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Here, we show that mice lacking the\n                    <jats:italic>Trp53<\/jats:italic>\n                    alternatively spliced (AS) exon, thereby expressing the canonical p53 protein but not isoforms with the AS C-terminus, have unexpectedly lost a male-specific protection against Myc-induced B-cell lymphomas. Lymphomagenesis was delayed in\n                    <jats:italic>\n                      Trp53\n                      <jats:sup>+\/+<\/jats:sup>\n                      E\u03bc-Myc\n                    <\/jats:italic>\n                    males compared to\n                    <jats:italic>\n                      Trp53\n                      <jats:sup>\u0394AS\/\u0394AS<\/jats:sup>\n                      E\u03bc-Myc\n                    <\/jats:italic>\n                    males, but also compared to\n                    <jats:italic>\n                      Trp53\n                      <jats:sup>+\/+<\/jats:sup>\n                      E\u03bc-Myc\n                    <\/jats:italic>\n                    and\n                    <jats:italic>\n                      Trp53\n                      <jats:sup>\u0394AS\/\u0394AS<\/jats:sup>\n                      E\u03bc-Myc\n                    <\/jats:italic>\n                    females. Pre-tumoral splenic cells from\n                    <jats:italic>\n                      Trp53\n                      <jats:sup>+\/+<\/jats:sup>\n                      E\u03bc-Myc\n                    <\/jats:italic>\n                    males exhibited a higher expression of\n                    <jats:italic>Ackr4,<\/jats:italic>\n                    encoding an atypical chemokine receptor with tumor suppressive effects. We identified\n                    <jats:italic>Ackr4<\/jats:italic>\n                    as a p53 target gene whose p53-mediated transactivation is inhibited by estrogens, and as a male-specific factor of good prognosis relevant for murine\n                    <jats:italic>E\u03bc-Myc<\/jats:italic>\n                    -induced and human Burkitt lymphomas. Furthermore, the knockout of\n                    <jats:italic>ACKR4<\/jats:italic>\n                    increased the chemokine-guided migration of Burkitt lymphoma cells. These data demonstrate the functional relevance of alternatively spliced p53 isoforms and reveal sex disparities in Myc-driven lymphomagenesis.\n                  <\/jats:p>","DOI":"10.7554\/elife.92774","type":"journal-article","created":{"date-parts":[[2024,1,10]],"date-time":"2024-01-10T12:17:20Z","timestamp":1704889040000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.92774","source":"Crossref","is-referenced-by-count":3,"title":["Mutant mice lacking alternatively spliced p53 isoforms unveil Ackr4 as a male-specific prognostic factor in Myc-driven B-cell lymphomas"],"prefix":"10.7554","volume":"13","author":[{"given":"Anne","family":"Fajac","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/04t0gwh46","id-type":"ROR","asserted-by":"publisher"}],"name":"Genetics of Tumor Suppression, Institut Curie","place":["Paris, France"]},{"id":[{"id":"https:\/\/ror.org\/02feahw73","id-type":"ROR","asserted-by":"publisher"}],"name":"CNRS UMR3244","place":["Paris, 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