EASL Recognition Awardee 2012
Authors: Michael Trauner
Journal: Journal of Hepatology (2012)

The EASL Recognition Award has been created by our Association to honor men and women who have shaped European Hepatology as scientists, physicians and teachers. In this regard, Peter Jansen matches every criteria for such an illustrious award. Peter was born in March 1946 in Hertogenbosch, The Netherlands. In 1975, he obtained his PhD in Pharmacology from the Radboud University Nijmegen and in 1977 his MD from the same University. This strategy in obtaining his academic degrees indicates that Peter approached his aims slightly differently, with his own vision of becoming a physician scientist and a scientific physician. Peter became initially infected by the research virus as a student during a Summer Research Lab visit with Norman Javitt in Upstate New York in 1967 where he cannulated the bile ducts of rats in a project on bilirubin metabolism. From 1973 to 1976 Peter was trained as a research fellow at the Albert Einstein College of Medicine in New York, USA, which at that time was already one of the places to be in liver research. There, he worked in the laboratory of Win Arias, who was extremely influential as a role model for Peter’s future scientific career. Both are still connected by a close personal friendship and share many common interests beyond science. Many of us would consider Peter Jansen as the European counterpart of Win Arias, not only through their common interests in biliary physiology and pathophysiology, but even more by their creative and innovative approaches in addressing new research questions and solving tricky problems. The New York years were also very important for Peter’s young and growing family. Peter was accompanied by his charming wife Tineke and two of their three children were born during that time in the United States. Apart from Peter’s scientific progress and success during his time abroad, his family had a wonderful time while making longlasting friendships with many international colleagues such as Jayanta and Namita Roy Chowdhury and the late Marcos Rojkind. After returning from the States, Peter continued his career in the Netherlands and moved through the academic ranks in Nijmengen before he was recruited by Prof. Guido Tytgat in 1986 as Associate Professor to the Amsterdam Medical Center, where he shaped the Liver Unit. In 1993, Peter was appointed Full Professor and Chair of Gastroenterology and Hepatology at the University of Groningen, from where he returned to Amsterdam in 2003 as Professor and Head of the Liver Unit. As Division Chief and Liver Unit Head, Peter has shaped and led the liver programs in Groningen and Amsterdam and brought them both to the highest international level as we know them today. Peter is a much sought after visiting professor around the globe, respected editor, and has a list of very impressive publications, with many of his articles published in the most prestigious journals of our discipline. A few words must be said of Peter Jansen, the man. Actually, it is already all in his first name if you take it as an acronym.-P as in brilliant physician scientist, bridge builder, a creative thinker who is able to translate clinical problems into basic research questions and answer them.-Enthusiastic and energetic, driven by an immense curiosity.-T as in tough, he is very charming but can be tough as nails when it comes to taking scientifc challenges and solving clinical problems of his patients, he is a great team player, shaping research consortia to solve tricky questions.-Emphatic towards his patients and colleagues.-Role model, so it’s all in Peter’s first name – he is a role model physician scientist! Clearly, such personal attributes were bound to result in scientific excellence. Peter has made landmark contributions unraveling the molecular mechanisms of jaundice and cholestasis. His discoveries have had a major impact on the field, although I have to admit that I may be biased in my judgement as a bile aficionado. The work of Peter and his colleagues on bilirubin glucuronidation and transport into bile paved the path for our understanding of the molecular and genetic basis of Gilbert’s and Crigler–Najjar syndrome [1van Es H.H. Goldhoorn B.G. Paul-Abrahamse M. Elferink R.P. Jansen P.L. Immunochemical analysis of uridine diphosphate-glucuronosyltransferase in four patients with the Crigler–Najjar syndrome type I.J Clin Invest. 1990; 85: 1199-1205Crossref PubMed Scopus (46) Google Scholar, 2Bosma P.J. Goldhoorn B. Elferink R.P.J.O. Sinaasappel M. Oostra B.A. Jansen P.L.M. A mutation in bilirubin uridine 5′-diphosphate-glucuronosyltransferase isoform-1 causing Crigler–Najjar syndrome type-I.Gastroenterology. 