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Additional file 10: of Induction of cell cycle arrest and inflammatory genes by combined treatment with epigenetic, differentiating, and chemotherapeutic agents in triple-negative breast cancer

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posted on 2018-11-28, 05:00 authored by Vanessa Merino, Soonweng Cho, Nguyen Nguyen, Helen Sadik, Athira Narayan, Conover Talbot, Leslie Cope, Xian Zhou, Zhe Zhang, Balázs Győrffy, Saraswati Sukumar
Figure S3. ED induces interferon gamma genes associated with an increase in tumor lymphocytes. (A) Hierarchical supervised clustering of expression of interferon-gamma (IFN-G) genes against signatures of MDA-MB-231 cells following treatments. (B) qRT-PCR of (a) IFN-G in MDA-MB-231 and (b) CXCL10 and TRIM48 in SUM-159 cells treated with EAD singly and in combinations (doxorubicin 12.5 and 200 nM). (C) Unsupervised hierarchical cluster analysis of tumor-infiltrating lymphocyte genes [57], used in Fig. 3C to classify immune infiltration (low, medium, and high) in TCGA RNA-seq breast cancer patient dataset [58]. (D) Hierarchical supervised clustering of expression of IFN-γ genes against TCGA RNA-seq breast cancer patient dataset. Bars above identify different tumor subtypes (PAM50) and inflammatory cell content (immune, low–high) identified in (C). (E) One-way ANOVA showed significant difference across one or more groups (#1 low, #2 medium, #3 high immune cells) and post-hoc pairwise Student t test revealed statistically significant differences across all groups (p < 0.05). (F) IFN-γ score correlation with immune infiltration. *p < 0.05, **p < 0.01, ***p < 0.001. (PPTX 538 kb)

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