Antibody-Mediated BRCC36 Silencing: A Novel Approach for Targeted Breast Cancer Therapy

Abstract

The significant mortality associated with metastatic breast cancer suggests a clear need to improve current therapeutic strategies. Breast tumor cells with defective BRCA1 are believed to be more sensitive to the DNA-damage based therapies. We propose that the aberrant expression (gain or loss) or activity of protein(s) in BRCA1-associated pathways will lead to a BRCA1 null-like phenotype and DNA damage hypersensitivity in breast cancer cells. Previous studies have demonstrated that BRCC36 is overexpressed in the vast majority of invasive breast cancers and that depletion of BRCC36 sensitizes breast cancer cells to IR via the BRCA1 DNA repair pathway. Therefore, we are examining if abrogation of BRCC36 will sensitize breast tumors to the DNA damage based therapies. We have tested a cancer cell-specific or smart therapeutic approach utilizing the conjugation of anti- HER2 antibodies and protamine to deliver BRCC36 siRNA to HER2 positive breast cancer cells. This approach should lead to improving the targeting of breast tumor cells while reducing non-specific toxicity.

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Document Details

Document Type
Technical Report
Publication Date
Jun 01, 2010
Accession Number
ADA551844

Entities

People

  • Xiaowei Chen

Organizations

  • Fox Chase Cancer Center

Tags

DTIC Thesaurus Topics

  • Breast Cancer
  • Carcinoma
  • Cell Physiological Processes
  • Cells
  • Department Of Defense
  • Genetics
  • Ionizing Radiation
  • Mammary Glands
  • Metabolic Diseases
  • Neoplasms
  • Oncology
  • Ovarian Cancer
  • Proteins
  • Skin Diseases
  • Transcription Factors
  • Two Dimensional
  • United States

Fields of Study

  • Biology
  • Medicine

Readers

  • Molecular Genetics
  • Neurodegenerative Parkinson's Disease and Rickettsial Disease handbook, including the data level of dopamine, BC, neurons, and PD.
  • Oncology (Cancer Research).

Technology Areas

  • Biotechnology
  • Biotechnology - Cancer Biotech