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. 2020 Oct 27;10:18316. doi: 10.1038/s41598-020-75529-0

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© The Author(s) 2020

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Akt isoform-specific effects on thyroid cancer development and progression. PVPV-AktWT (●), PVPV-Akt1KO (○), PVPV-Akt2KO (■), and PVPV-Akt3KO (□). A minimum of three mice were sacrificed at 3 months and seven mice at 6, 9, and 12 months for each genotype. Tumor development (A; ^#p = 0.053) and capsular invasion (B; *p = 0.012) trended toward or were significantly delayed/reduced only in the PVP-Akt1KO mice, respectively. Vascular invasion (C; *p < 0.05; **p = 0.061) and lung metastasis (D; *p = 0.018; ***p = 0.004) were decreased with loss of Akt isoforms vs control. (E) shows mouse number of each age for each genotype. Graph images were created using Graphpad Prism version 8.4.2 (https://graphad.com).