{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,16]],"date-time":"2026-07-16T10:48:22Z","timestamp":1784198902208,"version":"3.55.0"},"reference-count":25,"publisher":"National Academy of Sciences","issue":"7","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[1997,4]]},"abstract":"<jats:p>\n                    The A-\n                    <jats:italic>myb<\/jats:italic>\n                    gene is a transcription factor that shares structural and functional similarities with the v-\n                    <jats:italic>myb<\/jats:italic>\n                    oncogene. To date, v-\n                    <jats:italic>myb<\/jats:italic>\n                    is the only\n                    <jats:italic>myb<\/jats:italic>\n                    gene directly implicated in tumorigenesis, a property attributed to its transactivating ability. Recent studies have demonstrated that A-\n                    <jats:italic>myb<\/jats:italic>\n                    , like v-\n                    <jats:italic>myb<\/jats:italic>\n                    , is a potent transcriptional activator, raising the possibility that A-\n                    <jats:italic>myb<\/jats:italic>\n                    may also participate in oncogenesis. To test this hypothesis, we generated fusion constructs that contained the human A-\n                    <jats:italic>myb<\/jats:italic>\n                    cDNA under control of the mouse metallothionein promoter and the mouse mammary tumor virus long terminal repeat. These constructs were inserted into the germ line of mice, and the functional consequences of ectopic A-\n                    <jats:italic>myb<\/jats:italic>\n                    expression were examined. Although transgene expression was detected in a wide range of tissues, abnormalities were confined primarily to hematopoietic tissues. After a 9-month latency, A-\n                    <jats:italic>myb<\/jats:italic>\n                    transgenic mice developed hyperplasia of the spleen and lymph nodes. Enlarged tissues contained a polyclonally expanded B lymphocyte population that expressed a germinal center-cell phenotype. Transgenic B lymphocytes showed increased DNA synthesis in response to low dose mitogen stimulation, suggesting that A-\n                    <jats:italic>myb<\/jats:italic>\n                    may contribute to hyperplasia by increasing the rate of B cell proliferation.\n                  <\/jats:p>","DOI":"10.1073\/pnas.94.7.3240","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:35:50Z","timestamp":1027679750000},"page":"3240-3244","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":19,"title":["Ectopic expression of A-\n                    <i>myb<\/i>\n                    in transgenic mice causes follicular hyperplasia and enhanced B\u2009lymphocyte\u2009proliferation"],"prefix":"10.1073","volume":"94","author":[{"given":"Susan E.","family":"DeRocco","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, Kimmel Cancer Center, and Department of Pathology, Anatomy, and Cell Biology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Renato","family":"Iozzo","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Kimmel Cancer Center, and Department of Pathology, Anatomy, and Cell Biology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"XiaoPing","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Kimmel Cancer Center, and Department of Pathology, Anatomy, and Cell Biology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roland","family":"Schwarting","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Kimmel Cancer Center, and Department of Pathology, Anatomy, and Cell Biology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Peterson","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Kimmel Cancer Center, and Department of Pathology, Anatomy, and Cell Biology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bruno","family":"Calabretta","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Kimmel Cancer Center, and Department of Pathology, Anatomy, and Cell Biology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[1997,4]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/16.23.11075"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/335835a0"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(19)38844-1"},{"key":"e_1_3_3_4_2","first-page":"2469","volume":"9","author":"Golay J","year":"1994","unstructured":"J Golay, L Loffarelli, M Luppi, M Castellano, M Introna Oncogene 9, 2469\u20132479 (1994).","journal-title":"Oncogene"},{"key":"e_1_3_3_5_2","first-page":"2481","volume":"9","author":"Foos G","year":"1994","unstructured":"G Foos, S Grimm, K H Klempnauer Oncogene 9, 2481\u20132488 (1994).","journal-title":"Oncogene"},{"key":"e_1_3_3_6_2","first-page":"6512","volume":"54","author":"Ma X","year":"1994","unstructured":"X Ma, B Calabretta Cancer Res 54, 6512\u20136516 (1994).","journal-title":"Cancer 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