Paul Bornstein is currently Emeritus Professor of Biochemistry and Medicine at the University of Washington. He received his BA from Cornell University and MD from New York University. He trained in Surgery and Internal Medicine at Yale New Haven Hospital, and then spent a year as an Arthritis Foundation Postdoctoral Fellow at the Pasteur Institute in Paris.
In 1963, Dr. Bornstein joined the US Public Health Service as a Research Investigator and worked for four years on collagen biochemistry with Karl Piez at the National Institutes of Health. He was discharged from the USPHS in 1967 as a Senior Surgeon, with a rank of Commander in the US Coast Guard.
After leaving NIH, Dr Bornstein accepted a position as Assistant Professor of Medicine at the University of Washington, and in the following year obtained a joint appointment in Biochemistry. In 1973 he achieved the rank of full professor in Biochemistry and Medicine Over the years, Dr Bornstein’s research interests have changed from protein chemistry to the cell biology of cell-matrix interactions, and then to the molecular biology of thrombospondins and other matricellular proteins. He has held positions as Visiting Professor at UCSD, with Jonathan Singer, at Louis Pasteur University in Strasbourg with Pierre Chambon, and at the Whitehead Institute, MIT, with Rudolph Jaenisch.
Dr. Bornstein has been awarded a Lederle Medical Faculty Award, a Research Career Development Award from the NIH, a Josiah Macy Faculty Scholar Award, a John Simon Guggenheim Memorial Fellowship, a MERIT Award from the NIH, and most recently a Solomon Berson Alumni Achievement Award in Basic Science from NYU School of Medicine. He has been elected to membership in the American Society for Clinical Investigation and in the Association for American Physicians. He has also served on many Editorial Boards including the American Journal for Cell Biology, and the Journal of Biological Chemistry.
Dr. Bornstein founded the American Society for Matrix Biology in 2000 and served as its second Vice-President and President; he also served as Vice-President and President of the International Society for Matrix Biology, chaired two Gordon Conferences in the matrix field, and served on numerous Academic and Industrial Advisory Boards He is the author of nearly 300 research papers, reviews and book chapters.
Edward J. Calabrese is a Professor of Toxicology at the University of Massachusetts, School of Public Health and Health Sciences, Amherst. Dr. Calabrese has researched extensively in the area of host factors affecting susceptibility to pollutants, and is the author of over 600 papers in scholarly journals, as well as more than 10 books, including Principles of Animal Extrapolation; Nutrition and Environmental Health, Vols. I and II; Ecogenetics; Multiple Chemical Interactions; Air Toxics and Risk Assessment; and Biological Effects of Low Level Exposures to Chemicals and Radiation. Along with Mark Mattson (NIH) he is a co-editor of the recently published book entitled: Hormesis: A Revolution in Biology, Toxicology and Medicine.
Dr. Calabrese has been a member of the U.S. National Academy of Sciences and NATO Countries Safe Drinking Water committees, and on the Board of Scientific Counselors for the Agency for Toxic Substances and Disease Registry (ATSDR). Dr. Calabrese also serves as Chairman of the Biological Effects of Low Level Exposures (BELLE) and as Director of the Northeast Regional Environmental Public Health Center at the University of Massachusetts. Dr. Calabrese was awarded the 2009 Marie Curie Prize for his body of work on hormesis.
Over the past 20 years Professor Calabrese has redirected his research to understanding the nature of the dose response in the low dose zone and underlying adaptive explanatory mechanisms. Of particular note is that this research has led to important discoveries which indicate that the most fundamental dose response in toxicology and pharmacology is the hormetic-biphasic dose response relationship. These observations are leading to a major transformation in improving drug discovery, development, and in the efficiency of the clinical trial, as well as the scientific foundations for risk assessment and environmental regulation for radiation and chemicals.
After 18 years as Director of the Kolling Institute of Medical Research at the University of Sydney, Rob Baxter stepped down in January 2012 to continue his research on the biochemistry, cell biology, and endocrinology of the insulin-like growth factors and their binding proteins. He remains at the Kolling Institute where he heads the Hormones and Cancer Division.
His research has contributed to understanding both the regulation of normal tissue and body growth, and the aberrant cellular growth in cancer and overgrowth syndromes. His group’s achievements include characterizing the protein complexes that carry IGFs in the circulation, and discovering how IGF binding proteins affect cancer cell growth by modulating cell signaling pathways. His collaborative clinical studies have significantly advanced understanding of the role of these proteins in a variety of conditions including pregnancy, tumor-related hypoglycemia, and critical illness. He also heads the laboratory for Cellular and Diagnostic Proteomics in the Kolling Institute, and is involved in biomarker discovery studies in breast and pancreatic cancers, and growth disorders.
