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. 2018 Jun 13;8:9043. doi: 10.1038/s41598-018-27454-6

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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In vivo competitive inhibition. In AsPC-1 xenografts, blocking with cetuximab (EGFR block) showed an almost 2-fold decrease in ⁸⁹Zr-MEHD7945A uptake, whereas blocking HER3 with DL3.6b did not change probe uptake. (A) In BxPC-3 xenografts, blocking with cetuximab (EGFR block) showed a slight decrease in ⁸⁹Zr-MEHD7945A, whereas blocking with DL3.6b (HER3 block) showed a statistically significant, increase in probe accumulation. (B) IHC staining in BxPC-3 tumors blocked with 25× cetuximab (25x EGFR, left), 25x DL3.6b (25x HER3, middle) or left unblocked (right) were assessed by IHC for EGFR (top) and HER3 (bottom) expression, and showed an increase in EGFR and HER3 in both blocked cohorts. (C) Tumor sections depicted for IHC are shown in 100×. Densitometry analysis of western blots on tumor lysates (n = 2) from AsPC-1 (left) and BxPC-3 (right) that were untreated, exposed to EGFR-block with cetuximab and a HER3-block with DL3.6b. (D) Densitometry is shown as a ratio of target protein/loading control.