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. 2021 May 24;21:593. doi: 10.1186/s12885-021-08085-z

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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. 4 — Genetic alterations in select pathways. Oncoprint generated from 64 tumor samples with sequencing data. Percentages shown indicate the deleterious gene alteration frequencies. *Only FGFR1 and FGFR3 alterations were identified; no FGFR2 alterations were observed. ^†Only one alteration type is presented when multiple alteration types were found within a single gene. ^‡Includes truncating rearrangements. DDR DNA damage repair; HRD homologous recombination deficiency; PD progressive disease; PR partial response; NA not applicable; NE not evaluable; SD stable disease