{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,24]],"date-time":"2023-10-24T20:58:20Z","timestamp":1698181100186},"reference-count":32,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2006,7,14]],"date-time":"2006-07-14T00:00:00Z","timestamp":1152835200000},"content-version":"vor","delay-in-days":5857,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes Chromosomes &amp; Cancer"],"published-print":{"date-parts":[[1990,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Stable integration of polyoma viral DNA into the host\u2010cell genome is a prerequisite for continuous expression of the transformed phenotype. In this study we have mapped the chromosomal location of integrated viral DNA sequences in a polyoma\u2010induced mouse salivary gland adenocarcinoma. By in situ hybridization, a major integration site was assigned to chromosome 14, band B. The combined results from in situ hybridizations to metaphase chromosomes, primary tumors, and cultured tumor cells indicate the presence of both integrated and free polyoma viral DNA in the tumors. Cytogenetically, the tumors were characterized by a pronounced karyotypic instability. No abnormal cells with the same karyotype were observed in any of the tumors. Nevertheless, it was possible to recognize a preferential pattern of chromosome variation with certain common recurrent and sporadic deviations. Clonal gains and\/or losses of single chromosomes were seen in all tumors. It is concluded from these results that karyotypic instability may play an important role in the genesis and progression of polyoma virus\u2010induced salivary gland tumors.<\/jats:p>","DOI":"10.1002\/gcc.2870020206","type":"journal-article","created":{"date-parts":[[2007,2,21]],"date-time":"2007-02-21T22:52:36Z","timestamp":1172098356000},"page":"109-115","source":"Crossref","is-referenced-by-count":4,"title":["Karyotypic instability and viral integration in polyoma virus\u2010induced mouse salivary gland tumors"],"prefix":"10.1002","volume":"2","author":[{"given":"Jens","family":"Sandros","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G\u00f6ran","family":"Stenman","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,7,14]]},"reference":[{"key":"e_1_2_1_2_1","doi-asserted-by":"crossref","first-page":"373","DOI":"10.1128\/jvi.34.2.373-382.1980","article-title":"Chromatin conformation of integrated Moloney leukemia virus DNA sequences in tissues of BALB\/Mo mice and in virus\u2010infected cell lines","volume":"34","author":"Breindle M","year":"1980","journal-title":"J Virol"},{"key":"e_1_2_1_3_1","first-page":"193","article-title":"c\u2010myc and functionally related oncogenes induce both high rates of sister chromatid exchange and abnormal karyotypes in rat fibroblasts","volume":"132","author":"Cerni C","year":"1986","journal-title":"Curr 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