Full Text Journal Articles by
Author Markus Tschurtschenthaler


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Morphology Matters: A Critical Reappraisal of the Clinical Relevance of Morphologic Criteria From the 2019 WHO Classification in a Large Colorectal Cancer Cohort Comprising 1004 Cases.

Moritz Jesinghaus, Maxime Schmitt, Corinna Lang, Marianne Reiser, Alexander Scheiter, Björn Konukiewitz, Katja Steiger, Miguel Silva, Markus Tschurtschenthaler, Sebastian Lange, Sebastian Foersch, Karl F Becker, Dieter Saur, Helmut Friess, Kathrin Halfter, Jutta Engel, Melanie Boxberg, Nicole Pfarr, Dirk Wilhelm, Wilko Weichert,

The 2019 World Health Organization (WHO) classification of colorectal carcinoma (CRC) profoundly reclassified CRC subtypes and introduces tumor budding as a second major grading criterion, while condensing conventional grade into a 2-tiered system. So far it remains largely unexplored how these parameters interact with each other and whether they truly ... Read more >>

Am J Surg Pathol (The American journal of surgical pathology)
[2021, 45(7):969-978]

Cited: 0 times

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IDO1+ Paneth cells promote immune escape of colorectal cancer.

Sandra Pflügler, Jasmin Svinka, Irene Scharf, Ilija Crncec, Martin Filipits, Pornpimol Charoentong, Markus Tschurtschenthaler, Lukas Kenner, Monira Awad, Judith Stift, Marina Schernthanner, Romana Bischl, Dietmar Herndler-Brandstetter, Elisabeth Glitzner, Herwig P Moll, Emilio Casanova, Gerald Timelthaler, Maria Sibilia, Michael Gnant, Sigurd Lax, Josef Thaler, Mathias Müller, Birgit Strobl, Thomas Mohr, Arthur Kaser, Zlatko Trajanoski, Gerwin Heller, Robert Eferl,

Tumors have evolved mechanisms to escape anti-tumor immunosurveillance. They limit humoral and cellular immune activities in the stroma and render tumors resistant to immunotherapy. Sensitizing tumor cells to immune attack is an important strategy to revert immunosuppression. However, the underlying mechanisms of immune escape are still poorly understood. Here we ... Read more >>

Commun Biol (Communications biology)
[2020, 3(1):252]

Cited: 2 times

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ATG16L1 orchestrates interleukin-22 signaling in the intestinal epithelium via cGAS-STING.

Konrad Aden, Florian Tran, Go Ito, Raheleh Sheibani-Tezerji, Simone Lipinski, Jan W Kuiper, Markus Tschurtschenthaler, Svetlana Saveljeva, Joya Bhattacharyya, Robert Häsler, Kareen Bartsch, Anne Luzius, Marlene Jentzsch, Maren Falk-Paulsen, Stephanie T Stengel, Lina Welz, Robin Schwarzer, Björn Rabe, Winfried Barchet, Stefan Krautwald, Gunther Hartmann, Manolis Pasparakis, Richard S Blumberg, Stefan Schreiber, Arthur Kaser, Philip Rosenstiel,

A coding variant of the inflammatory bowel disease (IBD) risk gene <i>ATG16L1</i> has been associated with defective autophagy and deregulation of endoplasmic reticulum (ER) function. IL-22 is a barrier protective cytokine by inducing regeneration and antimicrobial responses in the intestinal mucosa. We show that ATG16L1 critically orchestrates IL-22 signaling in ... Read more >>

J Exp Med (The Journal of experimental medicine)
[2018, 215(11):2868-2886]

Cited: 34 times

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The Selective Autophagy Receptor Optineurin in Crohn's Disease.

Markus Tschurtschenthaler, Timon Erik Adolph,

Autophagy is a pathway that allows cells to target organelles, protein complexes, or invading microorganisms for lysosomal degradation. The specificity of autophagic processes is becoming increasingly recognized and is conferred by selective autophagy receptors such as Optineurin (OPTN). As an autophagy receptor, OPTN controls the clearance of <i>Salmonella</i> infection and ... Read more >>

Front Immunol (Frontiers in immunology)
[2018, 9:766]

Cited: 6 times

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Intestinal epithelial cell endoplasmic reticulum stress promotes MULT1 up-regulation and NKG2D-mediated inflammation.

Shuhei Hosomi, Joep Grootjans, Markus Tschurtschenthaler, Niklas Krupka, Juan D Matute, Magdalena B Flak, Eduardo Martinez-Naves, Manuel Gomez Del Moral, Jonathan N Glickman, Mizuki Ohira, Lewis L Lanier, Arthur Kaser, Richard Blumberg,

Endoplasmic reticulum (ER) stress is commonly observed in intestinal epithelial cells (IECs) and can, if excessive, cause spontaneous intestinal inflammation as shown by mice with IEC-specific deletion of X-box-binding protein 1 (<i>Xbp1</i>), an unfolded protein response-related transcription factor. In this study, <i>Xbp1</i> deletion in the epithelium (<i>Xbp1<sup>ΔIEC</sup></i> ) is shown ... Read more >>

J Exp Med (The Journal of experimental medicine)
[2017, 214(10):2985-2997]

Cited: 23 times

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Defective ATG16L1-mediated removal of IRE1α drives Crohn's disease-like ileitis.

