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. 2019 Jun 20;9:8908. doi: 10.1038/s41598-019-45210-2

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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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Summary of 303 distinct tumour samples examined for chromosome 9p21 in the CDKN2A region (CDKN2A (chr9:21,967,753–21,995,301); MTAP (chr9:21,802,636–21,865,971); and CDKN2B (chr9:22,002,903–22,009,363) showing that 204 of these samples (67%) showed no evidence of a CN change. Among the 99 samples showing a CN change, various patterns are observed, the majority of which impacted in CDKN2A, the known target of common alteration for melanoma. Three lines of evidence support the findings from the bioinformatic analysis: (A) (bottom left) gene expression analysis of regions of p16 (a protein product of CDKN2A) are associated with the extent of deletion in keeping with tumour heterogeneity and subsets of cells having a deletion (see also Supplementary Fig. 11); (B) (bottom centre) replication of results in a subset of tumours via MLPA. MLPA mean ratios (red dots) are superimposed (see Supplementary Table 2); and (C) evidence that a germline CN variant, esv36200012 (chr9: 23362412–23378071), can be detected reliably. The bottom right panel shows that the measured extent of CN loss matches the expected genotype.