ArticleJournal of advanced research2026
Pan-cancer epigenetic landscape of human tumor-associated macrophages reveals crucial enhancers governing their heterogenous formation by Pol II pausing modulation.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- High SIGLEC10-Expressing Tumor-Associated Macrophages Participate in Remodeling the Tumor Immune Microenvironment and Predict Poor Prognosis in Colorectal Cancer.Cancer medicine · 2026Article
- MeCP2 functions as a DNA methylation reader in immune homeostasis and cancer.Frontiers in epigenetics and epigenomics · 2026Review
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Authors and funding
7 authors.
Funding
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Abstract
introductionTumor-associated macrophages (TAMs) are a functionally heterogeneous population within the tumor microenvironments, exhibiting both anti-tumor and pro-tumor functions. Pro-tumorigenic TAMs can derive from peripheral monocytes or tissue-resident macrophages (TRMs). However, the epigenetic mechanisms driving the differentiation of these distinct cellular sources into specific TAM subtypes remain unclear.
objectivesHere, we sought to define the epigenetic mechanisms that drive the divergent differentiation of monocyte and TRM-derived TAMs. Through a pan-cancer analysis, we map the regulatory cascade, from cis-regulatory elements and key transcription factors to the release of RNA Polymerase II (Pol II) pausing, that specifies TAM heterogeneity.
methodsWe performed single-cell epigenetic profiling of macrophages derived from various human cancers, precancerous lesions, and healthy adult and fetal tissues using publicly available datasets, coupled with single-cell multi-omics integration. Key findings were validated through multi-omics analysis of mouse bone marrow-derived macrophage and CRISPR-based functional assays using in vitro human cell culture models.
resultsWe delineated the distinct epigenetic developmental trajectories by which peripheral monocytes and TRMs give rise to SPP1+ and C1QC + TAM, respectively. Along the monocyte-to-SPP1
conclusionOur work delineates the epigenetic and transcriptional circuitry that establishes TAM heterogeneity as potential therapeutic levers to enhance cancer immunotherapy.
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