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. 2020 Mar 17;8(1):e000326. doi: 10.1136/jitc-2019-000326

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© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See http://creativecommons.org/licenses/by-nc/4.0/.

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SX-682 plus bintrafusp alfa modulates tumor cell plasticity in Lewis lung carcinoma (LLC) tumors. (A, B) E-cadherin (green) expression in a representative section of a tumor in each treatment group (A) and quantification of E-cadherin expression from three individual tumors in each group (B). Shown are the average mean fluorescence intensities (MFI) of total fluorescence. (C, D) Versican (red) expression in a representative section of a tumor in each treatment group (C), and qPCR quantification of versican mRNA in CD45 negative cells isolated from three tumors in each group (D). Error bars indicate mean±SD of biological replicates. *P≤0.05; ****p≤0.0001 for one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test in (B, D). (E) Synopsis of the proposed mechanism of action of the combination SX-682 plus bintrafusp alfa.; ECM, extracellular matrix; G-MDSC, granulocytic myeloid-derived suppressor cell; PD-1, programmed death-1 receptor; PD-L1, programmed death ligand 1; TGF, transforming growth factor; TIL, tumor-infiltrating lymphocyte.