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Karyotypic instability and viral integration in polyoma virus‐induced mouse salivary gland tumors
Author(s) -
Sandros Jens,
Stenman Göran
Publication year - 1990
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/gcc.2870020206
Subject(s) - biology , salivary gland , chromosome instability , karyotype , metaphase , chromosome , virus , microbiology and biotechnology , dna , genome , phenotype , polyoma virus , in situ hybridization , virology , gene , genetics , gene expression , biochemistry
Stable integration of polyoma viral DNA into the host‐cell 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‐induced 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‐induced salivary gland tumors.