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. Author manuscript; available in PMC: 2019 Jul 1.
Published in final edited form as: Clin Cancer Res. 2018 Oct 16;25(1):210–221. doi: 10.1158/1078-0432.CCR-18-1278

Figure 5:

Figure 5:

(A) DLL3 immunohistochemistry of FFPE sample of a SCBC patient-derived xenograft (PDX) model and (B) isotype control (IgG1) of same FFPE sample showing lack of staining. (C) Tumor volumes across time in 4 groups of NOD/SCID mice implanted with BL100 tumor cells (SCBC PDX model) and treated with either vehicle, Cisplatin/Etoposide, SC16LD6.5 (antibody-drug conjugate Rova-T), or huIgG1LD6.5 (isotype antibody control ADC) (D) Estimated residual tumor initiating cell (TIC) frequency in tumors previously treated with vehicle, huIgG1LD6.5 or SC16LD6.5, suggesting that TIC suppression by SC16LD6.5 (Rova-T) is the mechanism that induces durable responses to Rova-T treatment