!!Markus M. Lerch MD FRCP - Biography

Markus Lerch is a professor of medicine, physician-in-chief and CEO of LMU University Hospital in Munich, one of Europe’s leading institutions for medical research, education and patient care.
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He grew up in the Rhineland and majored in Philosophy and Art History before attending Medical School in Freiburg, Glasgow, Toronto and at the University of Massachusetts. In 1984 he completed his MD in Freiburg with experiments using isolated pancreatic lobules, his first exposure to the pancreas field that has never since ceased to fascinate him. After a Pathology Internship in Freiburg he completed a residency in Internal Medicine at the Technical University of Aachen. Supported by the German Research Council (DFG) he worked as a post doc with Michael Steer and Ashok Saluja in Boston[1|1], interrupted by training in cell biology with Jacopo Meldolesi in Milano, Italy, and followed by a faculty appointment at Harvard. On his return to Germany in 1992 he was board certified in Gastroenterology and obtained a second doctorate from the University of Ulm (Habiliation, D.Sc. equivalent) for work on the cell biology of pancreatitis, and was promoted to reader and clinical consultant. In 1994 he moved to the Max-Planck-Institute for Biochemistry and the lab of Axel Ullrich in Munich as a staff scientist and was later board certified in Biochemistry. From 1996 he worked as an assistant professor and consultant gastroenterologist in Homburg (Saar), and as tenured associate professor at the University of Münster (1997-2003) before he accepted a full professorship at the University of Greifswald (founded in 1456), where he served as chairman of the Department of Medicine A and Vice Dean for Research and Clinical Affairs until 2020. 
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The research of his group has been continuously funded, is focused on the pathophysiology, cell biology and genetics of pancreatic disorders, remained by design translational, and has resulted in more than 760 publications ([https://orcid.org/0000-0002-9643-8263]). It has defined pancreatic acinar cell as the primary site of injury in pancreatitis[2|2] and discovered (transient) blockage of pancreatic secretion[3|3] and missorted endocytosis[4|4] as initiating events of gallstone-induced pancreatitis, a discovery subsequently confirmed in patients[5|5]. His group was the first to identify the type of calcium release from ER stores that leads to intracellular protease activation[6|6] and characterized the role of lysosomal enzymes in this process[7|7]. The observation that Magnesium can block trypsin activation[8|8] has initiated two clinical trials. More recent investigations have elucidated the role of immune cells, not only in the severity[9|9], but also the onset of pancreatitis[10|10], particularly the role of macrophages11 and the NLRP3 inflammasome[12|12]. Translational studies using population-based and patient cohorts permitted the identification of novel genetic risk factors, specifically ABO-blood type B and FUT2[13|13], of biomarker signatures for distinguishing pancreatitis from cancer[14|14], and established the exocrine pancreas as the most critical regulator of the intestinal microbiota compositon[15|15]. 
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Markus Lerch has served as secretary (2002 - 2007) and president (2018) of the European Pancreatic Club, president of the German Gastroenterological Society (DGVS, 2011 - 2017) and chairman/president of the German Society of Internal Medicine (DGIM, founded in 1882) from 2021 - 2022. He worked as associate editor for the journal Gut (2003 - 2009) and served on the editorial boards of Gastroenterology, Pancreas, Pancreatology and the Am. J. Physiology. He was awarded the EPC Lifetime Achievement Award in 2016, the George-Palade-Prize for Cell Biology of the International Pancreatic Association in 2018 and the American Pancreatic Association’s Vay Liang & Frisca Go Award for Lifetime Achievement in 2021. In 2001 he was elected an Honorary Fellow of the Glasgow Royal College of Physicians and Surgeons (FRCP), in 2015 appointed by the German President to the National Council of Science and Humanities (Wissenschaftsrat) and in 2016 elected as member to the European Academy of Science (Academia Europaea).
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__References__
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[1|#1] Lerch MM, Saluja AK, Dawra R, er al. The effect of chloroquine administration on two experimental models of acute pancreatitis. Gastroenterology. 1993 Jun;104(6):1768-79.

[2|#2] Lerch MM, Saluja AK, Dawra R, et al. Acute necrotizing pancreatitis in the opossum: earliest morphological changes involve acinar cells. Gastroenterology. 1992 Jul;103(1):205-13.

[3|#3] Lerch MM, Saluja AK, Rünzi M, et al. Pancreatic duct obstruction triggers acute necrotizing pancreatitis in the opossum. Gastroenterology. 1993 Mar;104(3):853-61.

[4|#4] Lerch MM, Saluja AK, Rünzi M, et al. Luminal endocytosis and intracellular targeting by acinar cells during early biliary pancreatitis in the opossum. J Clin Invest. 1995 May;95(5):2222-31.

[5|#5] Hernández CA, Lerch MM. Sphincter stenosis and gallstone migration through the biliary tract. Lancet. 1993 May 29;341(8857):1371-3.

[6|#6] Krüger B, Albrecht E, Lerch MM. The role of intracellular calcium signaling in premature protease activation and the onset of pancreatitis. Am J Pathol. 2000 Jul;157(1):43-50.

[7|#7] Wartmann T, Mayerle J, Kähne T, et al. Cathepsin L inactivates human trypsinogen, whereas cathepsin L-deletion reduces the severity of pancreatitis in mice. Gastroenterology. 2010 Feb;138(2):726-37.

[8|#8] Schick V, Scheiber JA, Mooren FC, et al. Effect of magnesium supplementation and depletion on the onset and course of acute experimental pancreatitis. Gut. 2014 Sep;63(9):1469-80.

[9|#9] Sendler M, Weiss FU, Golchert J, et al. Cathepsin B-Mediated Activation of Trypsinogen in Endocytosing Macrophages Increases Severity of Pancreatitis in Mice. Gastroenterology. 2018 Feb;154(3):704-718.e10. 

[10|#10] Mayerle J, Schnekenburger J, Krüger B, et al. Extracellular cleavage of E-cadherin by leukocyte elastase during acute experimental pancreatitis in rats. Gastroenterology. 2005 Oct;129(4):1251-67.

[11|#11] Sendler M, Weiss FU, Golchert J, et al. Cathepsin B-Mediated Activation of Trypsinogen in Endocytosing Macrophages Increases Severity of Pancreatitis in Mice. Gastroenterology. 2018 Feb;154(3):704-718.e10.

[12|#12] Sendler M, van den Brandt C, Glaubitz J, et al. NLRP3 Inflammasome Regulates Development of Systemic Inflammatory Response and Compensatory Anti-Inflammatory Response Syndromes in Mice With Acute Pancreatitis. Gastroenterology. 2020 Jan;158(1):253-269.e14.

[13|#13] Weiss FU, Schurmann C, Guenther A, et al. Fucosyltransferase 2 (FUT2) non-secretor status and blood group B are associated with elevated serum lipase activity in asymptomatic subjects, and an increased risk for chronic pancreatitis: a genetic association study. Gut. 2015 Apr;64(4):646-56.

[14|#14] Adam MG, Beyer G, Christiansen N, et al. Identification and validation of a multivariable prediction model based on blood plasma and serum metabolomics for the distinction of chronic pancreatitis subjects from non-pancreas disease control subjects. Gut. 2021 Nov;70(11):2150-2158.

[15|#15] Frost F, Kacprowski T, Rühlemann M, et al. Impaired exocrine pancreatic function associates with changes in intestinal microbiota composition and diversity. Gastroenterology. 2019 Mar;156(4):1010-1015.
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