Genetic Induction of Cytolytic Susceptibility in Breast Cancer Cells

Abstract

These studies continue to focus on defining the mechanisms by which the E1A oncogene sensitizes formerly resistant human tumor cells to destruction by proapoptotic injuries. Comparison and contrast between human breast cancer cells and NIH-3T3 cells continues to be used to analyze genetic mechanisms and traits that are common among species and unique to human tumor cells. Other types of human tumor cells have been contrasted with breast cancer cells for this same reason. The original two tasks continue to provide the focus for this work. In the first task, cDNA array analysis of E1A-induced differential gene expression has progressed. Resulting studies have focused on assessment of the possible relevance of E1A modulation of osteopontin gene expression in determining cellular susceptibility to proapoptotic injuries. In the second task, studies have focused on developing cell systems to test E1A-induce repression of antiapoptotic cellular mechanisms. Initial results show that E1A blockade of the cellular NF-kB defense against cytokine-induced apoptosis is one mechanism of sensitization to apoptosis. Tests of the generalization of this observation to breast cancer cells, among different breast cancer cell lines and among different types of human tumors are under way.

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Document Details

Document Type
Technical Report
Publication Date
Jul 01, 2001
Accession Number
ADB274793

Entities

People

  • James L. Cook

Organizations

  • University of Illinois at Chicago

Tags

DTIC Thesaurus Topics

  • Antineoplastic Agents
  • Breast Cancer
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Health Services
  • Lymphocytes
  • Medical Personnel
  • Papillomavirus Infections
  • Proteins
  • Tumor Cell Line

Fields of Study

  • Biology
  • Medicine

Readers

  • Molecular and genetic basis of cancer.
  • Oncology (Cancer Research).

Technology Areas

  • Biotechnology
  • Biotechnology - Cancer Biotech