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. 2019 Jan 30;9:975. doi: 10.1038/s41598-018-37389-7

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© The Author(s) 2019

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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Schema of the inferred tumour clonal evolution path of the CLL patient 2. CLL therapy could induce novel mutagenesis and/or accelerate clonal evolution by “killing” a clone and selecting other containing mutations in genes that might confer resistance. Sustained treatment with targeted antigen-specific immunotherapy with anti-CD20 and subsequent anti-CD37 monoclonal antibodies might interfere with stem cell plasticity and provoke tumor escape through clonal evolution with acquisition of additional genetic alterations responsible for histological transformation. FCR: fludarabine, cyclophosphamide, rituximab; TRU-Benda: TRU-016-bendamustine; RCMP: rituximab, liposomal doxorubicin and prednisone.