{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T11:07:06Z","timestamp":1790248026573,"version":"4.1.0"},"reference-count":48,"publisher":"American Society for Microbiology","issue":"5","license":[{"start":{"date-parts":[[2001,3,1]],"date-time":"2001-03-01T00:00:00Z","timestamp":983404800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2001,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Human T-cell leukemia virus type 1 (HTLV-1) is the etiologic agent of adult T-cell leukemia\/lymphoma (ATLL). The HTLV-1 Tax protein has been strongly linked to oncogenesis and is considered to be the transforming protein of this virus. A Tax transgenic mouse model was utilized to study the contribution of p53 inactivation to Tax-mediated tumorigenesis. These mice develop primary, peripheral tumors consisting of large granular lymphocytic (LGL) cells, which also infiltrate the lymph nodes, bone marrow, spleen, liver, and lungs. Primary Tax-induced tumors and tumor-derived cell lines exhibited functional inactivation of the p53 apoptotic pathway; such tumors and tumor cell lines were resistant to an apoptosis-inducing stimulus. In contrast,\n            <jats:italic>p53<\/jats:italic>\n            mutations in tumors were found to be associated with secondary organ infiltration. Three of four identified mutations inhibited transactivation and apoptosis induction activities in vitro. Furthermore, experiments which involved mating Tax transgenic mice with p53-deficient mice demonstrated minimal acceleration in initial tumor formation, but significantly accelerated disease progression and death in mice heterozygous for\n            <jats:italic>p53<\/jats:italic>\n            . These studies suggest that functional inactivation of p53 by HTLV-1 Tax, whether by mutation or another mechanism, is not critical for initial tumor formation, but contributes to late-stage tumor progression.\n          <\/jats:p>","DOI":"10.1128\/jvi.75.5.2185-2193.2001","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T10:06:37Z","timestamp":1027764397000},"page":"2185-2193","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":29,"title":["Analysis of p53 Inactivation in a Human T-Cell Leukemia Virus Type 1 Tax Transgenic Mouse Model"],"prefix":"10.1128","volume":"75","author":[{"given":"Toni","family":"Portis","sequence":"first","affiliation":[{"name":"<!--label omitted: 1-->Departments of Medicine, Pathology, and Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri 63110,1 and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William J.","family":"Grossman","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Departments of Medicine, Pathology, and Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri 63110,1 and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John C.","family":"Harding","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Departments of Medicine, Pathology, and Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri 63110,1 and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jay L.","family":"Hess","sequence":"additional","affiliation":[{"name":"<!--label omitted: 2-->Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 191042"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lee","family":"Ratner","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Departments of Medicine, Pathology, and Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri 63110,1 and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.65.12.6892-6899.1991"},{"key":"e_1_3_2_3_2","first-page":"3791","article-title":"p53 mutations in C57BL\/6J murine thymic lymphomas induced by gamma-irradiation and N-methylnitrosourea","volume":"52","author":"Brathwaite O.","year":"1992","unstructured":"Brathwaite O. Bayona W. Newcomb E. W. p53 mutations in C57BL\/6J murine thymic lymphomas induced by gamma-irradiation and N-methylnitrosourea.Cancer Res. 52 1992 3791 3795","journal-title":"Cancer Res."},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1006\/viro.1997.8509"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/318571a0"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V88.5.1551.1551"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V80.12.3205.3205"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1128\/mcb.7.8.2745-2752.1987"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.8023157"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.12.5545"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V86.10.3619.bloodjournal86103619"},{"key":"e_1_3_2_12_2","first-page":"1023","article-title":"HTLV-I Tax induces expression of various immediate early serum responsive genes","volume":"6","author":"Fujii M.","year":"1991","unstructured":"Fujii M. 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