1993; 105: 216-220Abstract PubMed Scopus (0) Google Scholar, 3Bosma P.J. Seppen J. Goldhoorn B. Bakker C. Oude Elferink R.P. Chowdhury J.R. et al.Bilirubin UDP-glucuronosyltransferase 1 is the only relevant bilirubin glucuronidating isoform in man.J Biol Chem. 1994; 269: 17960-17964Abstract Full Text PDF PubMed Google Scholar, 4Seppen J. Bosma P.J. Goldhoorn B.G. Bakker C.T. Chowdhury J.R. Chowdhury N.R. et al.Discrimination between Crigler–Najjar type I and II by expression of mutant bilirubin uridine diphosphate-glucuronosyltransferase.J Clin Invest. 1994; 94: 2385-2391Crossref PubMed Scopus (156) Google Scholar, 5Bosma P.J. Chowdhury J.R. Bakker C. Gantla S. de Boer A. Oostra B.A. et al.The genetic-basis of the reduced expression of bilirubin udp-glucuronosyltransferase-1 in gilberts-syndrome.N Engl J Med. 1995; 333: 1171-1175Crossref PubMed Scopus (1274) Google Scholar], his work elucidated the bilirubin and organic anion transport defects in a rat model explaining Dubin–Johnson syndrome [6Jansen P.L.M. Peters W.H. Lamers W.H. Hereditary chronic conjugated hyperbilirubinemia in mutant rats caused by defective hepatic anion transport.Hepatology. 1985; 5: 573-579Crossref PubMed Scopus (338) Google Scholar, 7Jansen P.L.M. Groothuis G.M.M. Peters W.H.M. Meijer D.F.M. Selective hepatobiliary transport defect for organic-anions and neutral steroids in mutant rats with hereditary-conjugated hyperbilirubinemia.Hepatology. 1987; 7: 71-76Crossref PubMed Scopus (119) Google Scholar, 8Elferink R.P. Ottenhoff R. Liefting W. de Haan J. Jansen P.L. Hepatobiliary transport of glutathione and glutathione conjugate in rats with hereditary hyperbilirubinemia.J Clin Invest. 1989; 84: 476-483Crossref PubMed Google Scholar, 9Jansen P.L. van Klinken J.W. van Gelder M. Ottenhoff R. Elferink R.P. Preserved organic anion transport in mutant TR-rats with a hepatobiliary secretion defect.Am J Physiol. 1993; 265: G445-G452PubMed Google Scholar] and jaundice of sepsis [[10]Roelofsen H. VanderVeere C.N. Ottenhoff R. Schoemaker B. Jansen P.L.M. Elferink R.P.J.O. Decreased bilirubin transport in the perfused liver of endotoxemic rats.Gastroenterology. 1994; 107: 1075-1084Abstract PubMed Scopus (0) Google Scholar]. In addition, he identified the principal mechanisms (e.g., multidrug resistance-related protein 1) which allow rescue of the liver and tumor cells from toxic compound overload [[11]Müller M. Meijer C. Zaman G.J. Borst P. Scheper R.J. Mulder N.H. et al.Overexpression of the gene encoding the multidrug resistance-associated protein results in increased ATP-dependent glutathione s-conjugate transport.Proc Natl Acad Sci U S A. 1994; 91: 13033-13037Crossref PubMed Scopus (637) Google Scholar]. His equally important later work uncovered the spectrum of hereditary bile salt export pump defects ranging from progressive familial intrahepatic cholestasis (PFIC) to benign recurrent intrahepatic cholestasis (BRIC) type 2 [12Jansen P.L. Strautnieks S.S. Jacquemin E. Hadchouel M. Sokal E.M. Hooiveld G.J. et al.Hepatocanalicular bile salt export pump deficiency in patients with progressive familial intrahepatic cholestasis.Gastroenterology. 1999; 117: 1370-1379Abstract Full Text Full Text PDF PubMed Scopus (377) Google Scholar, 13Plass J.R.F. Mol O. Heegsma E. de Bruijn J. Faber K.N. Jansen P.L.M. Effect of PFIC2 mutations on function and sorting of the bile salt export pump.Hepatology. 2002; 36: 587Google Scholar, 14van Mil S.W. van der Woerd W.L. van der Brugge G. Sturm E. Jansen P.L. Bull L.N. et al.Benign recurrent intrahepatic cholestasis type 2 is caused by mutations in ABCB11.Gastroenterology. 2004; 127: 379-384Abstract Full Text Full Text PDF PubMed Scopus (284) Google Scholar]. More recent work has helped understand the role of fibroblast-growth factor (FGF) 19 as novel bile acid-induced hormone in the enterobiliary tract [15Schaap F.G. van der Gaag N.A. Gouma D.J. Jansen P.L.M. High expression of the bile salt-homeostatic hormone fibroblast growth factor 19 in the liver of patients with extrahepatic cholestasis.Hepatology. 2009; 49: 1228-1235Crossref PubMed Scopus (209) Google Scholar, 16Zweers S.J. Booij K.A. Komuta M. Roskams T. Gouma D.J. Jansen P.L. et al.The human gallbladder secretes fibroblast growth factor 19 into bile: towards defining the role of fibroblast growth factor 19 in the enterobiliary tract.Hepatology. 2012; 55: 575-583Crossref PubMed Scopus (96) Google Scholar], the new metabolic role of bile acids and FGF-19 in non-alcoholic fatty liver disease [17Schreuder T.C. Marsman H.A. Lenicek M. van Werven J.R. Nederveen A.J. Jansen P.L. et al.The hepatic response to FGF19 is impaired in patients with nonalcoholic fatty liver disease and insulin resistance.Am J Physiol Gastrointest Liver Physiol. 2010; 298: G440-G445Crossref PubMed Scopus (118) Google Scholar, 18van Werven J.R. Schreuder T.C. Aarts E.O. Nederveen A.J. Meijer J.W. Berends F.J. et al.Hepatic steatosis in morbidly obese patients undergoing gastric bypass surgery: assessment with open-system 1H-MR spectroscopy.Am J Roentgenol. 2011; 196: W736-W742Crossref PubMed Scopus (15) Google Scholar], as well as micro RNAs in liver cancer [[19]Borel F. Konstantinova P. Jansen P.L. Diagnostic and therapeutic potential of miRNA signatures in patients with hepatocellular carcinoma.J Hepatol. 