Melbourne, Australia. He graduated in medicine from the University of Melbourne, before completing a PhD at WEHI, and a post-doc at Stanford. He is best known for his work on Bcl-2, having found in 1988 that it acted, unlike other oncogenes known at the time, to inhibit cell death, rather than promoting cell proliferation. By showing human Bcl-2 could inhibit developmental cell death in C. elegans, he showed that apoptosis and programmed cell death were the same, evolutionarily conserved process. He was among those who first identified the mammalian inhibitor of apoptosis (IAP) proteins, and their mammalian antagonists, such as Smac/Diablo. He is currently on the Scientific Advisory Board of TetraLogic Pharmaceuticals.
Professor Andreas Villunger conducted his undergraduate studies in Biology in Salzburg and Innsbruck, Austria, and obtained his Master and PhD degrees for research on cytokine signalling in multiple myeloma. After post-doctoral work in the Ras/PKC signalling field, Andreas moved to the Walter and Eliza Hall Institute, Melbourne, Australia, to conduct research on the role of Bcl-2 family proteins in lymphocyte development and transformation. After his return to Austria in 2003, he continued to work on Bcl-2 family proteins in the immune system and started to explore the role of caspases in tumor suppression. He has been awarded the prestigious START Prize by the Austrian Science Fund and the Novartis Prize for Medical Research. In 2009, he was appointed full professor at the Medical University Innsbruck and is head of the Division of Developmental Immunology.
Professor Karen Vousden is the Director of the Cancer Research UK Beatson Institute in Glasgow. The Beatson Institute carries out a program of world-class science directed at understanding key aspects of cancer cell behavior, and provides a state of the art facility where basic and clinical scientists can work together to translate these discoveries into new therapies and diagnostic/prognostic tools to help cancer patients. Karen's own research focuses on the regulation and function of the tumour suppressor protein p53. Karen received her Ph.D. in Genetics from the University of London, followed by postdoctoral fellowships with Chris Marshall at the Institute of Cancer Research in London and Douglas Lowy at the National Cancer Institute in the USA.
After joining the Ludwig Institute for Cancer Research in London moved back to the NCI in 1995 where she was Chief of the Regulation of Cell Growth Laboratory, before taking up her current position in 2002. Karen has been elected to the Royal Society, the Royal Society of Edinburgh, EMBO, the Academy of Medical Sciences and the European Academy of Sciences, and received honorary DScs from the Universities of London and Strathclyde. She was awarded the Tenovus Gold Medal in 1998, the Sir Frederick Gowland Hopkins Medal in 2008, the Royal Medal from the Royal Society of Edinburgh in 2009 and was honoured as Commander of the British Empire in 2010. She is presently on the Board of Directors of the AACR.
Dr. Hong Zhang is an Investigator in the Institute of Biophysics, Chinese Academy of Sciences (CAS). He graduated from Albert Einstein College of Medicine and had his postdoc training in Massachusetts General Hospital Cancer Center, Harvard Medical School. Before joining the Institute of Biophysics, CAS in 2012, he was an Assistant Investigator (2004-2009) and Associate Investigator (2009-2012) of the National Institute of Biological Sciences, Beijing. The research in his lab currently focuses on the molecular mechanisms of the autophagic machinery, the regulation of autophagy activity during development and the physiological function of autophagy. The awards he has won in recent years include the 6th C.C.Tan (Jia-Zhen Tan) Life Science Award (2013), National Outstanding Young Scientist Award (2012) and HHMI International Early Career Scientist Award (2012). Dr. Hong Zhang is on the Board of Reviewing Editors for eLife, is an Associate Editor for Autophagy and is also on the editorial Board for Journal of Cell Science, EMBO reports, JBC and Cell Death and Differentiation.
Professor Laurence Zitvogel, MD (clinical oncology), PhD (tumor immunology), PU-PH Faculty Paris Sud, University Paris XI (Clinical Biology), graduated in Medical Oncology from the School of Medicine of the University of Paris in 1992. She started her scientific career when she was at the University of Pittsburgh in the USA in Michael Lotze’s laboratory. She became Research Director at Institut National de la Santé et Recherche Médicale U1015, in a laboratory located at Institut Gustave Roussy, a large cancer Center in Villejuif/France and the Head of the Center for Clinical Investigations CICBT 507 for vaccine developments at Villejuif. She has been actively contributing to the field of cancer immunology and immunotherapy, and she brought together basic and translational research, including the design of cancer therapies through combined animal studies and Phase I patient trials. Her expertise is mainly dendritic cell and innate effector biology and relevance during tumour development as well as exosome-based vaccine designs. She pioneered the concept of immunogenic cell death and showed that chemotherapy, radiotherapy and inhibitors of tyrosine kinase mediate their tumoricidal activity, at least partly through the immune system. She is currently working on the mode of action of immune checkpoint blockers.