The Role of Ras in Myc-induced Mammary Tumorigenesis

Abstract

We have previously demonstrated that MYC or Wnt1 oncogene induction in the murine mammary epithelium results in the formation of mammary tumors. Kras2 mutations in either MYC or Wnt1-induced tumors correlate with oncogene-independent growth while Hrasl mutations do not. Kras2 mutations in MYC and Wnt1-induced tumors also exhibit higher levels of ras and MAPK pathway activation than do tumors that are wild-type for ras or tumors harboring Hrasl mutations. The next phase of this project includes introducing regulatable activated Kras2 and Hrasl alleles into MYC and Wnt1-induced tumors. Although attempts at constructing a mifepristone-inducible system and using retroviral vectors were not successful future efforts may require creating a different inducible system or adjusting the retroviral infection protocol to manipulate Kras2 or Hrasl independently of MYC or Wnt1.

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Document Details

Document Type
Technical Report
Publication Date
May 01, 2006
Accession Number
ADA484104

Entities

People

  • Joanne Jang

Organizations

  • University of Pennsylvania

Tags

DTIC Thesaurus Topics

  • Acquisition
  • Alkynes
  • Amplification
  • Biological Sciences
  • Biomedical Research
  • Breast Cancer
  • Cancer
  • Cell Line
  • Cells
  • Contrast
  • Department Of Defense
  • Glands
  • Infection
  • Mammary Glands
  • Mutations
  • Neoplasms
  • Wound Infections

Readers

  • Molecular Biology and Genetics
  • Molecular Genetics