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. 2022 May 28;36(7):1887–1897. doi: 10.1038/s41375-022-01597-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. 3 — A GSEA analysis using hallmark gene sets showed that 23 pathways were upregulated and 7 downregulated (FDR q-value<0.2, NES > 1.3) at late stage (latest available PD sample) versus early (1^st sample). The top upregulated pathways were E2F targets and G2M checkpoint involved in cell division and cell cycle. FDR: False discovery rate. B Heatmap showing the top 50 upregulated genes and their expression levels (log2(TPM + 1), z scored) in early and late samples. C The figure shows the evolvement in proliferative index (PI) between early and late samples in deceased patients. There was significant increase in PI in end-stage disease. D The figure shows diagnosis-1^st PD paired samples, and shows that patients with high PI at 1^st PD have different cytogenetic backgrounds. Mutation load and increase from diagnosis, time from diagnosis (TFD), and time to death/last control (TTD) are shown for patients with high PI at 1^st PD. E There was no significant difference in PI increase in diagnosis-first available PD sample between cytogenetic subgroups. This did not change when dividing the HRD group into cyclinD1 or cyclinD2 expressers (Fig. S6). CCND2, CCND3 and MAFs were not included due to few samples. F Heatmap for selected pathways showing ssGSEA for early-late pairs. Information on mutation load and presence of the most frequently enriched/acquired genomic aberrations at PD (KRAS, NRAS, amp1q21, and TP53) as well as intervening treatment received between the two BM sample timepoints are shown. In heatmaps patients are sorted horizontally by increasing PI of the late samples (right half) and the same patient order is used for the early samples (left half). SR standard risk according to ISS/R-ISS, HR High risk, ESD End-stage disease (<12 months from death). Cytogenetic subgroups; t(11;14)/CCND1, t(12;14)/ CCND2, t(6;14)/CCND3, t(4;14)/WHSC1(NSD2/MMSET), t(8;14)/MAFA are shown (Table S12). IMID Immunomodulatory drug, ProtInhib Proteasome inhibitor.