Risk for Sporadic Breast Cancer in Ataxia Telangiectasia Heterozygotes
Abstract
The discovery of p73, a gene that in certain experimental conditions behaves just like p53, requires us to determine what role it plays in breast cancer, whether a crosstalk exists between p73 and p53 actions and to clearly delineate the differences and similarities between these two genes concerning their biological role and signaling pathways. Our understanding of p53's role in breast cancer has been made hazier again by the advent of p73's discovery. For example, it has already been shown that p73's transactivation and apoptotic function is inhibited by tumor-derived p53 mutants. This opens the possibility that the phenotype of mutant p53 tumor cells might in fact be due to an interference with normal p73 function. Conversely, certain p73 isoforms could be dominant negative over p53 in heterotypic interactions. In this context it was already shown among the various p73 isoforms that, depending on the combination, synergistic or antagonistic biologic effects can ensue. This scenario could be the underlying explanation why only 30% of breast cancers have mutated their p53 gene In this case, dominant negative p73 isoforms, when deregulated in breast cancer, could interfere with p53 and p73-mediated growth suppression. About 40% of breast cancers overexpress p73, indicating its role in breast cancer tumorigenesis. A better insight into p73's function will add greatly to our understanding of its role in this disease.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 2000
- Accession Number
- ADA394063
Entities
People
- Ute M. Moll
Organizations
- State University of New York