ArticleMedical oncology (Northwood, London, England)2022
Identification of prostate cancer subtypes based on immune signature scores in bulk and single-cell transcriptomes.
Article in Medical oncology (Northwood, London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- The innate immune mediator group IIA secreted phospholipase AFrontiers in cell and developmental biology · 2026Article
- Quantitative profiling of intratumor immune heterogeneity identifies loss of immune diversity as a hallmark of cancer progression.NPJ precision oncology · 2025Article
- Molecular mechanisms and clinical significance of perineural invasion in malignancies: the pivotal role of tumor-associated Schwann cells in cancer progression and metastasis.Medical oncology (Northwood, London, England) · 2025Review
- Application and new findings of scRNA-seq and ST-seq in prostate cancer.Cell regeneration (London, England) · 2024Review
- Metastatic hormone-naïve prostate cancer: a distinct biological entity.Trends in cancer · 2024Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer (PC) is heterogeneous in the tumor immune microenvironment (TIME). Subtyping of PC based on the TIME could provide new insights into intratumor heterogeneity and its correlates of clinical features. Based on the enrichment scores of 28 immune cell types in the TIME, we performed unsupervised clustering to identify immune-specific subtypes of PC. The clustering analysis was performed in ten different bulk tumor transcriptomic datasets and in a single-cell RNA-Seq (scRNA-seq) dataset, respectively. We identified two PC subtypes: PC immunity high (PC-ImH) and PC immunity low (PC-ImL), consistently in these datasets. Compared to PC-ImL, PC-ImH displayed stronger immune signatures, worse clinical outcomes, higher epithelial-mesenchymal transition (EMT) signature, tumor stemness, intratumor heterogeneity (ITH) and genomic instability, and lower incidence of TMPRSS2-ERG fusion. Tumor mutation burden (TMB) showed no significant difference between PC-ImH and PC-ImL, while copy number alteration (CNA) was more significant in PC-ImL than in PC-ImH. PC-ImH could be further divided into two subgroups, which had significantly different immune infiltration levels and clinical features. In conclusion, "hot" PCs have stronger anti-tumor immune response, while worse clinical outcomes versus "cold" PCs. CNA instead of TMB plays a crucial role in the regulation of TIME in PC. TMPRSS2-ERG fusion correlates with decreased anti-tumor immune response while better disease-free survival in PC. The identification of immune-specific subtypes has potential clinical implications for PC immunotherapy.
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