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. 2021 Mar 11;12(3):259. doi: 10.1038/s41419-021-03542-w

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© The Author(s) 2021

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. 4 — A RT-PCR data representing fold change in Bcl2 and CD34 levels using BM aspirates derived from CML patient samples (y-axis = log2 scale). B Heatmap demonstrating relative expression profile of anti-apoptotic genes (Bcl2, Bcl2l1/Bcl-xL, Bcl2l2/Bcl-w) and stem cell marker (CD34) using matched CML samples. Most of the patients were in chronic phase at diagnosis (CP Dx.) with progression to lymphoid Blast crisis (LBC) or myeloid blast crisis (MBC). Two patients were in accelerated phase at diagnosis (AP Dx.) and progressed to MBC. The pattern of expression signifies the change in the trend of regulation of BCL2, BCl2L1, CD34, MCL-1 in progressive, poor responder CML patients. C Boxplot representing the distribution of Shh target genes BCL2, Mcl-1, and CD34 expression at various stages of the disease using data from Branford et al. D Significant upregulation of Bcl2 (P value = 6.1 × 10^–6) and CD34 (P value = 1 × 10^–6) in LBC is observed, while Mcl-1 expression is downregulated in progressive cases. Statistical analysis done using one-way ANOVA test.