Evidence map›Paper›PMID 42707646›Full record

ArticleJournal of inflammation research2026

OLR1 as a Key Inflammatory Regulator Associated with Poor Response to Neoadjuvant Immunochemotherapy in Resectable Lung Cancer.

Xinxin Chen, Siang Zhang, Xuefeng Ai, Yongfei Fan, Wenjie Chen

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Article in Journal of inflammation research, 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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1 · What the graph read from it

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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.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Xinxin Chen *Department of Thoracic Surgery, Shanghai Changzheng Hospital, Second Affiliated Hospital of Naval Military Medical University, Shanghai, People's Republic of China.ORCID 0000-0002-0940-0946
Siang Zhang *Department of Thoracic Surgery, Shanghai Changzheng Hospital, Second Affiliated Hospital of Naval Military Medical University, Shanghai, People's Republic of China.ORCID 0000-0001-6418-9314
Xuefeng Ai *Department of Thoracic Surgery, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, People's Republic of China.
Yongfei FanDepartment of Thoracic Surgery, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, People's Republic of China.ORCID 0009-0005-7782-6411
Wenjie ChenDepartment of Thoracic Surgery, Shanghai Changzheng Hospital, Second Affiliated Hospital of Naval Military Medical University, Shanghai, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Poor pathological response to neoadjuvant immunotherapy combined with chemotherapy (nICT) limits long-term survival in resectable lung cancer. How to improve response rates and the regulatory mechanism of tumor inflammatory signaling in nICT efficacy remain unclear. Methods: In this study, patients were stratified into molecular subgroups using unsupervised consensus clustering based on inflammatory response genes (IRGs) expression profiles. Single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics were applied to characterize tumor inflammatory states, immune microenvironment heterogeneity, and spatial organization between major pathological response (MPR) and non-MPR (NMPR) patients. Differentially expressed gene (DEG) analysis was performed to identify potential therapeutic targets, followed by preliminary functional validation to explore their biological roles. Results: Consensus clustering identified four molecular subgroups with distinct survival outcomes and clinical characteristics. scRNA-seq profiling uncovered that intratumoral inflammatory activation was markedly elevated in NMPR patients relative to MPR patients, with neutrophil subsets exhibiting the most robust inflammatory response among all immune cell populations. Further subset analysis identified two pro-inflammatory neutrophil populations (N3_CXCL8 and N4_VCAN), which were enriched in hypoxic tumor regions and contributed to immune evasion and angiogenesis. OLR1 was identified as a key regulatory hub associated with inflammatory activation, immunosuppression, and pro-angiogenic signaling. In addition, OLR1 Conclusion: This study identifies an OLR1-associated inflammatory regulatory axis that contributes to impaired response to nICT in lung cancer. Targeting OLR1 may represent a promising strategy to enhance immunotherapy efficacy and improve clinical outcomes in patients with resectable lung cancer. However, the study is limited by a relatively small validation cohort and a strong reliance on bioinformatics analyses, underscoring the need for further translational research and clinical validation to facilitate potential therapeutic application.

Indexed as

immune escapeimmunotherapyOLR1pathological angiogenesistumor-associated inflammation

Identifiers

PMID42707646
PMCPMC13548991

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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.