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. 2023 Sep 13;7:90. doi: 10.1038/s41698-023-00438-0

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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 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. 7 — a Table summarizing association of PFS with major cell cycle genes across cohorts of patients. b Heatmap showing expression of these genes across pretreatment biopsies. This unsupervised clustering is able to stratify luminal A patients from other subtypes (mainly luminal B). c Kaplan–Meier plot showing progression-free survival difference between the two groups stratified by unsupervised clustering. p = 0.0035 by log rank test. d–l Testing for power of single genes in stratifying patients for progression-free survival using gene expression data from pretreatment biopsies. For CCNE1 in the combined, AI, and FUL cohorts, p = 0.0843, p = 0.4007, and p = 0.0257 by log rank test, respectively. For CDK6 in the combined, AI, and FUL cohorts, p = 0.0252, p = 0.0087, and p = 0.815 by log rank test, respectively. For CCND2 in the combined, AI, and FUL cohorts, p = 0.047, p = 0.77, and p < 0.001 by log rank test, respectively.