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. 2023 Dec 14;28:590. doi: 10.1186/s40001-023-01576-8

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© The Author(s) 2023

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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 8 — ACBD3 mutation in various tumors of TCGA. A The alteration type and frequency. Among the many alteration types of ACBD3, “Amplification” was the most common type in patients with breast invasive carcinoma (BRCA) (9.22% alteration frequency) and liver hepatocellular carcinoma (LIHC) (5.38% alteration frequency). B The 3D structure of ACBD3 protein. C The number, sites, and types of the ACBD3 genetic alteration. “Missense Mutation” was the most dominant type of mutation. The alteration of R484Q/* and R516W in GOLD-2 is able to lead to the missense mutation of ACBD3. D–F The correlation between ACBD3 alternation and clinical outcomes in different tumors. For BRCA, cases with ACBD3 alternation had a worse prognosis in both progression-free survival and disease-specific survival. Patients with LIHC with ACBD3 alternation had a better prognosis in overall survival