Institutrice Titulaire (Certificat d’Aptitude Professionnelle) Education Nationale
Maitresse d’Application (Certificat d’Aptitude Ecole d’Application) Education Nationale
Professeur des Ecoles Education Nationale
Financial Manager Laboratoire d’Oncologie Virale et Moléculaire Université Paris 7 – D. Diderot
Secretary of the International CCN Society
Treasurer of the International CCN Society
Administrative Manager and Coordinator JCCS-ICCNS
Foreign Postings
Glasgow Preschool, Scotland
Los Angeles, USA French Primary School – Mission Laique
Lecturer Holmes Junior High School
Istituto Rizzoli Bologna, Italy
Professional training
Desktop Publishing Université de Sceaux, France
Advanced English Training British Council, Paris, France
Computer skills : Word, Excel, Power Point, Photoshop, Filemaker
Publications
Perbal B, Perbal M, Perbal A. Cooperation is the key: the CCN biological system as a gate to high complex protein superfamilies’ signaling. J Cell Commun Signal. 2023
Perbal A. The 11th international workshop on the CCN family of genes in pictures. J Cell Commun Signal. 2023 Mar;17(1):13-23.
Perbal A. Correction to: 10th international workshop on the CCN family of genes, Niagara Falls, Canada, October 21-24, 2019. J Cell Commun Signal. 2021 Mar;15(1):153
Perbal A. The disastrous boomerang effects of “citation mania”. J Cell Commun Signal. 2017 Sep;11(3):291-295.
Perbal A, Perbal B. The CCN family of proteins: a 25th anniversary picture. J Cell Commun Signal. 2016 Sep;10(3):177-190. Epub 2016 Aug 31.
Perbal A. 8th international workshop on the CCN family of genes-Nice November 3-8, 2015. J Cell Commun Signal. 2016 Mar;10(1):87-101
Perbal A, Perbal B. CCN proteins, microenvironment, communication and signaling: why did we need a new journal? J Cell Commun Signal. 2007 Jun;1(1):1-3. doi: 10.1007/s12079-007-0007-x. Epub 2007 May 25. No abstract available.
Organization of International Conferences
International Workshop on Retroviral Pathogenesis 1996, 2005, Saint-Malo, France
International Workshop on the CCN family of Genes Organizer,2000, 2002, 2004, Saint-Malo, France Co-Organiser, 2006, Okayama, Japan Co-Organiser, 2008, Toronto, Canada Co-Organiser, 2010, Newcastle, Ireland Organiser, 2013, Nice, France Organiser, 2015, Nice, France Organiser, 2017, Saint-Malo, France Co-Organiser, 2019, Niagara Falls, Canada Organiser, 2022, Nice, France
The studies performed in the laboratory of Viral Oncology that I created in 1982 were aimed at understanding : • the molecular basis for the Myeloblastosis Associated Virus (MAV) tumorigenic potential. • the biochemical properties, mode of action and biological role of the CCN3 (NOV) protein in normal and pathological conditions with a particular emphasis to the potential use of the CCN3 protein as a new tool for molecular medicine The MAV strains usually induce osteopetrosis, lymphomas, and nephroblastomas in chicken (Perbal, 1995). MAV is the natural helper virus of Avian Myelobalstosis virus (AMV). Molecular cloning of a MAV strain inducing specifically nephroblastoma when injected in day-old chicken (Perbal 1985, Soret et al. 1985) allowed to establish that MAV-induced nephroblastoma represent a unique animal model for the Wilms’ tumor (Perbal 1994). The molecular cloning of MAV integration sites in the host genome, identified several genes whose viral induced alteration is associated to cancer development (Li et al. 2006). One of them, CCN3 was one of the three founding members of the CCN family of 6 proteins involved in the regulation of cell proliferation and differentiation in several normal and tumoral contexts (Joliot et al., 1992, Perbal , 2001). Functionally bipartite, with members acting negatively or positively on cell communication and signaling, the CCN proteins are subject to complex fine tuning regulation from which stemmed the concept of their biological properties being based on a spatio-temporal combinatorial events model (Perbal . 