Treatment Progress in Triple Negative Breast Cancer
Stefan Krämer, Christoph Rogmans, Dilek Saylan, Dominique Friedrich, Clayton N. Kraft, Gunther Rogmans, M Wirtz, Michael Friedrich, Enrique Hernández, M Hammond, D Hayes, M Dowsett, D Allred, K Hagerty, S Badve, Meh Hammond, D Hayes, M Dowsett, D Allred, K Hagerty, S Badve, A Wolff, Meh Hammond, D Hicks, M Dowsett, L Mcshane, K Allison, S Swain, K Trivers, M Lund, P Porter, J Liff, E Flagg, R Coates, B Lehmann, J Bauer, X Chen, M Sanders, A Chakravarthy, Y Shyr, A Gonzalez-Angulo, K Timms, S Liu, H Chen, J Litton, J Potter, R Millikan, B Newman, C Tse, P Moorman, K Conway, L Dressler, C Parise, K Bauer, M Brown, V Caggiano, L Carey, C Perou, C Livasy, L Dressler, D Cowan, K Conway, A Phipps, R Chlebowski, R Prentice, A Mctiernan, J Wactawski-Wende, L Kuller, J Palmer, E Viscidi, M Troester, C Hong, P Schedin, T Bethea, M Pierobon, C Frankenfeld, R Dent, M Trudeau, K Pritchard, W Hanna, H Kahn, C Sawka, K Collett, I Stefansson, J Eide, A Braaten, H Wang, G Eide, C Livasy, G Karaca, R Nanda, M Tretiakova, O Olopade, D Moore, M Burstein, A Tsimelzon, G Poage, K Covington, A Contreras, Saw Fuqua
Abstract
Triple-negative breast cancer (TNBC) lacks expression of the three biomarkers (the estrogen receptor (ER), progesterone receptor (PR), and the human epidermal growth factor receptor 2 (HER2) protein) and are typically higher grade. While the triple-negative clinical phenotype is heterogeneous, the basal-like molecular subtype comprises a large proportion, particularly for breast cancer susceptibility gene 1 (BRCA1)-associated breast cancer. New treatment options are checkpoint inhibitors like inhibition of PD-L1 pathway with pembrolizumab and atezolizumab, parp-inhibition with olaparib or talozoparib and treatment with the an antibody drug conjugate sacituzumab-govitecan.