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. 2022 Oct 11;8:416. doi: 10.1038/s41420-022-01206-y

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© The Author(s) 2022

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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Fig. 2 — A Lung cancer or MPM. A Aa–c TTFields combined with radiation causes DNA damage but reduces DNA damage repair by inhibiting the expression of FANCA, FANCD2, FANCJ, and BRCA. A Ad In addition, TTFields promotes the phosphorylation of AKT, which in turn promotes the phosphorylation of FOXO3A, reduces the nuclear entry of FOXO3A, and inhibits the expression of BIM, which ultimately leads to the weakening of the efficacy of Osimertinib. B Breast cancer. B Ba TTFields enhances breast cancer sensitivity to Trastuzumab by inhibiting AKT phosphorylation. C Glioblastoma. C Ca TTFields inhibits the phosphorylation of AKT, JUN, P38, and ERK, resulting in enhanced radiosensitivity while inhibiting ciliogenesis and enhancing the sensitivity of GBM to Temozolomide. C Cb In addition, TTFields combined with Sorafenib or hyperthermia resulted in cell death by inhibiting STAT3. C Cc TTFields inhibits ciliogenesis, thereby suppressing sensitivity to Temozolomide.