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. 2021 Aug 9;14:121. doi: 10.1186/s13045-021-01111-4

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© The Author(s) 2021

Open AccessThis 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. 7 — The interactions between BCR-ABL and MYC in B-cell lymphocytic leukemia with t(9;22). Dashed arrows represent an indirect pathway of action, and thick arrows show the mediator's direct effect. Both mature and immature BCR signaling cascades are able to increase the MYC expression. sIgM signaling increases the MYC mRNA stability, which results in a higher level of MYC, and increase the BCR-ABL expression. BCR-ABL can induce MYC expression. Pre-BCR signaling can increase MYC stability and expression. Inhibitors of these signaling mediators can significantly reduce the activity and expression of MYC