ArticleCancer research communications2026
Compartment-Specific CD8 Infiltration and Disease-Specific Survival in Resected Ampullary Adenocarcinoma.
Article in Cancer research communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Ampullary adenocarcinoma is rare, and its immune biomarker landscape is incompletely characterized. This article evaluated mismatch repair (MMR), programmed cell death ligand 1 (PD-L1; CD274), and compartment-specific CD3 (CD3E)/CD8 (CD8A) tumor-infiltrating lymphocytes (TIL) in resected tumors and explored associations with disease-specific survival (DSS). Ninety-nine patients underwent pancreaticoduodenectomy at Vancouver General Hospital (VGH) between 1984 and 2013. Duplicate 0.6-mm tissue microarrays (TMA) were assessed for MMR proteins, PD-L1 combined positive score (CPS), and stromal and intraepithelial CD3 and CD8 counts. DSS was estimated using the Kaplan-Meier method. Exploratory Cox models were adjusted for age, histologic subtype, pathologic tumor (pT) group, pathologic node (pN) status, and adjuvant chemotherapy. There were 44 DSS events. MMR deficiency (dMMR) was present in 37 of 99 (37.4%) tumors. PD-L1 was evaluable in 87 tumors; 57 of 87 (65.5%) tumors had CPS ≥1, and 24 of 87 (27.6%) tumors had CPS ≥10. Intraepithelial CD8+ T cells were present in 23 of 98 (23.5%) tumors. PD-L1 CPS ≥1, PD-L1 CPS ≥10, and MMR status were not associated with DSS by log-rank testing (P = 0.35, P = 0.98, and P = 0.74, respectively). In the pT-adjusted model, intraepithelial CD8 presence was associated with lower disease-specific hazard [hazard ratio (HR), 0.422; 95% confidence interval (CI), 0.144-0.994; likelihood-ratio P = 0.048], although the Wald sensitivity test was not significant (P = 0.074). Continuous log-transformed intraepithelial CD8 counts showed a concordant, method-dependent signal. dMMR and PD-L1 expression were common in this historical resected cohort. Intraepithelial CD8 infiltration was associated with DSS, but the borderline and inferential method-dependent estimates require external validation. These prognostic data do not establish benefit from immune checkpoint blockade. SIGNIFICANCE: Ampullary cancer is a rare disease in which treatment is extrapolated from other gastrointestinal cancers. In this cohort, immune features varied among tumors with functioning MMR. CD8+ T cells within the tumor epithelium showed an exploratory association with improved DSS, which supports the prospective evaluation of immune stratification, not immediate treatment selection.
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.