Molecular profiling of triple negative breast cancer

Issue title: Triple Negative Breast Cancer: Breast Cancer Research in Evolution

Guest editors: Jennifer Eng-Wongx and Jo Anne Zujewskiy

Article type: Research Article

Authors: Ma, Cynthia X.^{a; c; *} | Luo, Jingqin^{b; c} | Ellis, Matthew J.^{a; c}

Affiliations: [a] Section of Breast Oncology, Division of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA | [b] Division of Biostatistics, Washington University School of Medicine, St. Louis, MO, USA | [c] Siteman Cancer Center, Washington University School of Medicine, St. Louis, MO, USA | [x] Lombardi Comprehensive Cancer Center, Georgetown University, Washington DC, USA | [y] Clinical Trial Evaluation Program (CTEP), National Cancer Institute, Bethesda MD, USA

Correspondence: [*] Corresponding author: Cynthia Ma, Section of Breast Oncology, Division of Oncology, Department of Medicine, Campus box 8056, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA. E-mail: cma@dom.wustl.edu

Abstract: Advances in high-throughput technology and bioinformatics have made it possible to analyze tumors in an unbiased manner at the genomic level. These techniques aim to produce novel prognostic and predictive biomarkers, and most importantly, mechanistic insights that can be translated into ground-breaking therapeutic hypotheses. Genome-wide analysis is particularly relevant to the study of triple negative breast cancer (TNBC), as effective targeted therapy would make a considerable impact. At the transcriptome level, TNBC most frequently overlaps the intrinsic subtype referred to as “Basal-like”. However other less common subtypes, including “Claudin-low”, “HER2-enriched but without HER2 gene amplification”, “Luminal B”, “Luminal A” and “Molecular apocrine'' subtypes have also been described in TNBC. Additionally TNBC tumors that arise in the setting of a germ-line BRCA1 mutation may be considered a separate entity because of their potential susceptibility to poly ADP ribose polymerase (PARP) inhibitor therapy. With the advent of whole genome sequencing, we envision further classification of TNBC that is based on genetic abnormalities linked to targeted therapeutics.

DOI: 10.3233/BD-2010-0309

Journal: Breast Disease, vol. 32, no. 1-2, pp. 73-84, 2011