Identification and Characterization of Distinct Apoptotic Pathways in Cancer Cells Activated in Response to Treatment with Different Anti-Cancer Agents
Abstract
Apoptosis is a programmed form of cell death that plays an important role in malignancy by shifting the balance from tumor proliferation to its regression. Anticancer drugs act by activating apoptosis in tumor cells. Mutations in apoptotic pathways can lead to anticancer drug resistance and therefore can promote tumor progression. Our lab is working to elucidate the molecular mechanisms of apoptosis in oncogenically-transformed primary Mouse Embryo Fibroblasts (MEFs). We have chosen this model system because it lacks mutations and alterations that are common to immortal cell lines; of the ability to use genetic approach to study apoptosis (availability of knock-out mouse lines); of the ease of gene manipulations (retroviral mediated gene transfer technique) in MEFs. The adenovirus E1A oncoprotein sensitizes primary cells to undergo apoptosis following treatment with anticancer agents. It was shown that E1A induced sensitivity in MEFs is similar to chemosensitivity of spontaneous tumors. We expect that further insight into mechanisms of programmed cell death in oncogenically-transformed MEFs will provide a fuller understanding of the role of apoptosis in real tumor progression such as breast cancer and will lead to the developing new strategies for anti-cancer therapy.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 2000
- Accession Number
- ADB271166
Entities
People
- Julia Polyakova
Organizations
- Cold Spring Harbor Laboratory