ReviewFrontiers in immunology2026
Tumor-immune spatiotemporal co-evolution as a paradigm for overcoming therapy resistance in advanced prostate cancer.
Review in Frontiers in immunology, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- A TBX2-HLX Regulatory Axis Is Associated with Advanced Prostate Cancer.Biomedicines · 2026Article
- The glycobiology of prostate cancer: an update.Oncogene · 2026Review
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Therapeutic resistance in metastatic castration-resistant prostate cancer (mCRPC) is orchestrated not only by tumor-intrinsic genomic alterations but also by dynamic reprogramming of the tumor microenvironment (TME). This review introduces the tumor-immune spatiotemporal co-evolution paradigm, which reframes mCRPC resistance as an ecosystem-level adaptation unfolding across temporal (disease stage) and spatial (niche architecture) dimensions. We synthesize clinical and multi-omics data to map a probabilistic evolutionary trajectory from an immune-permissive state, through suppressive niche consolidation, to a terminal immune desert phenotype. In this review, we systematically apply the Oxford Centre for Evidence-Based Medicine (OCEBM) 2011 criteria to this field, grading all mechanistic claims to explicitly distinguish peer-reviewed, validated findings (Level 1-2b) from speculative hypotheses (Level 3-4), and delineate 5 evidence-graded core conclusions of the tumor-immune co-evolution paradigm. We delineate how spatially organized cancer-associated fibroblast (CAF) subsets architect immunosuppressive niches and engage in reciprocal metabolic symbiosis with tumor cells, and redefine therapeutics as dominant selective pressures that drive clonal-stromal co-selection to explain cross-resistance across treatment modalities. To translate this paradigm, we propose an integrative closed-loop
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