GENE EXPRESSION PROFILING OF INFLAMMATION-RELATED GENES IN BREAST CANCER TISSUES: INSIGHTS INTO THE TUMOR MICROENVIRONMENT
Abstract
Inflammation-related gene expression may provide insights into breast cancer biology; however, bulk tissue measurements do not directly determine immune infiltration or pathway activation. This study compared selected inflammatory transcripts in breast cancer and matched adjacent-normal tissues using an exploratory, quantitative, retrospective secondary analysis of six tissue pairs from GSE133998. After filtering, 23,813 features were analyzed with paired tests of log₂(CPM + 1) and Benjamini–Hochberg adjustment. Eight inflammatory genes and six expression signatures were evaluated. Negative binomial sensitivity analyses and external microarray comparisons supplemented the primary analysis. Seven genes were estimable, while TNF was not. TGFB1 demonstrated the largest positive mean paired difference (0.992; 95% confidence interval, 0.344–1.640; adjusted p = 0.139). TGFB1, IL1B, and NFKB1 had unadjusted p-values below 0.05, but none achieved genome-wide significance. No expression signature reached its adjusted significance threshold. TGFB1 met the panel-adjusted threshold in the pooled-dispersion sensitivity model (log₂ fold change, 1.007; adjusted p = 0.0096). External analysis identified 18,028 significant probes among 54,675, but did not establish gene-level replication. Inflammatory transcripts showed heterogeneous directional differences; however, primary analyses did not identify statistically significant differences in the selected genes or signatures after adjustment. TGFB1 merits further investigation, although its sensitivity finding depends on model specification and testing scope. The small sample size and incomplete analytical documentation limit interpretation. Larger, independently validated studies incorporating cellular and protein measurements are required.
Keywords
- Breast cancer; inflammation; gene expression; tumor microenvironment; RNA sequencing; quantitative analysis.
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