ArticleFrontiers in oncology2026
Tumor-cell PD-L1 expression, mismatch repair status, and survival outcomes in colorectal carcinoma: a retrospective Pakistani cohort study.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Tumor-cell programmed death-ligand 1 (PD-L1) expression has been investigated as a biomarker for colorectal carcinoma (CRC), but the reported positivity rates vary by antibody clone, scoring method, and threshold. Tumor-cell PD-L1 is not a validated companion diagnostic tool for CRC. We assessed whether PD-L1 expression scored with the ZR3 clone functions as a clinicopathological or prognostic biomarker in a Pakistani cohort, using microsatellite instability/mismatch-repair (MSI/MMR) status as the reference biomarker. Methods: We retrospectively evaluated 60 patients with CRC diagnosed between 2020 and 2023. PD-L1 expression was assessed using the tumor proportion score (TPS) and ZR3 antibody. MSI was determined using polymerase chain reaction-based fragment analysis, and MMR status was determined using four-protein immunohistochemistry. Associations between binary PD-L1 status and 10 clinicopathological variables were analyzed and adjusted using the Benjamini-Hochberg false discovery rate procedure. Overall survival (OS; n=60), disease-free survival (DFS; n=44), and progression-free survival (PFS; n=16) were the exploratory outcomes. Results: At a TPS threshold of ≥1%, PD-L1 positivity was identified in 43 of 60 tumors (71.7%), including 31 low-positive and 12 high-positive tumors. This rate exceeded that of most CRC TPS series and likely reflected clone- and threshold-specific assay behavior. No clinicopathological variables were associated with binary PD-L1 status after multiplicity correction. MSI-H/dMMR was present in 12 cases (20.0%) and was associated with the three-level PD-L1 category (Fisher-Freeman-Halton p=0.0017; Cramer's V = 0.485), but not with binary positivity (p=0.151); the association was confined to the high-positive group. PD-L1 status was not associated with OS (HR 1.43, 95% CI 0.40-5.05; p=0.580), DFS (HR 0.46, 95% CI 0.15-1.45; p=0.185), or PFS (HR 0.67, 95% CI 0.20-2.20; p=0.505). Older age, rather than PD-L1 status, was associated with mortality (adjusted HR 1.68 per 10 years, 95% CI 1.09-2.57; p=0.018). Conclusions: ZR3-based tumor-cell PD-L1 TPS was not associated with clinicopathological characteristics or survival in this cohort. The high positivity rate should be interpreted as assay-specific, while the enrichment of MSI-H/dMMR tumors in the high-positive tier was consistent with established biology. ZR3-based TPS should remain a research measure and should not independently guide immunotherapy selection; MSI/MMR testing remains the clinically actionable biomarker for CRC.
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