ReviewDiscover oncology2026
Biomarker guided combination strategies and perioperative integration for immune cold microsatellite stable colorectal cancer.
Review in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMost colorectal cancers (CRC) are microsatellite stable (MSS) and show little benefit from single-agent immune checkpoint inhibition (ICI). A rapidly expanding body of work now focuses on combination strategies to remodel the tumor microenvironment (TME) and convert immune-“cold” MSS disease into an immune-responsive state. MAIN BODY: We synthesize (i) biological liabilities that underpin MSS immune resistance; (ii) clinical evidence across key combination classes—anti-angiogenic/VEGFR + ICI (randomized AtezoTRIBE suggests a progression-free survival benefit when atezolizumab is added to FOLFOXIRI + bevacizumab), multikinase TKI + PD-1/PD-L1 (mixed activity and geographic/site heterogeneity; LEAP-017 was negative for overall survival), dual-checkpoint or next-generation CTLA-4 backbones (phase-1 botensilimab + balstilimab with durable responses in heavily pretreated MSS mCRC), EGFR- or HER2-targeted plus ICI (signals in molecularly defined subsets; e.g., CAVE rechallenge), and RT/ablation + ICI (biologically compelling but heterogeneous outcomes in pMMR-dominant settings). We emphasize biomarker-anchored selection—topology of disease (especially active liver metastases), inflammatory gene programs, and ctDNA kinetics—and propose peri-operative/oligometastatic integration frameworks relevant to surgical teams. Conclusions: Converting MSS CRC from cold to hot appears feasible in biologically selected contexts and with rational sequences. The next wave should stratify by liver involvement, embed ctDNA-anchored endpoints, and leverage surgery-embedded window studies to verify on-treatment immune conditioning.
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