Progression of well differentiated rat mammary adenocarcinomas to very anaplastic phenotypes was found to correlate with a systematic and significant amplification of a mutant HRAS allele. Tumors with high amplification levels of this oncogene were analyzed by chromosomal in situ hybridization; in four of the cases the amplified sequences did not reside at the native chromosome 1 locus but were localized in a novel marker chromosome. The model described has potential as a reproducible system for the study of the chromosomal and cellular mechanisms operative uin vivo” for oncogene amplification.
|Number of pages||6|
|State||Published - Nov 1993|