ArticlePLoS computational biology2022
An individualized causal framework for learning intercellular communication networks that define microenvironments of individual tumors.
Article in PLoS computational biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Microbiome-metabolite signaling networks in gastrointestinal disease: systems biology, network rewiring, and precision therapeutics.Archives of microbiology · 2026Review
- Causal modeling reveals cell-cell communication dynamics in the tumor microenvironment during anti-PD-1 therapy in breast cancer patients.Briefings in bioinformatics · 2026Article
- Inferring Personalized Cell-Cell Communication Networks in Colorectal Cancer with Individualized Causal Discovery.bioRxiv : the preprint server for biology · 2025Article
- Unraveling the immune evasion mechanisms in the tumor microenvironment of head and neck squamous cell carcinoma.Frontiers in immunology · 2025Review
- Inferring pattern-driving intercellular flows from single-cell and spatial transcriptomics.Nature methods · 2024Article
- Measuring the composition of the tumor microenvironment with transcriptome analysis: past, present and future.Future oncology (London, England) · 2024Review
- scGEM: Unveiling the Nested Tree-Structured Gene Co-Expressing Modules in Single Cell Transcriptome Data.Cancers · 2023Article
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
Cells within a tumor microenvironment (TME) dynamically communicate and influence each other's cellular states through an intercellular communication network (ICN). In cancers, intercellular communications underlie immune evasion mechanisms of individual tumors. We developed an individualized causal analysis framework for discovering tumor specific ICNs. Using head and neck squamous cell carcinoma (HNSCC) tumors as a testbed, we first mined single-cell RNA-sequencing data to discover gene expression modules (GEMs) that reflect the states of transcriptomic processes within tumor and stromal single cells. By deconvoluting bulk transcriptomes of HNSCC tumors profiled by The Cancer Genome Atlas (TCGA), we estimated the activation states of these transcriptomic processes in individual tumors. Finally, we applied individualized causal network learning to discover an ICN within each tumor. Our results show that cellular states of cells in TMEs are coordinated through ICNs that enable multi-way communications among epithelial, fibroblast, endothelial, and immune cells. Further analyses of individual ICNs revealed structural patterns that were shared across subsets of tumors, leading to the discovery of 4 different subtypes of networks that underlie disparate TMEs of HNSCC. Patients with distinct TMEs exhibited significantly different clinical outcomes. Our results show that the capability of estimating individual ICNs reveals heterogeneity of ICNs and sheds light on the importance of intercellular communication in impacting disease development and progression.
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