The Tumor Suppressor Protein p53 and its Physiological Splicing Variant p53as in a Mouse Mammary Cancer Model
Abstract
Mouse mammary cell lines ranging from hyperplasia to highly tumorigenic were used to study distinct p53 protein forms during carcinogenesis. All contained p53 and an endogenous alternatively spliced form, p53as. p53/p53as mutation was neither sufficient nor required for the low tumorigenic phenotype, but mutated p53 accompanied high tumongenicity. Genistein induced p53 and p53as (mutant or wild type) early, peaking 3 hours post treatment and was transient, in contrast to the sustained induction of p53as in epidermal and fibroblast cells.
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 1997
- Accession Number
- ADA340579
Entities
People
- Molly Kulesz-martin
Organizations
- Health Research, Incorporated