ArticleJournal of inflammation research2025
Identifying Chemokine System-Related Phenotype to Predict Immune Feature in Pan-Cancer and Prognostic Signature for Lung Adenocarcinoma.
Article 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 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
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
No grant is acknowledged in the PubMed record.
Abstract
Background: The chemokine system modulates tumor cell characteristics and influences immune cell function. This research investigates the roles of chemokines and their receptors (CaCRs) across multiple cancers and establishes a reliable CaCRs-based prognostic model for lung adenocarcinoma (LUAD). Methods: Gene expression data were sourced from the UCSC-Xena platform and the GEO database. The chemokine score was calculated using the ssGSEA algorithm. A CaCRs-based prognostic signature was constructed and validated for LUAD. Expression levels of signature genes in lung cancer tissues were verified. Results: Dysregulation of CaCRs expression was observed in multiple cancers. The chemokine score has shown prognostic features in various tumors. In the LUAD cohort, a seven-gene signature of CaCRs (CCR2, CCR4, CCR6, XCR1, CCL20, CXCL17, and XCL2) was constructed as a prognostic model, identifying a poorer prognosis for high-risk groups. mRNA levels of CCR2, CCR4, CCR6, and XCR1 were significantly reduced in lung cancer tissues compared to adjacent normal tissues, while CCL20 was markedly overexpressed in tumor tissues. Furthermore, CCL20 promoted A549 cell proliferation via the MAPK pathway, with JNK inhibitors effectively blocking CCL20-induced proliferation. Conclusion: This study highlights the substantial role of CaCRs in immunity and prognosis. The identified seven-gene signature of CaCRs provides a new prognostic tool for LUAD.
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.