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. 2024 Sep 18;131(8):1298–1308. doi: 10.1038/s41416-024-02739-y

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© Waters Technologies Corporation and The Author(s) 2024

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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Fig. 4 — Scheme of ω6 fatty acid metabolism a indicating selected enzymes involved, and the role of PI3K signaling in the liberation of arachidonic acid from the cell membrane by cPLA2. Fatty acids measured in the current study, emphasize pathways that contribute to tissue pools of arachidonic acid. Boxplots in b from a subset of data stratified by PIK3CA genotype indicate relative concentrations of the sum of selected fatty acids in normal breast adipose (N, N = 82) compared to tumor tissue harboring wildtype (WT, N = 12) or mutant (Mut, N = 23) PIK3CA. There was a significant difference in the level of all fatty acids between N and WT/Mut with all p < 0.005. c Boxplots of ratio analysis showing the change in the overall fatty acid metabolism.