2013, 2018, 2023) Disregulation of the ccn3 gene expression and abnormal production, processing or localization of the CCN3 protein is associated to malignancy in several tumor cases. CCN3 detection in tumor samples is associated to a favorable outcome in several types of tumors and in some documented cases its expression is associated to metastatic potentiality of the tumor cells (Planque and Perbal 2003, Perbal 2003). The value of CCN3 as a prognostic marker has been established in the case of osteosarcomas (Perbal et al. 2008) and melanomas (Vallacchi et al. 2008). CCN3 is reducing the tumorigenic potential of glioblastomas, choriocarcinomas, Ewing’s tumors and melanomas. These observations set the stage for developing protocols for genetic therapy of these tumors. Proteins and ligands interacting with CCN3 allow it to play its regulatory role in the control of cell attachement, spreading, proliferation and differentiation. After biologically active truncated CCN3 proteins with different sub cellular localization (Perbal 2004, Planque et al. 2006), were identified in our laboratory, several groups reported the existence of truncated and rearranged forms of other CCN proteins (Perbal et al. 2023). Since the nuclear CCN3 proteins detected in cancer cells have been shown to regulate transcription, we have proposed that a balanced production of secreted CCN3 protein with anti-proliferative activity and nuclear CCN3 protein with pro-proliferative and oncogenic activities is required for the spatio temporal combinatorial events control of its biological activities (Perbal et al 2023). Recent Orientations My interest in the molecular basis of genetic diseases which stemmed from my early retrovirology studies, led me to undertake investigations in the legal aspects related to genetic information protection of human. Further to the COVID pandemic and interrogations expressed by the public, I became interested in social approches of medical diseases and the combination power of my scientific and legal activities culminated in my certification as a couple therapist and sexologist.
Selected Publications in the field of cell communication and signaling
Perbal B, Perbal M, Perbal A. Cooperation is the key: the CCN biological system as a gate to high complex protein superfamilies’ signaling.J Cell Commun Signal. 2023 Jun;17(2):233-253. doi: 10.1007/s12079-023-00749-8.PMID: 37166690Free PMC article. 2
Perbal B.J Time has come to address the spatiotemporal combinatorial model for CCN proteins biological activitites by spatial transcriptomics and genome wide association studies. Cell Commun Signal. 2023 Mar;17(1):1-3.
Kubota S, Kawaki H, Perbal B, Takigawa M, Kawata K, Hattori T, Nishida T. Do not overwork: cellular communication network factor 3 for life in cartilage.J Cell Commun Signal. 2023 Jun;17(2):353-359.
Perbal B. The power of combined spatial transcriptomics and genome wide association studies (GWAS) approaches to heritable prostate cancer. J Cell Commun Signal. 2023 Mar;17(1):5-6. doi:10.1007/s12079-023-00724-3.6
Yeger H, Perbal B. The CCN axis in cancer development and progression. J Cell Commun Signal. 2021Dec;15(4):491-517.
Perbal B.J Cell Commun Signal. 2019 Dec;13(4):437-439. doi: 10.1007/s12079-019-00543-5. CCN proteins are part of a multilayer complex system: a working model.
Perbal B, Tweedie S, Bruford E.J The official unified nomenclature adopted by the HGNC calls for the use of the acronyms, CCN1-6, and discontinuation in the use of CYR61, CTGF, NOV and WISP 1-3 respectively.Cell Commun Signal. 2018 Dec;12(4):625-629. doi: 10.1007/s12079-018-0491-1. Epub 2018 Nov5.
Perbal B. The concept of the CCN protein family revisited: a centralized coordination network. J Cell Commun Signal. 2018 Mar;12(1):3-12. doi: 10.1007/s12079-018-0455-5. Epub 2018 Feb 22.
Dombrowski Y, O’Hagan T, Dittmer M, Penalva R, Mayoral SR, Bankhead P, Fleville S,Eleftheriadis G, Zhao C, Naughton M, Hassan R, Moffat J, Falconer J, Boyd A,Hamilton P, Allen IV, Kissenpfennig A, Moynagh PN, Evergren E, Perbal B, Williams AC, Ingram RJ, Chan JR, Franklin RJM, Fitzgerald DC.Regulatory T cells promote myelin regeneration in the central nervous system Nat Neurosci. 2017 May;20(5):674-680. doi: 10.1038/nn.4528. Epub 2017 Mar 13.
