{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,25]],"date-time":"2026-10-25T02:41:00Z","timestamp":1792896060610,"version":"4.5.0"},"reference-count":69,"publisher":"American Society of Hematology","issue":"17","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2021,4,29]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Chronic graft-versus-host disease (cGVHD) is a major life-threatening complication of allogeneic hematopoietic stem cell transplantation. The molecular mechanisms underlying cGVHD remain poorly understood, and targeted therapies for clinical use are not well established. Here, we examined the role of the canonical WNT pathway in sclerodermatous cGVHD (sclGVHD). WNT signaling was activated in human sclGVHD with increased nuclear accumulation of the transcription factor \u03b2-catenin and a WNT-biased gene expression signature in lesional skin. Treatment with the highly selective tankryase inhibitor G007-LK, the CK1\u03b1 agonist pyrvinium, or the LRP6 inhibitor salinomycin abrogated the activation of WNT signaling and protected against experimental cGVHD, without a significant impact on graft-versus-leukemia effect (GVL). Treatment with G007-LK, pyrvinium, or salinomycin almost completely prevented the development of clinical and histological features in the B10.D2 (H-2d) \u2192 BALB\/c (H-2d) and LP\/J (H-2b) \u2192 C57BL\/6 (H-2b) models of sclGVHD. Inhibition of canonical WNT signaling reduced the release of extracellular matrix from fibroblasts and reduced leukocyte influx, suggesting that WNT signaling stimulates fibrotic tissue remodeling by direct effects on fibroblasts and by indirect inflammation-dependent effects in sclGVHD. Our findings may have direct translational potential, because pyrvinium is in clinical use, and tankyrase inhibitors are in clinical trials for other indications.<\/jats:p>","DOI":"10.1182\/blood.2020008720","type":"journal-article","created":{"date-parts":[[2021,2,5]],"date-time":"2021-02-05T14:33:31Z","timestamp":1612535611000},"page":"2403-2416","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":21,"title":["Targeting of canonical WNT signaling ameliorates experimental sclerodermatous chronic graft-versus-host disease"],"prefix":"10.1182","volume":"137","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3004-9935","authenticated-orcid":false,"given":"Yun","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Internal Medicine III\u2013Rheumatology and Immunology, University of Erlangen-Nuremberg, Erlangen, Germany;"},{"name":"Deutsches Zentrum f\u00fcr Immuntherapie (DZI), Friedrich-Alexander-Universit\u00e4t Erlangen-N\u00fcrnberg\u2013University Hospital Erlangen, Erlangen, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lichong","family":"Shen","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine III\u2013Rheumatology and Immunology, University of Erlangen-Nuremberg, Erlangen, Germany;"},{"name":"Deutsches Zentrum f\u00fcr Immuntherapie (DZI), Friedrich-Alexander-Universit\u00e4t Erlangen-N\u00fcrnberg\u2013University Hospital Erlangen, Erlangen, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katja","family":"Drei\u00dfigacker","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine III\u2013Rheumatology and Immunology, University of Erlangen-Nuremberg, Erlangen, Germany;"},{"name":"Deutsches Zentrum f\u00fcr Immuntherapie (DZI), Friedrich-Alexander-Universit\u00e4t Erlangen-N\u00fcrnberg\u2013University Hospital Erlangen, Erlangen, 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