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Alliance"],"accepted":{"date-parts":[[2026,6,11]]},"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:p>\n                    We generated two mouse models, p21\n                    <jats:sup>+\/Tert<\/jats:sup>\n                    and p21\n                    <jats:sup>+\/TertCi<\/jats:sup>\n                    , expressing either telomerase reverse transcriptase (Tert) or a catalytically inactive variant under the control of the p21 promoter. By 18\u201320 mo of age, \u223c15% of mice from both genotypes developed liver tumors with histopathological features resembling human hepatocellular carcinoma (HCC). Whole-exome sequencing identified activating Ctnnb1 mutations and recurrent PP1 subunit alterations in p21\n                    <jats:sup>+\/Tert<\/jats:sup>\n                    tumors, whereas p21\n                    <jats:sup>+\/TertCi<\/jats:sup>\n                    tumors harbored activating Hras\n                    <jats:sup>Gln61Lys<\/jats:sup>\n                    mutations associated with elevated C\u00a0&gt;\u00a0A transversions. Both models exhibited chromosomal aberrations commonly observed in human HCC. Transcriptomic analyses revealed that \u03b2-catenin\u2013activated tumors recapitulated gene expression signatures of human HCC, whereas MAPK-mutated tumors showed profiles consistent with MAPK\/ERK pathway activation. All HCCs suppressed the gluconeogenic genes\n                    <jats:italic>Fbp1<\/jats:italic>\n                    and\n                    <jats:italic>AldoB<\/jats:italic>\n                    , but diverged into two distinct groups based on their glycolytic and\n                    <jats:italic>NRF2<\/jats:italic>\n                    target gene expression profiles. Spatial profiling further revealed reduced HNF4\u03b1-positive hepatocytes across tumors, independent of HNF4\u03b1 transcription, and markedly diminished immune cell infiltration, particularly in \u03b2-catenin\u2013activated tumors. Collectively, these findings uncover telomere-independent functions of Tert and identify molecular and metabolic features with potential relevance for predicting immunotherapy response.\n                  <\/jats:p>","DOI":"10.26508\/lsa.202603660","type":"journal-article","created":{"date-parts":[[2026,6,12]],"date-time":"2026-06-12T06:21:41Z","timestamp":1781245301000},"page":"e202603660","update-policy":"https:\/\/doi.org\/10.26508\/lsa.crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["TERT drives liver tumorigenesis beyond telomere elongation"],"prefix":"10.26508","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8958-3817","authenticated-orcid":true,"given":"Laura","family":"Braud","sequence":"first","affiliation":[{"name":"CRCM, Inserm, CNRS, Institut Paoli-Calmettes, Aix-Marseille University Marseille, \u00c9quipe labellis\u00e9e par la Ligue Nationale Contre le Cancer, Marseille, 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