Accession Number:

ADA300274

Title:

Regulation of Epidermal Growth Factor Receptor (EGFR) Expression by PML in Human Breast Cancer.

Descriptive Note:

Annual rept. 1 Aug 94-31 Jul 95,

Corporate Author:

ROBERT WOOD JOHNSON MEDICAL SCHOOL PISCATAWAY NJ

Personal Author(s):

Report Date:

1995-08-15

Pagination or Media Count:

12.0

Abstract:

Overexpression of epidermal growth factor receptor EGFR, HER-2lneu, and myc oncogenes are some of the well described patterns of genetic changes that occur frequently in breast cancer. In addition, deletions of chromosomal loci that are thought to be associated with putative tumor suppressors and other genes, also contribute to more aggressive phenotype and metastasis of breast cancer. These genetic changes have important prognostic implication in the clinical outcome of breast cancer. Our laboratory is interested in exploring the role of PML, a novel tumor suppressor, on the regulation of EOFR expression in breast cancer. We show recently that PML suppresses the clonogenicity and tumorigenicity of cells derived from acute promyelocytic leukemia APL. Furthermore, PML suppresses the transformation of REF and NIH3T3 cells by oncogenes. We also show that PML specifically represses the activity of EOFR gene promoter. These results suggest that PML is a tumor suppressor gene and that the chromosomal translocation in APL involving PML and retinoic acid receptor-a RARa disrupts the biological function of PML as a tumor suppressor. In the current study, we propose to investigate the interaction between PML and EOFR, and its consequence in the development of breast cancer.

Subject Categories:

  • Medicine and Medical Research
  • Anatomy and Physiology

Distribution Statement:

APPROVED FOR PUBLIC RELEASE