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. 2019 Sep 13;9:13259. doi: 10.1038/s41598-019-49853-z

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© The Author(s) 2019

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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Human patient derived xenografts recapitulate the human tumor of origin and express FAK. (A) Hematoxylin and eosin staining (top panels) of the human specimens (left) and the tumors harvested from the mice (right) showed that the PDX tumors recapitulated the histology of the human specimens from which they were derived. Immunohistochemistry staining for neuron-specific enolase (bottom panels), a marker for neuroendocrine neoplasms, showed similar staining between the human specimens and the PDX tumors. (B) Immunoblotting of tumor lysates for total and phosphorylated (Y397) FAK demonstrated baseline expression of FAK and pFAK (Y397) in both COA3 and COA6 cells. In both cell lines treatment with FAK inhibitors PF and Y15 resulted in a decrease in both phosphorylated and total FAK in a dose-dependent manner.