Abstract
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.
Original language | English |
---|---|
Pages (from-to) | 5339-5344 |
Number of pages | 6 |
Journal | Cancer Research |
Volume | 53 |
Issue number | 22 |
State | Published - Nov 1993 |