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Breast tumor copy number aberration phenotypes and genomic instability

BMC Cancer · 2006 · Vol. 6(1) · pp. 96–96
Jane FridlyandAntoine M. SnijdersBauke YlstraHua LiAdam B. OlshenRichard SegravesShanaz H. DairkeeTaku A. TokuyasuBritt‐Marie LjungAjay N. JainJane McLennanJohn L. ZieglerKoei ChinSandy DeVriesHeidi S. FeilerJoe W. GrayFrederic M. WaldmanDaniel PinkelDonna G. Albertson

Abstract

Many of the genes associated with higher frequency of copy number aberrations are direct targets of E2F, supporting the hypothesis that deregulation of the Rb pathway is a major contributor to chromosomal instability in breast tumors. These observations are consistent with failure to find mutations in sporadic tumors in genes that have roles in maintenance or manipulation of the genome.

Genomic variations and chromosomal abnormalitiesCancer Genomics and DiagnosticsDNA Repair MechanismsGenome instabilityChromosome instabilityBiologyComparative genomic hybridizationTelomereCopy-number variationGeneticsPhenotypeGeneDNA repair

MeSH terms

AdultAgedBreast NeoplasmsChromosome AberrationsChromosomes, HumanDNA, NeoplasmFemaleHumansKaryotypingMiddle AgedNeoplasm ProteinsNucleic Acid HybridizationPhenotypeSignal TransductionGene Expression Regulation, Neoplastic

Funding

  • U.S. Department of Energy
  • Avon Foundation for Women
  • National Institutes of Health
  • University of California, San Francisco
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