Trial reportAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
PRDM1+ Malignant Cells Mediate an Immunosuppressive Landscape and Resistance to Neoadjuvant Chemoradiotherapy and Immunotherapy in Esophageal Squamous Cell Carcinoma.
Trial report in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03940001 (A Study of Anti-PD-1 Antibody, Sintilimab Plus Chemoradiation Before Surgery for Esophageal Cancer), which is not on this map. Cited by 1 paper.
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.
A Study of Anti-PD-1 Antibody, Sintilimab Plus Chemoradiation Before Surgery for Esophageal Cancer
Who cites it
1 citing paper in PubMed.
- PRDM Proteins Orchestrate Colorectal Cancer Tumorigenesis.International journal of molecular sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
The mechanisms underlying resistance to neoadjuvant immunotherapy and chemoradiotherapy (nICRT) in locally advanced esophageal squamous cell carcinoma (ESCC) remain poorly understood. Through a single-arm phase II trial (n = 22) with 44.4-month median follow-up, we observed a significant survival disparity: patients achieving major pathologic response (MPR) exhibited superior 3-year event-free survival (EFS) and overall survival (OS), with no recurrence in MPR patients versus 71.4% recurrence in non-major pathological response (NMPR) patients (HR = 17.69, 95% CI 2.25-139.20, p = 0.0063). Integrating single-cell RNA/TCR sequencing and functional validation, we identified a PRDM1+ malignant cell subcluster enriched in NMPR patients and associated with treatment resistance. These cells exhibit strong lipid peroxidation characteristics, a state linked to the transcriptional activation of CTSB and MFSD12 mediated by PRDM1. This state renders the PRDM1+ malignant cell cluster more susceptible to ferroptosis induction. PRDM1+ cells further recruited immunosuppressive regulatory T cells (Tregs) through IL1A-IL1R2 interactions and activated lipid-metabolizing TREM2+ macrophages via CD47-SIRPA signaling, fostering an immune-evasive microenvironment. Conversely, MPR patients displayed expanded cytotoxic T-effector clones with enhanced tumor-killing capacity. Our findings identify PRDM1 as a key factor associated with nICRT resistance and suggest that targeting ferroptosis pathways or disrupting PRDM1+ cell-mediated immune suppression may represent a viable strategy in ESCC. Clinical trial registration number: NCT03940001.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.