Perbal B, Tweedie S, Bruford E The official unified nomenclature adopted by the HGNC calls for the use of the acronyms, CCN1-6, and discontinuation in the use of CYR61, CTGF, NOV and WISP 1-3 respectively. J Cell Commun Signal. 2018 Dec;12(4):625-629
Perbal B. The concept of the CCN protein family revisited: a centralized coordination network. J Cell Commun Signal. 2018 Mar;12(1):3-12.
Yeger H, Perbal B. CCN family of proteins: critical modulators of the tumor cell microenvironment. J Cell Commun Signal. 2016 Sep;10(3):229-240.
Zhang C, van der Voort D, Shi H, Zhang R, Qing Y, Hiraoka S, Takemoto M, Yokote K, Moxon JV, Norman P, Rittié L, Kuivaniemi H, Atkins GB, Gerson SL, Shi GP, Golledge J, Dong N, Perbal B, Prosdocimo DA, Lin Z. Matricellular protein CCN3 mitigates abdominal aortic aneurysm. J Clin Invest. 2016 May 2;126(5):2012.
Perbal B CCN Proteins : A Centralized Communication System. J Cell Commun Signal. 2013 Aug;7(3):169-77..May;180(5):1979-90.
Ouellet V, Tiedemann K, Mourskaia A, Fong JE, Tran-Thanh D, Amir E, Clemons M, Perbal B, Komarova SV, Siegel P. CCN3 impairs osteoblast and stimulates osteoclast differentiation to favor breast cancer metastasis to boneAm J Pathol 2011 May;178(5):2377-88
Rittié L,Perbal B,Castellot JJ, Orringer JS, Voorhees JJ, Fisher GJ Spatial-temporal modulation of CCN proteins during wound healing in human skin in vivo J Cell Commun Signal. 2011 Mar;5(1):69-80
Lin Z, Natesan V, Shi H, Hamik A, Kawanami D, Hao C, Mahabaleshwar GH, Wang W, Jin ZG, Atkins GB, Firth SM, Rittié L, Perbal B, Jain MK A novel role of CCN3 in regulating endothelial inflammation. J Cell Commun Signal. 2010 Oct;4(3):141-53.
Perbal B, Lazar N, Zambelli D, Lopez-Guerrero JA, Llombart-Bosch A, Scotlandi K, Picci P. Prognostic relevance of CCN3 in Ewing sarcoma. Hum Pathol. 2009 Oct;40(10):1479-86. Epub 2009 Aug 19.
Perbal B. Alternative splicing of CCN mRNAs…. it has been upon us. J Cell Commun Signal. 2009 Jun;3(2):153-7. Epub 2009 Apr 28.
Holbourn KP, Acharya KR, Perbal B. The CCN family of proteins: structure-function relationships. Trends Biochem Sci. 2008 Oct;33(10):461-73. Epub 2008 Sep 11.
Kawaki H, Kubota S, Suzuki A, Lazar N, Yamada T, Matsumura T, Ohgawara T, Maeda T, Perbal B, Lyons KM, Takigawa M. Cooperative regulation of chondrocyte differentiation by CCN2 and CCN3 shown by a comprehensive analysis of the CCN family proteins in cartilage. J Bone Miner Res. 2008 Nov;23(11):1751-64.
Yeger H, Perbal B. The CCN family of genes: a perspective on CCN biology and therapeutic potential. J Cell Commun Signal. 2008 Jun 21. [Epub ahead of print]
Perbal B, Zuntini M, Zambelli D, Serra M, Sciandra M, Cantiani L, Lucarelli E, Picci P, Scotlandi K. Prognostic value of CCN3 in osteosarcoma. Clin Cancer Res. 2008 Feb 1;14(3):701-9.
