alexa Triple Negative Breast Cancer: Its Time to Kick the Can down the Road | Open Access Journals
ISSN: 2476-2261
Journal of Oncology Translational Research
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Triple Negative Breast Cancer: Its Time to Kick the Can down the Road

Sandra S Hatch*

Department of Radiation Oncology, University of Texas Medical Branch, Galveston, Texas, USA

*Corresponding Author:
Sandra S Hatch
Department of Radiation Oncology
University of Texas Medical Branch, Galveston, Texas, USA
E-mail: [email protected]

Received date: June 17, 2016; Accepted date: June 17, 2016; Published date: June 24, 2016

Citation: Hatch SS (2016) Triple Negative Breast Cancer: It’s Time to Kick the Can down the Road. Oncol Trans Res 2:e101. doi:10.4172/jotr.1000e101

Copyright: © 2016 Hatch SS. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Introduction

Breast cancer as an entity represents classic disease diversity. Yet we continue to define a subset of patients as triple negative breast cancer (TNBC) based on solely the absence of expression profiling of ER, PR and Her2 neu. These biomarkers are obtained since therapies exist to target breast cancer treatment. By definition TNBC does not have measurable detection of these biomarkers and therefore does not have an associated targeted therapy.

Approximately 15% of breast cancer patients will be diagnosed with TNBC [1]. TNBC appear to be more common in young women and those that are BRCA mutation carriers. In fact, about 70% of the cancers identified in BRCA1 mutation carriers will be triple-negative [2-4]. It is also found more commonly in black women compared to white women [2].

TNBC are actually a heterogeneous population. While the clinical phenotype includes the basal-like molecular subtype, the two are not synonymous [5]. The basal TNBC is characterized by genomic expression of the basal cluster. The basal cluster includes the epidermal growth factor receptor, EGFR that is also called Her1. The cluster of genes also contains the basal cytokeratins of 5 and 6. In addition the cluster encompasses the proto-oncogene c-Kit, the proliferation cluster, the hormone receptors and Her 2 genes [6,7]. Historically, tissue microarray IHC studies have identified 2 groups of TNBCs with differing cytogenetic alterations and protein expression patterns [8,9]. Lehmann and colleagues identified 6 TNBC subtypes using cluster analysis. These subtypes displayed unique gene expression profiles and properties. The subtypes were defined by 2 basal-like (BL1, BL2), a mesenchymal stem-like (MSL), a mesenchymal (ML), an immunomodulatory (IM) and a luminal androgen receptor (LAR) [10]. This classification has been demonstrated to correlate to response to inductive chemotherapy and therefore can serve to guide treatment [11]. The possible identification of these cell subtypes may prove predictive for outcomes to treatment response and drivers for targeted therapy. There is also an evolving body of research exploring the role of CDK4 and CDK6 that contributes to the understanding of the molecular biology of TNBC and clinical behavior. While the standard of care in TNBC is chemotherapy, the use of platinum based chemotherapy, PARP inhibitors and VEGF-directed monoclonal antibodies may be influenced by these sub-classifications.

It is important that we apply the lessons learned to date regarding the influence of biological, molecular and behavioral differences in the management of our breast cancer patients. We have entered an era where guidelines should embrace the histology and move beyond ER, PR and Her 2 neu status. With the clinicians’ recognition, targeted therapies will evolve into the true concept of precision medicine.

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