Abstract：
:Initiation of tumorigenesis in mouse skin can be accomplished by mutagenesis of the H-ras gene by treatment with chemical carcinogens. A mouse model system has been developed to study the additional genetic events that take place during tumor progression. Skin carcinomas were induced in F1 hybrid mice exhibiting restriction fragment length polymorphisms at multiple chromosomal loci. Analysis of loss of heterozygosity in such tumors showed that imbalance of alleles on mouse chromosome 7, on which the H-ras gene is located, occurs very frequently in skin carcinomas. The chromosomal alterations detected, which included both nondisjunction and mitotic recombination events, were only seen in tumors that have activated ras genes. We conclude that gross chromosomal alterations that elevate the copy number of mutant H-ras and/or lead to loss of normal H-ras are a consistent feature of mouse skin tumor development.
journal_name
Celljournal_title
Cellauthors
Bremner R,Balmain Adoi
10.1016/0092-8674(90)90523-hsubject
Has Abstractpub_date
1990-05-04 00:00:00pages
407-17issue
3eissn
0092-8674issn
1097-4172pii
0092-8674(90)90523-Hjournal_volume
61pub_type
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