Table 1.

Clinical genomic studies of chemotherapy resistance in breast cancer.

Publications 2010–2018	Clinical Endpoint and Sample Size	Genomic Platform	Primary Genes and Pathways Discovered
Balko et al. 2012 [16] Balko et al. 2014 [17] Balko et al. 2016 [18]	Relapse-free survival (RFS) n = 74	Targeted RNA and DNA sequencing	DUSP4 low expression, MYC high expression, and JAK2 amplification were associated with RFS.
Lips et al. 2015 [19]	Pathologic complete response (pCR) and RFS n = 56	Targeted DNA sequencing	No statistically significant genes
Kim et al. 2018 [20]	pCR was not defined after NACT n = 20	Bulk DNA sequencing, single nucleus RNA- seq/DNA-seq	Chemoresistance gene signatures are enriched in EMT, CDH1, AKT1, hypoxia, angiogenesis, and extracellular matrix degradation signaling pathways.
Laura et al. 2013 [21]	pCR n = 106	Affymetrix	Significant genes enriched in Wnt, HIF1, p53, and Rho GTPases signaling pathways were associated with poor response to chemotherapy drugs.
Korde et al. 2010 [22]	pCR n = 21	Affymetrix	MAP-2, MACF1,VEGF-B, and EGFR showed high expression in patients without pCR after chemotherapy.
Silver et al. 2010 [23]	pCR n = 28	Affymetrix	BRCA1 promoter methylation and E2F3 activation contribute to good cisplatin response.
Stover et al. 2015 [24]	pCR n = 446	Affymetrix, Agilent	Low proliferation and immune-predicted resistance, with stem-like phenotype and Ras-Erk were associated with chemotherapy resistance.