Abstract：
:Nonrandom chromosome rearrangements, observed in a variety of human and animal tumours, are associated in some cases with enhanced expression or deregulation of cellular oncogenes. Recently, it was shown that normal, diploid rodent cells are neoplastically transformed following transfection with two cooperating oncogenes, for example myc plus ras. However, the number of steps necessary to convert a normal cell into a malignant cell is unknown. If activation of two oncogenes is sufficient for tumorigenicity, tumours derived from diploid cells transformed by the transfected oncogenes may remain diploid or have only random chromosome alterations. We have performed cytogenetic analyses of tumours formed after transfection of Syrian hamster embryo cells with either v-Ha-ras plus v-myc DNAs or polyoma DNA alone. Whereas polyoma-induced, tumour-derived cells were diploid, tumours induced by v-Ha-ras plus v-myc oncogenes were monoclonal and had a nonrandom chromosome change, monosomy of chromosome 15. Thus, an additional change, loss of chromosome 15, is required for or is advantageous for tumorigenicity induced by v-Ha-ras plus v-myc oncogenes. These results suggest that the neoplastic progression of normal, diploid cells requires more than two steps under certain conditions.
journal_name
Naturejournal_title
Natureauthors
Oshimura M,Gilmer TM,Barrett JCdoi
10.1038/316636a0subject
Has Abstractpub_date
1985-08-15 00:00:00pages
636-9issue
6029eissn
0028-0836issn
1476-4687journal_volume
316pub_type
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