Molecular Basis of Genomic Instability in Breast Cancer: Regulation of the Centrosome Duplication Cycle

Abstract

This award (DAMD 17-02-1-0344) supports the study of genomic instability in breast cancer cells from the June 1st, 2002 to the May 31st, 2005. The hypothesis that centrosome abnormality may induce genomic instability was studied focusing on a mitotic kinases: Aurora kinases, which overexpression induces centrosome amplification, cellular transformation and aneuploidy. Two experimental approaches were taken: one was a genetic screen looking for its protein partners using two-hybrid screen performed in S. cerevisiae (annual report 2003 and 2005). Aurora-A interacting protein NM23-H1 and astrin were identified and characterized biochemically and geneticly. The second proteomic approach was taken to purify and identify the Aurora-A protein complex (annual report 2004 and 2005). p160ROCK were characterized as an Aurora-A kinase substrate and a genetic suppressor, which the interaction promotes the genomic instability in cancer cell lines. The results are published in Nuclei Acid Research (2002), PNAS (2004), and submitted (see key research accomplishment1-3), as well as reported in various scientific meetings (reportable outcomes 1-5).

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Document Details

Document Type
Technical Report
Publication Date
Jun 01, 2005
Accession Number
ADA444650

Entities

People

  • Gregory Hannon
  • Jianbin Du

Organizations

  • Cold Spring Harbor Laboratory

Tags

Communities of Interest

  • Biomedical

DTIC Thesaurus Topics

  • Amino Acids
  • Biological Sciences
  • Breast Cancer
  • Cell Division
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Chromosome Aberrations
  • Culture Techniques
  • Cytoskeleton
  • Genetics
  • Genomic Instability
  • Medical Personnel
  • Neoplasms
  • Proteins

Fields of Study

  • Biology

Readers

  • Molecular Biology and Genetics

Technology Areas

  • Biotechnology