Window of Opportunity Trial of Entinostat in Patients With Newly Diagnosed Stage I-IIIC,TNBC

Primary Objective and Endpoint To identify decrease in Ki-67 mRNA following treatment with entinostat across TNBC breast cancers. Secondary Objectives and Endpoints To identify messenger ribonucleic acid (mRNA) gene expression changes following treatment with entinostat, across TNBC. To evaluate changes in the proliferation signature by mRNA expression following treatment with entinostat across TNBC. To identify differential kinome activation before and after treatment with entinostat across TNBC To correlate mutation and/or copy number variations by whole exome sequencing (WES) with mRNA gene expression changes and reduction of proliferation signature following treatment with entinostat across TNBC. To correlate protein lysine hyperacetylation in peripheral blood and tumor from pre- and post-entinostat treated TNBCs. To explore molecular subtype, Programmed death-ligand 1 (PD-L1) and other immune checkpoint molecule expression, immune gene and innate anti-programed cell death-1 resistance (IPRES) expression signatures and phenotypes of tumor-infiltrating lymphocytes, including delineation of effector and regulatory T cells, and define T cell receptor (TCR) repertoire prior to and following entinostat treatment in TNBCs. We will also explore mutation and copy number variation status, and predicted major histocompatibility complex (MHC) class I neoantigen burden. To document safety of entinostat in patients with TNBC prior to their scheduled surgical resection per National Cancer Institute - Common Terminology for Adverse Events (NCI-CTCAE v4.0).