Rob received his PhD in Biochemistry from the University of Sydney in 1973, was awarded a DSc in 1990, and was elected a Fellow of the Australian Academy of Science in 2004. He has over 300 research publications, cited >18,000 times. He has served on journal Editorial Boards including Endocrinology, American Journal of Physiology (Endo & Metabolism), and Journal of Biological Chemistry. He has given keynote plenary lectures at conferences in Australia, Europe, South America and the USA, and has received several major research awards including the Dale Medal (Society for Endocrinology, UK), Wellcome Australia Medal, Lemberg Medal (ASBMB) and Ramaciotti Medal for Excellence in Biomedical Research. He served as president of the Endocrine Society of Australia from 1988-1990, chaired the National Committee for Biomedical Sciences of the Australian Academy of Science from 2006-2009, and is currently Vice-President of the International Society for IGF Research.
Carlo M. Croce, MD, is the Professor and Chair of Molecular Virology, Immunology and Medical Genetics, Director of the Human Cancer Genetics Program, and Director of the Institute of Genetics at The Ohio State University Comprehensive Cancer Center. His research has revealed the variety of mutated genes involved in leukemias, lymphomas and other cancers.
Dr. Croce is world-renowned for his contributions involving the genes and genetic mechanisms implicated in the pathogenesis of human cancer. During the course of his career, he discovered the juxtaposition of the human immunoglobulin genes to the MYC oncogene, the deregulation of MYC in Burkitt lymphoma, the ALL1 gene involved in acute leukemias, the TCL1 gene associated with T-cell leukemias, and cloned and characterized the BCL2 gene involved in follicular lymphoma.
Dr. Croce has also uncovered the early events involved in the pathogenesis of lung, nasopharyngeal, head and neck, esophageal, gastrointestinal and breast cancers. His discoveries have led to revolutionary innovations in the development of novel and successful approaches to cancer prevention, diagnosis, monitoring and treatment, based on gene-target discovery, verification and rational drug development.
He is a member of the National Academy of Sciences, Institute of Medicine, American Academy of Arts and Sciences and an AAAS Fellow. He is principal investigator on seven federal research grants and has more than 1000 peer-reviewed, published research papers.
Judith Campisi received a PhD in Biochemistry from the State University of New York at Stony Brook, and postdoctoral training in cell cycle regulation and cancer at the Dana-Farber Cancer Institute and Harvard Medical School.
As an Assistant Professor at the Boston University Medical School, she began studying the role of cellular senescence in suppressing the development cancer. However, she soon became convinced that senescent cells also contributed to aging. She left Boston University as an Associate Professor to accept a Senior Scientist position at the Lawrence Berkeley National Laboratory in 1991. In 2002, she established a laboratory at the Buck Institute for Age Research, where she is a Professor.
At both institutions, Judith Campisi established a broad program to understand various aspects of aging, with an emphasis on the interface between cancer and aging. Her laboratory made several pioneering discoveries in these areas, and her research continues to challenge and alter existing paradigms.
In recognition of the quality of her research and leadership, Judith Campisi has received numerous awards. These include two MERIT awards from the US National Institute on Aging, awards from the AlliedSignal Corporation, Gerontological Society of America and American Federation for Aging Research, the Longevity prize from the international IPSEN Foundation, the Bennett Cohen award from the University of Michigan and the Schober award from Halle University (Germany).
Judith Campisi is an elected a fellow of the American Association for the Advancement of Science, and serves on numerous national and international editorial and scientific advisory boards.
On the occasion of the ICCNS-Springer Award, Professor Campisi will give a presentation entitled :
Cancer and aging: Rival demons and signaling mechanisms
SYNOPSIS: Aging is the single largest risk factor for developing a panoply of diseases, including diseases as diverse as neurodegeneration and cancer. I will discuss recent progress in the common signaling mechanisms and cell fate responses that drive disparate age-related diseases. At the heart of this convergence is the cell fate decision termed cellular senescence. The pleiotropic senescence response entails a complex signaling cascade that ultimately determines important physiological responses ranging from tumor suppression to wound healing.
Dr. Meenhard Herlyn is Caspar Wistar Professor for Melanoma Research and Director of the Melanoma Research Center at The Wistar Institute in Philadelphia, as well as Founding President of the Society for Melanoma Research. Born and educated in Germany, Dr. Herlyn received his D.V.M. at the University of Veterinary Medicine, Hanover in 1970 and went on to receive a D.Sc. in medical microbiology at the University of Munich in 1976. That same year he came to The Wistar Institute as an associate scientist, where he worked in the emerging field of monoclonal antibodies, a technology that formed the basis of a portion of today’s new targeted therapeutics.
In 1981, Dr. Herlyn became an assistant professor and established a laboratory that is, today, one the largest and best-known research groups on the study of melanoma biology. Current major efforts include the ability to model the microenvironment of normal and diseased human tissue through 3-D artificial skin, providing his laboratory with a unique insight into cancer research. His laboratory also seeks to further define the various signaling pathways that work in cancer cells in order to discover new opportunities to inhibit cancer growth through targeted therapeutics. Since therapy is increasingly guided by the genetic aberrations in tumors, Dr. Herlyn and colleagues are developing combinations of compounds that take into account the genetic signature of tumors, with the specific goal of individualized cancer therapy.