Markus Tschurtschenthaler, Timon E Adolph, Jonathan W Ashcroft, Lukas Niederreiter, Richa Bharti, Svetlana Saveljeva, Joya Bhattacharyya, Magdalena B Flak, David Q Shih, Gwenny M Fuhler, Miles Parkes, Kenji Kohno, Takao Iwawaki, C Janneke van der Woude, Heather P Harding, Andrew M Smith, Maikel P Peppelenbosch, Stephan R Targan, David Ron, Philip Rosenstiel, Richard S Blumberg, Arthur Kaser,

ATG16L1<sup>T300A</sup>, a major risk polymorphism in Crohn's disease (CD), causes impaired autophagy, but it has remained unclear how this predisposes to CD. In this study, we report that mice with Atg16l1 deletion in intestinal epithelial cells (IECs) spontaneously develop transmural ileitis phenocopying ileal CD in an age-dependent manner, driven by ... Read more >>

J Exp Med (The Journal of experimental medicine)
[2017, 214(2):401-422]

Cited: 59 times

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Paternal chronic colitis causes epigenetic inheritance of susceptibility to colitis.

Markus Tschurtschenthaler, Priyadarshini Kachroo, Femke-Anouska Heinsen, Timon Erik Adolph, Malte Christoph Rühlemann, Johanna Klughammer, Felix Albert Offner, Ole Ammerpohl, Felix Krueger, Sébastien Smallwood, Silke Szymczak, Arthur Kaser, Andre Franke,

Inflammatory bowel disease (IBD) arises by unknown environmental triggers in genetically susceptible individuals. Epigenetic regulation of gene expression may integrate internal and external influences and may thereby modulate disease susceptibility. Epigenetic modification may also affect the germ-line and in certain contexts can be inherited to offspring. This study investigates epigenetic ... Read more >>

Sci Rep (Scientific reports)
[2016, 6:31640]

Cited: 3 times

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Type I interferon signalling in the intestinal epithelium affects Paneth cells, microbial ecology and epithelial regeneration.

Markus Tschurtschenthaler, Jun Wang, Cornelia Fricke, Teresa M J Fritz, Lukas Niederreiter, Timon E Adolph, Edina Sarcevic, Sven Künzel, Felix A Offner, Ulrich Kalinke, John F Baines, Herbert Tilg, Arthur Kaser,

<h4>Objective</h4>Intestinal epithelial cells (IECs) at the internal/external interface orchestrate the mucosal immune response. Paneth cells secrete antimicrobial peptides and inflammatory mediators, protect from pathogens and shape the commensal microbiota. Prompted by the genetic association of the locus harbouring the type I interferon (IFN) receptor (IFNAR1) with Crohn's disease, and a ... Read more >>

Gut (Gut)
[2014, 63(12):1921-1931]

Cited: 49 times

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Paneth cells as a site of origin for intestinal inflammation.

Timon E Adolph, Michal F Tomczak, Lukas Niederreiter, Hyun-Jeong Ko, Janne Böck, Eduardo Martinez-Naves, Jonathan N Glickman, Markus Tschurtschenthaler, John Hartwig, Shuhei Hosomi, Magdalena B Flak, Jennifer L Cusick, Kenji Kohno, Takao Iwawaki, Susanne Billmann-Born, Tim Raine, Richa Bharti, Ralph Lucius, Mi-Na Kweon, Stefan J Marciniak, Augustine Choi, Susan J Hagen, Stefan Schreiber, Philip Rosenstiel, Arthur Kaser, Richard S Blumberg,

The recognition of autophagy related 16-like 1 (ATG16L1) as a genetic risk factor has exposed the critical role of autophagy in Crohn's disease. Homozygosity for the highly prevalent ATG16L1 risk allele, or murine hypomorphic (HM) activity, causes Paneth cell dysfunction. As Atg16l1(HM) mice do not develop spontaneous intestinal inflammation, the ... Read more >>

Nature (Nature)
[2013, 503(7475):272-276]

Cited: 321 times

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ER stress transcription factor Xbp1 suppresses intestinal tumorigenesis and directs intestinal stem cells.

Lukas Niederreiter, Teresa M J Fritz, Timon E Adolph, Anna-Maria Krismer, Felix A Offner, Markus Tschurtschenthaler, Magdalena B Flak, Shuhei Hosomi, Michal F Tomczak, Nicole C Kaneider, Edina Sarcevic, Sarah L Kempster, Tim Raine, Daniela Esser, Philip Rosenstiel, Kenji Kohno, Takao Iwawaki, Herbert Tilg, Richard S Blumberg, Arthur Kaser,

Unresolved endoplasmic reticulum (ER) stress in the epithelium can provoke intestinal inflammation. Hypomorphic variants of ER stress response mediators, such as X-box-binding protein 1 (XBP1), confer genetic risk for inflammatory bowel disease. We report here that hypomorphic Xbp1 function instructs a multilayered regenerative response in the intestinal epithelium. This is ... Read more >>

J Exp Med (The Journal of experimental medicine)
[2013, 210(10):2041-2056]

Cited: 65 times

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