Genetic Induction of Cytolytic Susceptibility in Breast Cancer Cells
Abstract
These studies focus on mechanisms by which the E1A oncogene sensitizes tumor cells to destruction by cytolytic lymphocytes and other injuries. The preliminary observation that E1A sensitizes cells to proapoptotic injuries, but not injuries that trigger cellular necrosis has been confirmed. Our speculation that E1A functions independently of the p53 transcription factor has been confirmed. Other studies showed that co-expression of the Bcl-2-like molecule, E1B 19 kD, does not block the E1A sensitizing effect. These data further focus the proposed Tasks. Thus, the search for El A-modulated cellular genes whose altered expression renders cells sensitive to cytolytic injury (Task 1) can now be focused on a p53-independent apoptosis pathway that is not blocked by Bcl-2 activity. RHKO mutagenesis, differential display and PCR-based subtractive hybridization studies have provided limited information on E1A modulation of cellular genes and are being replaced by plans for studies using cDNA chip technology.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 1999
- Accession Number
- ADB259955
Entities
People
- James L. Cook
Organizations
- National Jewish Health