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. 2019 Mar 14;33(8):2111–2115. doi: 10.1038/s41375-019-0444-6

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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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Fig. 1 — Type, incidence and prognostic impact of KRAS, NRAS and BRAF mutations. a Lollipop plots of mutations found in KRAS, NRAS, and BRAF genes. Sites and frequency of missense point mutations, and schematic presentation of the protein structure and functional domains are shown (MutationMapper, cBioPortal Version 1.14.0, Gao et al. Sci. Signal. 2013 and Cerami et al. Cancer Discov. 2012). Gray boxes indicate amino acids (aa) regions corresponding to the sequenced amplicons. RBD, Ras-binding domain; C1_1, phorbol esters/diacylglycerol binding domain (C1 domain); Pkinase_Tyr, protein tyrosine kinase domain. b Co-mutation plot of 534 CLL analyzed for KRAS, NRAS, BRAF mutations. Incidence of trisomy 12, KRAS, NRAS, and BRAF missense mutations, NOTCH1 aberrations and IGHV status are shown. c Kaplan–Meier curves of treatment-free survival (TFS) of 442 CLL patients stratified by the presence of KRAS and/or NRAS mutations. d Kaplan–Meier curves of TFS of 61 CLL patients in the IGHV unmutated/trisomy 12-only/NOTCH1-wt group stratified by the presence of KRAS mutations