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Baumeister T, Ingermann J, Marcazzan S, et al. Anti-inflammatory chemoprevention attenuates the phenotype in a mouse model of esophageal adenocarcinoma. Carcinogenesis. 2021;42(8):1068-1078doi: 10.1093/carcin/bgab032.
Baumeister, T., Ingermann, J., Marcazzan, S., Fang, H. Y., Oellinger, R., Rad, R., Engleitner, T., Kleigrewe, K., Anand, A., Strangmann, J., Schmid, R. M., Wang, T. C., & Quante, M. (2021). Anti-inflammatory chemoprevention attenuates the phenotype in a mouse model of esophageal adenocarcinoma. Carcinogenesis, 42(8), 1068-1078. https://doi.org/10.1093/carcin/bgab032
Baumeister, Theresa, et al. "Anti-inflammatory chemoprevention attenuates the phenotype in a mouse model of esophageal adenocarcinoma." Carcinogenesis vol. 42,8 (2021): 1068-1078. doi: https://doi.org/10.1093/carcin/bgab032
Baumeister T, Ingermann J, Marcazzan S, Fang HY, Oellinger R, Rad R, Engleitner T, Kleigrewe K, Anand A, Strangmann J, Schmid RM, Wang TC, Quante M. Anti-inflammatory chemoprevention attenuates the phenotype in a mouse model of esophageal adenocarcinoma. Carcinogenesis. 2021 Aug 19;42(8):1068-1078. doi: 10.1093/carcin/bgab032. PMID: 33878160; PMCID: PMC8374059.
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Carcinogenesis. 2021 Aug 19;42(8):1068-1078. doi: 10.1093/carcin/bgab032.

Anti-inflammatory chemoprevention attenuates the phenotype in a mouse model of esophageal adenocarcinoma.

Carcinogenesis

Theresa Baumeister, Jonas Ingermann, Sabrina Marcazzan, Hsin-Yu Fang, Rupert Oellinger, Roland Rad, Thomas Engleitner, Karin Kleigrewe, Akanksha Anand, Julia Strangmann, Roland M Schmid, Timothy C Wang, Michael Quante

Affiliations

  1. Department of Medicine II, Klinikum rechts der Isar, Technical University Munich (TUM), Ismaninger Str. 22, München, Germany.
  2. Chair of Biological Imaging, School of Medicine, Technische Universität München, Munich, Germany.
  3. Helmholtz Zentrum München, Institute of Biological and Medical Imaging, Neuherberg, Germany.
  4. Institute of Molecular Oncology and Functional Genomics, Klinikum rechts der Isar, Technical University Munich (TUM), Ismaninger Str. 22, München, Germany.
  5. Bavarian Center for Biomolecular Mass Spectrometry (BayBioMS), Technical University of Munich, Freising, Germany.
  6. Department of Medicine, Columbia University Irving Medical Center, New York, NY, USA.
  7. Innere Medizin II, Universitätskliniken Freiburg, Universität Freiburg, Freiburg, Germany.

PMID: 33878160 PMCID: PMC8374059 DOI: 10.1093/carcin/bgab032

Abstract

Barrett's esophagus (BE) is the main known precursor condition of esophageal adenocarcinoma (EAC). BE is defined by the presence of metaplasia above the normal squamous columnar junction and has mainly been attributed to gastroesophageal reflux disease and chronic reflux esophagitis. Thus, the rising incidence of EAC in the Western world is probably mediated by chronic esophageal inflammation, secondary to gastroesophageal reflux disease in combination with environmental risk factors such as a Western diet and obesity. However, (at present) risk prediction tools and endoscopic surveillance have shown limited effectiveness. Chemoprevention as an adjunctive approach remains an attractive option to reduce the incidence of neoplastic disease. Here, we investigate the feasibility of chemopreventive approaches in BE and EAC via inhibition of inflammatory signaling in a transgenic mouse model of BE and EAC (L2-IL1B mice), with accelerated tumor formation on a high-fat diet (HFD). L2-IL1B mice were treated with the IL-1 receptor antagonist Anakinra and the nonsteroidal anti-inflammatory drugs (NSAIDs) aspirin or Sulindac. Interleukin-1b antagonism reduced tumor progression in L2-IL1B mice with or without a HFD, whereas both NSAIDs were effective chemoprevention agents in the accelerated HFD-fed L2-IL1B mouse model. Sulindac treatment also resulted in a marked change in the immune profile of L2-IL1B mice. In summary, anti-inflammatory treatment of HFD-treated L2-IL1B mice acted protectively on disease progression. These results from a mouse model of BE support results from clinical trials that suggest that anti-inflammatory medication may be effective in the chemoprevention of EAC.

© The Author(s) 2021. Published by Oxford University Press. All rights reserved. For Permissions, please email: [email protected].

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