Another major effort of his laboratory is the study of therapy resistance and tumor dormancy. Tumor cells can become dormant in primary tumors or at any time after metastatic dissemination and can persist in the dormant state for many years, allowing tumors to resist treatment. Dr. Herlyn’s working hypothesis is that defined tumor subpopulations are central to dormancy and drug resistance due to their slow turnover and their non-responsiveness to growth signals. His efforts seek to define how tumor cells escape dormancy for growth, invasion, and metastasis, and how to best develop strategies for therapy. Because of the significance of immunotherapy in treatment of melanoma patients, the laboratory has developed two models that closely mimic the conditions in humans with the ultimate goal of combining targeted and immune therapies.
Dr. Herlyn has over 500 peer-reviewed publications, over 85% of which are on melanoma. He has presented at dozens of national and international congresses and meetings, and has received accolades from prestigious organizations such as the Melanoma Research Foundation, American Skin Association, American Cancer Society, Society for Melanoma Research and more. He serves on numerous national and international editorial and scientific advisory boards.
On the occasion of the ICCNS-Springer Award, Dr. Herlyn will give a presentation entitled:
Understanding the biology of stem cells and melanocytes to develop new strategies for melanoma therapy
SYNOPSIS:We have developed a series of in vitro and in vivo models to elucidate the functions of genes associated with normal skin homeostasis and melanoma progression and metastasis formation. Using cDNA and RNA interference constructs and libraries in viral vectors, we have investigated the crosstalk of genes associated with cell-cell and cell-matrix interactions, intracellular signaling and transcriptional regulation. Three-dimensional skin with a ‘dermis’ containing fibroblasts and neural crest-like stem cells and ‘epidermis’ of keratinocytes and melanocytes mimic the skin environment, which we begin to populate also with inflammatory and immune cells. The 3-D models allow us to investigate mechanisms of transformation for melanocytes and stem cells, which are obtained from patients with high susceptibility for melanoma.
Work on tumor subpopulations lead to the development of a dynamic model of tumor maintenance, in which cells remained quiescence for prolonged periods of time until signals from the microenvironment activate them for proliferation. Invasion may occur even during dormancy, a cellular state of high resistance to any conventional therapy. The laboratory has been active in the development of targeted therapies in melanoma using small molecule inhibitors specific for kinases in key signaling pathways for proliferation and survival and of target genes that play critical roles in melanocyte development and tumor invasion and metastasis. We are developing groups of melanomas amendable to therapy with combinations of three or more drugs to also kill those cells that survive even double agent therapies.
Major emphasis is on intrinsic (innate) and acquired resistance in melanoma, in which cells escape primary therapy but can be successfully eliminated with inhibitors that are specifically targeting subpopulations of cells. Signaling inhibitors are also combined with immunotherapeutics using for the in vivo studies mice humanized with CD34+ hematopoietic stem cells from cord blood or induced pluripotent (iPS) cells and HLA-matched or autologous patient-derived xenografts (PDX), respectively. Thus, our work spans basic biological to translational investigations with defined clinical outcome. Strong emphasis is placed on multi-disciplinary collaborations with intra- and inter-institutional research groups.
Cynthia Kenyon helped to pioneer the field of aging, showing that the aging process is plastic and subject to regulation. Her work with long-lived mutant roundworms stimulated an intensive study of the molecular regulation of aging, and led to the realization that a conserved endocrine network regulates the aging process throughout the animal kingdom. Dr. Kenyon was on the UCSF faculty for many years, and is currently Vice President of Aging Research at Calico Life Sciences, a Google/Alphabet company. Summary of the presentation to be given on October 21, 2019 Lifespan and aging were once thought to be immutable: we just wear out like old cars. This paradigm has been overturned completely by molecular genetic experiments initiated in the roundworm C. elegans and now extended to many species. Changing specific genes or cells can extend healthy lifespan dramatically while postponing age-related disease. In this lecture, the history of these discoveries and the possibilities they create for the future will be discussed. Promising new research frontiers, such as the immortality of the germ lineage, will be described as well.
One goal of the International CCN Society (ICCNS) is to to facilitate the diffusion of scientific information and promote contacts with other Scientific Societies.
As a first step along this line of action, the Journal of Cell Communication and Signaling (JCCS) has been created as the official journal of the ICCNS.
In an effort to broaden the scientific scope of the International Workshop on the CCN family of Genes, Professor Bernard Perbal, President of the ICCNS and Peter Butler, a former Editor at Springer, have agreed upon the creation of an award to be given to a scientist in recognition of his/her scientific merit and contribution to his/her field of interest.
In order to trigger interactions between scientists working in the CCN field with those working on related biological and biomedical areas it has been agreed that the recipient of the ICCNS award would be offered the possibility to present his main achievements in the frame of an International CCN workshop. Since 2019, Springer stopped sponsoring this event.
The Award presented by the ICCNS covers the full cost of meeting registration fees.
The name of the recipient and the topic of the Educational Session will be communicated by the President of the ICCNS.