Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8429614 | Biochimica et Biophysica Acta (BBA) - Reviews on Cancer | 2009 | 15 Pages |
Abstract
Breast cancer is the most common malignancy among women in developed countries, affecting more than a million women per year worldwide. Over the last decades, our increasing understanding of breast cancer biology has led to the development of endocrine agents against hormone receptor-positive tumors and targeted therapeutics against HER2-expressing tumors. However, no targeted therapy is available for patients with triple-negative breast cancer, lacking expression of hormone receptors and HER2. Overlap between BRCA1-mutated breast cancers and triple-negative tumors suggests that an important part of the triple-negative tumors may respond to therapeutics targeting BRCA1-deficient cells. Here, we review the features shared between triple-negative, basal-like and BRCA1-related breast cancers. We also discuss the development of novel therapeutic strategies to target BRCA1-mutated tumors and triple-negative tumors with BRCA1-like features. Finally, we highlight the utility of mouse models for BRCA1-mutated breast cancer to optimize (combination) therapy and to understand drug resistance.
Keywords
ICLORFNHEJBERAPCMRPPARPMRNGEMABCCGHpoly (ADP-ribose)BRCA2frizzledID4ATM and Rad3-relatedPARPiPALB2HDRGSIHER1DSBMre11/Rad50/Nbs1HER2MDREGFRCNACSCATRataxia telangiectasia mutatedFFPEloss of heterozygosityHomology-directed repairionizing radiationcomparative genomic hybridizationBase-excision repairParHedgehogATMcancer stem cellcytokeratindouble strand breaknon-homologous end joiningformalin-fixed paraffin-embeddedopen reading frameLOHMultidrug resistancePARP inhibitorγ-secretase inhibitorgenetically engineered mouseHomologous recombinationmultidrug resistance-associated proteinpoly (ADP-ribose) polymeraseBRCA1breast cancer susceptibility gene 1Fanconi anemiaCopy number alterationATP-binding cassetteEstrogen receptorEpidermal growth factor receptor
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Authors
Janneke E. Jaspers, Sven Rottenberg, Jos Jonkers,