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. 2023 Jun 2;11(6):e006388. doi: 10.1136/jitc-2022-006388

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© Author(s) (or their employer(s)) 2023. 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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Loss of ASS1 blunts the therapeutic response to MYXV-mediated oncolytic virotherapy: ASS1^WT or ASS1^KO (KO#1) tumors were established in C57Bl/6J mice and then treated with three doses of either PBS (mock) or 1×10⁵ FFU of MyxPD1/IL-12 intratumorally QOD over 5 days. Tumor burden was then monitored QOD in all cohorts. (A) Schematic of treatment regimen. (B) Spaghetti plots tracking individual tumor sizes over time. (C) Overall survival of mice. Statistical significance was determined using log-rank analysis. *P<0.05. Arg, arginine; ASS1, argininosuccinate synthetase 1; FFU, focus-forming unit; IL, interleukin; MYXV, myxoma virus; n.s., no significance; PBS, phosphate-buffered saline; QOD, every other day; WT, wild type.