{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T08:17:29Z","timestamp":1791274649974,"version":"4.1.0"},"reference-count":36,"publisher":"National Academy of Sciences","issue":"9","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2006,2,28]]},"abstract":"<jats:p>\n                    p53-binding protein 1 (53BP1) participates in the cellular response to DNA double-stranded breaks where it associates with various DNA repair\/cell cycle factors including the H2AX histone variant. Mice deficient for\n                    <jats:italic>53BP1<\/jats:italic>\n                    (\n                    <jats:italic>53BP1<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ) are sensitive to ionizing radiation and immunodeficient because of impaired Ig heavy chain class switch recombination. Here we show that, as compared with\n                    <jats:italic>p53<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice,\n                    <jats:italic>53BP1<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    \/\n                    <jats:italic>p53<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    animals more rapidly develop tumors, including T cell lymphomas and, at lower frequency, B lineage lymphomas, sarcomas, and teratomas. In addition, T cells from animals deficient for both\n                    <jats:italic>53BP1<\/jats:italic>\n                    and\n                    <jats:italic>p53<\/jats:italic>\n                    (\n                    <jats:italic>53BP1<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    \/\n                    <jats:italic>p53<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ) display elevated levels of genomic instability relative to T cells deficient for either\n                    <jats:italic>53BP1<\/jats:italic>\n                    or\n                    <jats:italic>p53<\/jats:italic>\n                    alone. In contrast to\n                    <jats:italic>p53<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    T cell lymphomas, which routinely display aneuploidy but not translocations,\n                    <jats:italic>53BP1<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    \/\n                    <jats:italic>p53<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    thymic lymphomas fall into two distinct cytogenetic categories, with many harboring clonal translocations (40%) and the remainder showing aneuploidy (60%). We propose that 53BP1, in the context of\n                    <jats:italic>p53<\/jats:italic>\n                    deficiency, suppresses T cell lymphomagenesis through its roles in both cell-cycle checkpoints and double-stranded break repair.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0511259103","type":"journal-article","created":{"date-parts":[[2006,2,21]],"date-time":"2006-02-21T23:03:47Z","timestamp":1140563027000},"page":"3310-3315","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":67,"title":["53BP1 and p53 synergize to suppress genomic instability and lymphomagenesis"],"prefix":"10.1073","volume":"103","author":[{"given":"Julio C.","family":"Morales","sequence":"first","affiliation":[{"name":"*Department of Biochemistry and Molecular Biology, University of Texas Health Sciences Center, Houston, TX 77030;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sonia","family":"Franco","sequence":"additional","affiliation":[{"name":"Center for Blood Research, Children\u2019s Hospital, Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael M.","family":"Murphy","sequence":"additional","affiliation":[{"name":"Center for Blood Research, Children\u2019s Hospital, Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Craig H.","family":"Bassing","sequence":"additional","affiliation":[{"name":"Center for Blood Research, Children\u2019s Hospital, Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kevin D.","family":"Mills","sequence":"additional","affiliation":[{"name":"Center for Blood Research, Children\u2019s Hospital, Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melissa M.","family":"Adams","sequence":"additional","affiliation":[{"name":"*Department of Biochemistry and Molecular Biology, University of Texas Health Sciences Center, Houston, TX 77030;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicole C.","family":"Walsh","sequence":"additional","affiliation":[{"name":"Joint Program in Transfusion Medicine, Department of Laboratory Medicine, Children\u2019s Hospital, and Department of Pathology, Harvard Medical School, Boston, MA 02115; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John P.","family":"Manis","sequence":"additional","affiliation":[{"name":"Joint Program in Transfusion Medicine, Department of Laboratory Medicine, Children\u2019s Hospital, and Department of Pathology, Harvard Medical School, Boston, MA 02115; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"George Z.","family":"Rassidakis","sequence":"additional","affiliation":[{"name":"Department of Hematopathology, University of Texas M. 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Anderson Cancer Center, Houston, TX 77030"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frederick W.","family":"Alt","sequence":"additional","affiliation":[{"name":"Center for Blood Research, Children\u2019s Hospital, Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Phillip B.","family":"Carpenter","sequence":"additional","affiliation":[{"name":"*Department of Biochemistry and Molecular Biology, University of Texas Health Sciences Center, Houston, TX 77030;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2006,2,21]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(02)00675-X"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1101\/gad.1161904"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2005.01.028"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.122228699"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1069398"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni1067"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200403021"},{"key":"e_1_3_3_8_2","first-page":"149","volume":"2","author":"Bassing C.","year":"2004","unstructured":"C. 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