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. 2019 Apr 5;9:5685. doi: 10.1038/s41598-019-42107-y

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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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Association of lincRNAs with genetic and clinical parameters. (a) Number of lincRNAs regulated by one or more driver gene(s) or differentially expressed upon copy number variation in the patient samples. (b) Number of lincRNAs regulated by one or more driver genes or differentially expressed upon copy number variation, for lincRNAs differentially expressed in both the patient samples and model systems. (c) Number of lincRNAs regulated by MYCN, associated with clinical and genetic features. (d) Representation of the genomic locus and RNAseq data of lnc-GOLGA6A-1. lnc-GOLGA6A-1 expression levels in ALK wild type and mutated samples, and MYCN amplified and single copy samples are shown, together with expression of the lincRNA upon crizotinib treatment, an ALK inhibitor. The boxplot shows the expression pattern of lnc-GOLGA6A-1 across the different cancer types.