ReviewJournal of inflammation research2025
Dual Targeting of Inflammatory and Immune Checkpoint Pathways to Overcome Radiotherapy Resistance in Esophageal Squamous Cell Carcinoma.
Review in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Dynamic survival prediction using longitudinal AGR in unresectable locally advanced esophageal squamous cell carcinoma.Frontiers in immunology · 2026Article
- From local control to immune modulation: hypofractionated radiotherapy as a backbone for cancer immunotherapy.Frontiers in oncology · 2026Review
- Mast cell driven immunometabolism as a therapeutic entry point in ESCC.Frontiers in cell and developmental biology · 2026Review
- Role of autophagy‑modulating long non‑coding RNAs in tumor radioresistance (Review).Oncology reports · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Esophageal squamous cell carcinoma (ESCC) is characterized by chronic inflammation, immune evasion, and resistance to RT. Inflammatory pathways such as nuclear factor-kappa B (NF-κB) and signal transducer and activator of transcription 3 (STAT3), and cyclooxygenase 2 (COX-2) promote tumor progression and reduce radiosensitivity. RT activates pro-inflammatory cytokines and upregulates immune checkpoints including programmed death 1 (PD-1) and cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), which contribute to immune suppression and treatment failure. Dual targeting of inflammatory and immune checkpoint pathways has shown potential to reverse radio resistance and enhance therapeutic response. Inhibition of COX-2 can reduce inflammation and improve tumor control, while blockade of PD-1 can restore T cell function and promote antitumor immunity. Strategies that integrate anti-inflammatory components, immune checkpoint inhibitors (ICIs), and RT guided by molecular profiling may improve treatment outcomes in ESCC. This review focuses on the biological basis of inflammation-mediated radio resistance and presents dual targeting approaches as promising options to overcome current therapeutic limitations.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.