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Molecular Types of TNBC and Treatment Options

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    Posted: Aug 20 2019 at 8:21am

Insights into Molecular Classifications of Triple-Negative Breast Cancer: Improving Patient Selection for Treatment


Triple-negative breast cancer (TNBC) remains the most challenging breast cancer subtype to treat. To date, therapies directed to specific molecular targets have rarely achieved clinically meaningful improvements in outcomes of patients with TNBC, and chemotherapy remains the standard of care. Here, we seek to review the most recent efforts to classify TNBC based on the comprehensive profiling of tumors for cellular composition and molecular features. Technologic advances allow for tumor characterization at ever-increasing depth, generating data that, if integrated with clinical–pathologic features, may help improve risk stratification of patients, guide treatment decisions and surveillance, and help identify new targets for drug development.

Significance: TNBC is characterized by higher rates of relapse, greater metastatic potential, and shorter overall survival compared with other major breast cancer subtypes. The identification of biomarkers that can help guide treatment decisions in TNBC remains a clinically unmet need. Understanding the mechanisms that drive resistance is key to the design of novel therapeutic strategies to help prevent the development of metastatic disease and, ultimately, to improve survival in this patient population.


Breast cancer is the most frequently diagnosed cancer and the second most common cause of cancer mortality in women worldwide (1). Breast tumors that are immunohistochemically characterized by lack of estrogen receptor (ER), progesterone receptor (PR), and HER2 (also defined by lack of HER2 amplification by FISH) are classified as triple-negative breast cancer (TNBC) and account for approximately 15% to 20% of all breast carcinomas (2). Compared with hormone receptor–positive or HER2-positive disease, TNBC has a highly aggressive clinical course, with earlier age of onset, greater metastatic potential, and poorer clinical outcomes as shown by the higher relapse and lower survival rates (2, 3). The molecular mechanisms that drive TNBC recurrence have not been fully elucidated. Consequently, to date, targeted therapies have not significantly improved survival in patients with TNBC, and chemotherapy remains the standard of care.

Major effort has been devoted over the past decade to classify TNBC into distinct clinical and molecular subtypes that could guide treatment decisions. Characterization of genomic, transcriptomic, proteomic, epigenomic, and microenvironmental alterations has expanded our knowledge of TNBC. Here, we review the most recent innovations in TNBC molecular taxonomy, the complex interaction between these classifications (Fig. 1), and their potential therapeutic implications.

To read the entire article:

DX IDC TNBC 6/09 age 49, Stage 1,Grade 3, 1.5cm,0/5Nodes,KI-67 48%,BRCA-,6/09bi-mx, recon, T/C X4(9/09)
11/10 Recur IM node, Gem,Carb,Iniparib 12/10,MRI NED 2/11,IMRT Radsx40,CT NED11/13,MRI NED3/15

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