Vallacchi V, Daniotti M, Ratti F, Di Stasi D, Deho P, De Filippo A, Tragni G, Balsari A, Carbone A, Rivoltini L, Parmiani G, Lazar N, Perbal B, Rodolfo M. CCN3/nephroblastoma overexpressed matricellular protein regulates integrin expression, adhesion, and dissemination in melanoma. Cancer Res. 2008 Feb 1;68(3):715-23. Erratum in: Cancer Res. 2008 Mar 15;68(6):2051.
Lazar N, Manara C, Navarro S, Bleau A-M, Llombart-Bosch A, Scotlandi K, Planque N, Perbal B. Domain-specific CCN3 antibodies asunique tools for structural and functional studies J. Cell Commun Signal. 2007 Sep;1(2):91-102. Epub 2007 Sep 8.
Fukunaga-Kalabis M, Martinez G, Telson SM, Liu ZJ, Balint K, Juhasz I, Elder DE, Perbal B, Herlyn M. Downregulation of CCN3 expression as a potential mechanism for melanoma progression. Oncogene. 2008 Apr 17;27(18):2552-60. Epub 2007 Oct 29.
van Roeyen CR, Eitner F, Scholl T, Boor P, Kunter U, Planque N, Grone HJ, Bleau AM, Perbal B, Ostendorf T, Floege J. CCN3 is a novel endogenous PDGF-regulated inhibitor of glomerular cell proliferation. Kidney Int. 2007 Oct 3; [Epub ahead of print]
Bleau AM, Planque N, Lazar N, Zambelli D, Ori A, Quan T, Fisher G, Scotlandi K, Perbal B. Antiproliferative activity of CCN3: Involvement of the C-terminal module and post-translational regulation. J Cell Biochem. 2007 Mar 5; [Epub ahead of print]
Perbal B. The CCN3 protein and cancer. Adv Exp Med Biol. 2006;587:23-40. Review.
Fukunaga-Kalabis M, Martinez G, Liu ZJ, Kalabis J, Mrass P, Weninger W, Firth SM, Planque N, Perbal B, Herlyn M. CCN3 controls 3D spatial localization of melanocytes in the human skin through DDR1. J Cell Biol. 2006 Nov 20;175(4):563-9. Epub 2006 Nov 13..
Perbal B. New insight into CCN3 interactions – Nuclear CCN3 : fact or fantasy? Cell Commun Signal. 2006 Aug 8;4:6.
McCallum L, Price S, Planque N, Perbal B, Pierce A, Whetton AD, Irvine AE. A novel mechanism for BCR-ABL action: stimulated secretion of CCN3 is involved in growth and differentiation regulation. Blood. 2006 Sep 1;108(5):1716-23. Epub 2006 May 2.
Planque N, Long Li C, Saule S, Bleau AM, Perbal B. Nuclear addressing provides a clue for the transforming activity of amino-truncated CCN3 proteins. J Cell Biochem. 2006 Sep 1;99(1):105-16.
Perbal B. NOV story: the way to CCN3. Cell Commun Signal. 2006 Feb 20;4:3.
Benini S, Perbal B, Zambelli D, Colombo MP, Manara MC, Serra M, Parenza M, Martinez V, Picci P, Scotlandi K. In Ewing’s sarcoma CCN3(NOV) inhibits proliferation while promoting migration and invasion of the same cell type. Oncogene. 2005 Jun 23;24(27):4349-61.
Bleau AM, Planque N, Perbal B. CCN proteins and cancer: two to tango. Front Biosci. 2005 May 1;10:998-1009.
Kyurkchiev S, Yeger H, Bleau AM, Perbal B. Potential cellular conformations of the CCN3(NOV) protein. Cell Commun Signal. 2004 Sep 10;2(1):9.
Fu CT, Bechberger JF, Ozog MA, Perbal B, Naus CC. CCN3 (NOV) interacts with connexin43 in C6 glioma cells: possible mechanism of connexin-mediated growth suppression. J Biol Chem. 2004 Aug 27;279(35):36943-50. Epub 2004 Jun 21.
Gellhaus A, Dong X, Propson S, Maass K, Klein-Hitpass L, Kibschull M, Traub O, Willecke K, Perbal B, Lye SJ, Winterhager E. Connexin43 interacts with NOV: a possible mechanism for negative regulation of cell growth in choriocarcinoma cells. J Biol Chem. 2004 Aug 27;279(35):36931-42. Epub 2004 Jun 4.
