Genetic Induction of Cytolytic Susceptibility in Breast Cancer Cells

Abstract

These studies continue to focus on defining the mechanisms by which the ElA oncogene sensitizes human tumor cells to destruction by proapoptotic, immunological and chemical injuries. Translation and testing of the key observations from an NIH-3T3 cell system to a human breast cancer cell system has been completed, and an important difference between these systems has been detected - i.e., in contrast to mouse fibroblasts, chemotherapy- induced injury of ElA-positive human tumor cells does not require expression of the wild type p53 gene. This finding has potentially important implications for the clinical relevance of the findings from this work. cDNA array studies of ElA-related differences in cellular gene expression that might be involved in the ElA-induced phenotypic change from apoptosis-resistant to apoptosis-sensitive has been initiated. Preliminary data indicate that some findings in mouse NTH-3T3 cells will be translatable into the human breast cancer cell system. A significant delay in the productivity of these studies has resulted from relocation of the research laboratory from one institution to another and the delayed transfer of funds from the original site to the new institution. As a result, the project has been extended for an additional year.

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Document Details

Document Type
Technical Report
Publication Date
Jul 01, 2000
Accession Number
ADA389502

Entities

People

  • James M Cook

Organizations

  • University of Illinois at Chicago

Tags

DTIC Thesaurus Topics

  • Apoptosis
  • Biomedical Research
  • Breast Cancer
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Chemotherapeutic Agents
  • Chemotherapy
  • Dna Microarrays
  • Fibroblasts
  • Gene Expression
  • Materials
  • Neoplasms
  • Observation
  • Programmed Cell Death
  • Proteins

Fields of Study

  • Biology

Readers

  • Oncology (Cancer Research).
  • Technical Research and Report Writing.

Technology Areas

  • Biotechnology
  • Biotechnology - Cancer Biotech