Primary Melanoma Tumors from CDKN2A Mutation Carriers Do Not Belong to a Distinct Molecular Subclass  Johan Staaf, Katja Harbst, Martin Lauss, Markus Ringnér, Anna Måsbäck, Jillian Howlin, Karin Jirström, Mark Harland, Abdlsattar Zebary, Jane M. Palmer, Christian Ingvar, Håkan Olsson, Julia Newton-Bishop, Johan Hansson, Nicholas Hayward, Nelleke Gruis, Göran Jönsson  Journal of Investigative Dermatology  Volume 134, Issue 12, Pages 3000-3003 (December 2014) DOI: 10.1038/jid.2014.272 Copyright © 2014 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 1 Gene expression landscape of melanomas from CDKN2A mutation carriers compared with sporadic melanomas. (a) Principal component analysis (PCA) 3D-plot highlighting the gene expression profile similarities between primary melanomas from CDKN2A carriers (black dots) and sporadic cases (yellow dots). mRNA levels for 7,752 genes in 297 samples, including 17 normal skin and nevi (light-gray dots), are included in the analysis. (b) Classification of primary melanomas in the four gene expression phenotypes based on 270 genes described by Harbst et al. (2012). Melanoma tumors (n=280) are ordered according to gene expression phenotype, CDKN2A mutation status, and centroid correlation coefficient. Melanomas from CDKN2A mutation carriers (n=43) are denoted by black bars. (c) Genes differentially expressed between melanomas from CDKN2A carriers and sporadic cases. Fold change is unlogged and is relative to the CDKN2A carriers; that is, STAT4 is downregulated in melanomas from carriers as compared with sporadic cases. (d) Comparison of molecular and clinical features in different subsets of melanomas. Journal of Investigative Dermatology 2014 134, 3000-3003DOI: (10.1038/jid.2014.272) Copyright © 2014 The Society for Investigative Dermatology, Inc Terms and Conditions