{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T08:08:28Z","timestamp":1769155708215,"version":"3.49.0"},"reference-count":52,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2003,1,15]],"date-time":"2003-01-15T00:00:00Z","timestamp":1042588800000},"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":[[2003,1,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The c\n            <jats:italic>-myb<\/jats:italic>\n            oncogene is a frequent target for retroviral activation in hemopoietic tumors of avian and mammalian species. While insertions can target the gene directly, numerous clusters of retroviral insertion sites have been identified which map close to c\n            <jats:italic>-myb<\/jats:italic>\n            and outside the transcription unit in T-lymphomas (\n            <jats:italic>Ahi-1<\/jats:italic>\n            ,\n            <jats:italic>fit-1<\/jats:italic>\n            , and\n            <jats:italic>Mis-2<\/jats:italic>\n            ) and monocytic and myeloid leukemias (\n            <jats:italic>Mml1<\/jats:italic>\n            ,\n            <jats:italic>Mml2<\/jats:italic>\n            ,\n            <jats:italic>Mml3<\/jats:italic>\n            , and\n            <jats:italic>Epi-1<\/jats:italic>\n            ). Previous analyses showed no consistent effect of these insertions on c\n            <jats:italic>-myb<\/jats:italic>\n            expression, raising the possibility that other nearby genes were the true targets. In contrast, our analysis of four cell lines established from lymphomas bearing insertions at\n            <jats:italic>fit-1<\/jats:italic>\n            (\n            <jats:italic>fti-1<\/jats:italic>\n            ) (feline leukemia virus) and\n            <jats:italic>Ahi-1<\/jats:italic>\n            (Moloney murine leukemia virus) shows that these display higher expression levels of c\n            <jats:italic>-myb<\/jats:italic>\n            RNA and protein compared to a panel of phenotypically similar cell lines lacking such insertions. An interesting feature of the cell lines with long-range c-\n            <jats:italic>myb<\/jats:italic>\n            insertions was that each also carried an activated\n            <jats:italic>Myc<\/jats:italic>\n            allele. The potential for oncogenic synergy between\n            <jats:italic>Myb<\/jats:italic>\n            and\n            <jats:italic>Myc<\/jats:italic>\n            in T-cell lymphoma was confirmed in transgenic mice overexpressing alleles of both genes in the T-cell compartment, lending further credence to the case for c-\n            <jats:italic>myb<\/jats:italic>\n            as the major target for long-range activation. In contrast, mapping and analysis of c-\n            <jats:italic>myb<\/jats:italic>\n            neighboring genes (\n            <jats:italic>HBS1<\/jats:italic>\n            and\n            <jats:italic>FLJ20069<\/jats:italic>\n            ) showed that the expression of these genes did not correlate well with the presence of proviral insertions. A possible explanation for the paradoxical behavior of c\n            <jats:italic>-myb<\/jats:italic>\n            was provided by one of the murine T-lymphoma lines bearing an insertion at\n            <jats:italic>Ahi-1<\/jats:italic>\n            (p\/m16i) that reproducibly down-regulated c\n            <jats:italic>-myb<\/jats:italic>\n            RNA and protein to very low levels or undetectable levels on prolonged culture. Our observations implicate c\n            <jats:italic>-myb<\/jats:italic>\n            as a key target of upstream and downstream retroviral insertions. However, overexpression may become dispensable during outgrowth in vitro, and perhaps during tumor progression in vivo, providing a potential rationale for the previously observed discordance between retroviral insertion and c\n            <jats:italic>-myb<\/jats:italic>\n            expression levels.\n          <\/jats:p>","DOI":"10.1128\/jvi.77.2.1059-1068.2003","type":"journal-article","created":{"date-parts":[[2002,12,26]],"date-time":"2002-12-26T19:42:51Z","timestamp":1040931771000},"page":"1059-1068","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":26,"title":["Long-Range Effects of Retroviral Insertion on c\n            <i>-myb<\/i>\n            : Overexpression May Be Obscured by Silencing during Tumor Growth In Vitro"],"prefix":"10.1128","volume":"77","author":[{"given":"L.","family":"Hanlon","sequence":"first","affiliation":[{"name":"Molecular Oncology Laboratory, Department of Veterinary Pathology, University of Glasgow, Bearsden, Glasgow G61 1QH"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"N. I.","family":"Barr","sequence":"additional","affiliation":[{"name":"Molecular Oncology Laboratory, Department of Veterinary Pathology, University of Glasgow, Bearsden, Glasgow G61 1QH"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K.","family":"Blyth","sequence":"additional","affiliation":[{"name":"Molecular Oncology Laboratory, Department of Veterinary Pathology, University of Glasgow, Bearsden, Glasgow G61 1QH"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"Stewart","sequence":"additional","affiliation":[{"name":"Molecular Oncology Laboratory, Department of Veterinary Pathology, University of Glasgow, Bearsden, Glasgow G61 1QH"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P.","family":"Haviernik","sequence":"additional","affiliation":[{"name":"Leukemogenesis Section, Laboratory of Cellular Oncology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-4255"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L.","family":"Wolff","sequence":"additional","affiliation":[{"name":"Leukemogenesis Section, Laboratory of Cellular Oncology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-4255"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K.","family":"Weston","sequence":"additional","affiliation":[{"name":"Cancer Research UK, Centre for Cell and Molecular Biology, Institute of Cancer Research, London SW3 6JB, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E. 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