LAUSR

e14186 Background: The human microbiome has been postulated to play a role in carcinogenesis, and there is evidence that commensal intestinal bacteria are capable of promoting tumor immunosurveillance and controlling the immune system’s response to therapy by modulating the tumor microenvironment. Methods: We characterized the stool microbiome of 30 patients (pts) with triple-negative breast cancer (TNBC) using 16S rRNA gene sequencing. Analysis of composition of microbiomes (ANCOM) was used to identify differential abundant exact-sequence-variants (ESVs) with p-values adjusted using Benjamini-Hochberg False Discovery Rate (pFDR) correction. We correlated the stool microbiome with clinicopathologic features and response to treatment. Results: The cohort included 7 pts with metastatic breast cancer and 23 pts with early-stage disease. 19 pts were treated with neoadjuvant chemotherapy (NACT). Bacteroides ovatus ESV was enriched (pFDR < 0.05) in black pts (n = 14), whereas ESV from Prevotella copri was abundant (pFDR < 0.05) in white pts (n = 13). ESVs from Clostridium and family Ruminococcaceae were enriched (pFDR < 0.05) in pts with distant metastatic recurrence (n = 6) compared to pts without metastatic disease. Notably, we identified specific taxa that differentiated between pts with a pathological complete response to NACT (pCR, n = 6) and those with residual disease (n = 13). ESVs from Bacteroides and Ruminococcaceae were relatively more abundant in pts with a pCR (pFDR < 0.05). Furthermore, among pts with residual disease after NACT, Bacteroides caccae was significantly enriched in pts with a partial response (n = 4) compared to pts with no response (n = 9). Conclusions: To our knowledge, this is the first time that 16S rRNA amplicon sequencing has been used to identify microbial signatures correlating with clinical phenotypes and response to treatment in pts with TNBC. This small study provides insight into the potential role of microbes in novel therapeutic interventions to correct dysbiosis and shift towards a gut microbial ecosystem that enhances the body’s immune response to TNBC.