2012; 56: 1371Abstract Full Text Full Text PDF PubMed Scopus (206) Google Scholar]. This broad and impressive spectrum of scientific inquiry is typical of Peter Jansen, who has always searched for new challenges and tasks to take on. These discoveries in biliary (patho) physiology were discussed with great passion at the Hochhausen Meetings where bile aficionados met in a modest but very familial and cordial atmosphere, with Peter being always in the center. The more lucky among us met at more exotic places such as Bora Bora – French Polynesia or the Falk Meetings – Peter always managed to be at both and presided and chaired many of them. As a highly successful academic mentor, Peter would give two main lines of advice to young and aspiring scientists. First, get abroad and get exposed to new thoughts and ideas, and second, make a good couple with a science partner! As an academic mentor Peter took his own advice seriously and – probably heavily influenced by the functional anatomy of the bile secretory apparatus – made couples – I am tempted to say hepatocyte couplets – with excellent basic scientists such as Ronald Oude Elferink, Michael Müller and Han Moshage, who in the meantime have become leaders of their own field as full professors and department chairs. More recent coworkers include Klaas Nico Faber and Frank Schaap who are ready to continue the legacy of Peter, together with Ulrich Beuers who has recently succeeded Peter as Professor and Head of the Liver Unit in Amsterdam. Peter is equally proud of his 24 PhD students who researched a broad range of topics beyond transport and cholestasis, such as viral hepatitis, fatty liver disease, inflammatory bowel disease, liver transplantation and liver cancer. Peter is also a very caring physician, who is loved and admired by his patients. He is not only an excellent hepatologist in his own subspecialty and research area (e.g. taking care of his Crigler Najjar patients), but his clinical work encompasses the whole spectrum of Clinical Hepatology. He is a complete hepatologist. His empathy for patients and vision for academic medicine are best reflected by quoting him from one of his papers which originated just around the turn of the last millennium: “The future of university-based research is uncertain. The staggering costs of research and limited career possibilities may force universities to the limited task of higher education, with as a result biotech companies, shareholders and corporate finance ruling the scientific waves in the next century. The 21st century patient will know the way in cyberspace and will go shopping for the best doctor, for the best treatment and for the best, or friendliest, hospital’’ [[20]Jansen P.L. Hepatology in the 21st century. Gene transfer, hepatocyte transplantation, DNA chips, cyberspace and ... a friendly hospital.Neth J Med. 1999; 55: 287-292Crossref PubMed Scopus (3) Google Scholar]. His deep understanding of our discipline and Medicine as a whole became also evident when Peter served our Association as Secretary General (1992–1993), and more recently as Educational Councilor (2007–2011). He was a visionary councilor and ambassador for our society acting with much oversight and great diplomacy. With his genuine interest in organizing educational programs worldwide, he opened EASL towards Asia and South America and was instrumental for making our Association to what it has become today – a more international liver society. Apart from being a successful physician scientist, he is also a profoundly and widely educated person and family man. He is a loving father of 3 children (2 girls, 1 son) and 5 grandchildren who were all raised in the international spirit of the Jansen family. Peter and his charming wife Tineke make a power couple for now more than 44 years. Peter enjoys outdoor activities such as golf and sailing, where he can exercise his natural born leadership as skipper. He also loves to travel, exploring new countries and cultures with great curiosity. When observing nature, Peter can be as dedicated and meticulous in his hobbies as he is as a scientist. So in a way, the private man Peter Jansen is very much alike the physician scientist Peter Jansen whom we respect and admire so much. All of us who know Peter well enough, are fully aware that formalities such as his recent retirement will not stop him. We hope for the benefit of the liver community that he will continue his inspiring and innovative work for many more years in excellent health and congratulate him with all our hearts with this EASL recognition award 2012 for his eminent contributions to the field of Hepatology. I wish to express my gratitude to the many colleagues, companions and friends of Peter Jansen for their help in obtaining additional insights into the professional and personal life of our awardee.