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. 2019 Dec 13;9:19107. doi: 10.1038/s41598-019-55710-w

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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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Identification of signaling pathways that are altered in each specific TNBC subtypes. (A) Classification of 205 TNBCs into subtypes, and activity of 25 different signaling pathways. (B,C) In both training and validation sets high MYC pathway activity alone stratifies BL1 TNBC into high and low risk groups. (D,E) E2F2 and TGFβ pathways are significantly elevated in BL2. (F,G) IFNα and IFNγ pathways are significantly induced in IM. (H) EGFR activity is significantly higher in MLS compared to all other TNBC subtypes. Only IFNα signalling affected clinical outcome (Supplemental Fig. 1).