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We have previously demonstrated the importance of Wnt\/\u03b2-catenin signaling in mouse models of PSC. In this study, we wished to determine the clinical relevance of \u03b2-catenin localization in patient samples. In livers explanted from patients diagnosed with PSC, the majority (12\/16; 75%) lacked \u03b2-catenin protein expression. Biopsies from patients post-transplant were classified as recurrent or non-recurrent based on pathology reports and then scored for \u03b2-catenin activation as a function of immunohistochemical localization. Despite lack of statistical significance, patients with recurrent primary disease (n\u2009=\u200911) had a greater percentage of samples with nuclear, transcriptionally active \u03b2-catenin (average 58.8%) than those with no recurrence (n\u2009=\u200910; 40.53%), while non-recurrence is correlated with \u03b2-catenin staining at the cell surface (average 52.63% for non-recurrent vs. 27.34% for recurrent), as determined by\u00a0three different methods of analysis. \u03b2-catenin score and years-to-endpoint are both strongly associated with recurrence status (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.017 and\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.00063, respectively). Finally, there was significant association between higher \u03b2-catenin score and increased alkaline phosphatase, a marker of biliary injury and disease progression. Thus, \u03b2-catenin expression and activation changes during the progression of PSC, and its localization may be a useful prognostic tool for predicting recurrence of this disease.\n                  <\/jats:p>","DOI":"10.1038\/s41598-021-04358-6","type":"journal-article","created":{"date-parts":[[2022,1,7]],"date-time":"2022-01-07T06:03:21Z","timestamp":1641535401000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Changes in beta-catenin expression and activation during progression of primary sclerosing cholangitis predict disease recurrence"],"prefix":"10.1038","volume":"12","author":[{"given":"Mary","family":"Ayers","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Silvia","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aatur D.","family":"Singhi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karis","family":"Kosar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pamela","family":"Cornuet","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kari","family":"Nejak-Bowen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2022,1,7]]},"reference":[{"key":"4358_CR1","doi-asserted-by":"publisher","first-page":"107","DOI":"10.1002\/cld.667","volume":"10","author":"J Lewis","year":"2017","unstructured":"Lewis, J. 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