Katsube K, Chuai ML, Liu YC, Kabasawa Y, Takagi M, Perbal B, Sakamoto K. The expression of chicken NOV, a member of the CCN gene family, in early stage development. Brain Res Gene Expr Patterns. 2001 Aug;1(1):61-5.
Perbal B. Communication is the key. Cell Commun Signal. 2003 Oct 27;1(1):3.
Perbal B. The CCN3 (NOV) cell growth regulator: a new tool for molecular medicine. Expert Rev Mol Diagn. 2003 Sep;3(5):597-604.
Planque N, Perbal B. A structural approach to the role of CCN (CYR61/CTGF/NOV) proteins in tumourigenesis. Cancer Cell Int. 2003 Aug 22;3(1):15.
Li CL, Martinez V, He B, Lombet A, Perbal B. A role for CCN3 (NOV) in calcium signalling. Mol Pathol. 2002 Aug;55(4):250-61.
Sakamoto K, Yamaguchi S, Ando R, Miyawaki A, Kabasawa Y, Takagi M, Li CL, Perbal B, Katsube K. The nephroblastoma overexpressed gene (NOV/ccn3) protein associates with Notch1 extracellular domain and inhibits myoblast differentiation via Notch signaling pathway. J Biol Chem. 2002 Aug 16;277(33):29399-405. Epub 2002 Jun 05.
Manara MC, Perbal B, Benini S, Strammiello R, Cerisano V, Perdichizzi S, Serra M, Astolfi A, Bertoni F, Alami J, Yeger H, Picci P, Scotlandi K. The expression of ccn3(nov) gene in musculoskeletal tumors. Am J Pathol. 2002 Mar;160(3):849-59.
Perbal B. Les protéines CCN : quand multimodulaire rime avec multifonctionnel. Médecine-Sciences. 2002 Jun;18 :745-56
Thomopoulos GN, Kyurkchiev S, Perbal B. Immunocytochemical localization of NOVH protein and ultrastructural characteristics of NCI-H295R cells. J Submicrosc Cytol Pathol. 2001 Jul;33(3):251-60.
Gupta N, Wang H, McLeod TL, Naus CC, Kyurkchiev S, Advani S, Yu J, Perbal B, Weichselbaum RR. Inhibition of glioma cell growth and tumorigenic potential by CCN3 (NOV). Mol Pathol. 2001 Oct;54(5):293-9.
Maillard M, Cadot B, Ball RY, Sethia K, Edwards DR, Perbal B, Tatoud R. Differential expression of the ccn3 (nov) proto-oncogene in human prostate cell lines and tissues Mol Pathol. 2001 Aug;54(4):275-80
Su BY, Cai WQ, Zhang CG, Martinez V, Lombet A, Perbal B. The expression of ccn3 (nov) RNA and protein in the rat central nervous system is developmentally regulated Mol Pathol 2001 Jun;54(3):184-91.
Perbal B. NOV (nephroblastoma overexpressed) and the CCN family of genes: structural and functional issues. Mol Pathol. 2001 Apr;54(2):57-79. doi: 10.1136/mp.54.2.57
Joliot V, Martinerie C, Dambrine G, Plassiart G, Brisac M, Crochet J, Perbal B . Proviral rearrangements and overexpression of a newcellular gene (nov) in myeloblastosis-associated virus type 1-induced nephroblastomas. Mol Cell Biol. 1992 Jan;12(1):10-21.
Paul Bornstein (1934-2013) Emeritus Professor of Biochemistry and Medicine at the University of Washington at the time he received this award. Holder pof a BA from Cornell University and MD from New York University, he trained in Surgery and Internal Medicine at Yale New Haven Hospital. He 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.
This page is meant to provide an open forum for discussions between recognized seniors and younger fellows on various scientific topics of interest. Depending upon the success and interest of this web page, it will become published on line wihtout any fee, after validation by the editorial office of the International CCN Society who will ascertain that the content of the proposed communications do not infringe any intellectual property right and that you only mention names of authors relating to the content of your posting.
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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 (1948 – 2024) 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 gave 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.
