ArticleThe American journal of pathology2011
Overexpression of CXCL5 is associated with poor survival in patients with pancreatic cancer.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 2 of them syntheses that pooled it.
What it found
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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.
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
100 citing papers in PubMed, 2 syntheses or guidelines pooled it, 177 citations in OpenAlex.
- CXCL5: A coachman to drive cancer progression.Frontiers in oncology · 2022Pooled it
- Six Novel Loci Associated with Circulating VEGF Levels Identified by a Meta-analysis of Genome-Wide Association Studies.PLoS genetics · 2016Pooled it
- CXCR2 knockdown reduces ERK and AKT signaling and migration in PANC-1 pancreatic cancer cells.microPublication biology · 2026Article
- Race-based differences in serum biomarkers for cancer-associated cachexia in a diverse cohort of patients with pancreatic ductal adenocarcinoma.Communications medicine · 2025Article
- CXCL5 neutralization mitigates cancer cachexia by disrupting CAF-cancer cell crosstalk.Journal of biomedical science · 2025Article
- TScience advances · 2025Article
- Tumor-derived CXCL5 promotes 5-fluorouracil resistance in colorectal cancer cells via p21 downregulation.Medical oncology (Northwood, London, England) · 2025Article
- Depletion of tumor-derived CXCL5 improves T cell infiltration and anti-PD-1 therapy response in an obese model of pancreatic cancer.Journal for immunotherapy of cancer · 2025Article
- Genetic risk variants implicate impaired maintenance and repair of periodontal tissues as causal for periodontitis-A synthesis of recent findings.Periodontology 2000 · 2025Review
- Article
- CXCL5 Promotes the Malignant Phenotype of Pancreatic Cancer and Is Associated With Immune Infiltration.Clinical Medicine Insights. Oncology · 2024Article
- Causal relationship between circulating cytokines and follicular lymphoma: a two-sample Mendelian randomization study.American journal of cancer research · 2024Article
- Article
- Review
- Small molecule antagonist of CXCR2 and CXCR1 inhibits tumor growth, angiogenesis, and metastasis in pancreatic cancer.Cancer letters · 2023Article
- L1CAM deployed perivascular tumor niche promotes vessel wall invasion of tumor thrombus and metastasis of renal cell carcinoma.Cell death discovery · 2023Article
- Targeting CXCL5 in Pancreatic Cancer Cells Inhibits Cancer Xenograft Growth by Reducing Proliferation and Inhibiting EMT Progression.Digestive diseases and sciences · 2023Article
- CXCL5 knockdown attenuated gemcitabine resistance of pancreatic cancer through regulation of cancer cells and tumour stroma.American journal of translational research · 2023Article
- The roles of phospholipase C-β related signals in the proliferation, metastasis and angiogenesis of malignant tumors, and the corresponding protective measures.Frontiers in oncology · 2023Review
- Regulation of pancreatic cancer therapy resistance by chemokines.Seminars in cancer biology · 2022Review
40 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Epithelial neutrophil-activating peptide-78 (CXCL5), a member of the CXC chemokine family, has been shown to be involved in angiogenesis, tumor growth, and metastasis. The objective of this study was to determine the relationship between CXCL5 expression and tumor progression in human pancreatic cancer and to elucidate the mechanism underlying CXCL5-mediated tumor angiogenesis and cancer growth. We report herein that CXCL5 is overexpressed in human pancreatic cancer compared with paired normal pancreas tissue. Overexpression of CXCL5 is significantly correlated with poorer tumor differentiation, advanced clinical stage, and shorter patient survival. Patients with pancreatic cancer and CXCL5 overexpression who underwent resection of cancer had a mean survival time 25.5 months shorter than that of patients who did not overexpress CXCL5. Blockade of CXCL5 or its receptor CXCR2 by small-interfering RNA knockdown or antibody neutralization attenuated human pancreatic cancer growth in a nude mouse model. Finally, we demonstrated that CXCL5 mediates pancreatic cancer-derived angiogenesis through activation of several signaling pathways, including protein kinase B (Akt), extracellular signal-regulated kinase (ERK), and signal transducer and activator of transcription (STAT) in human endothelial cells. These data suggest that CXCL5 is an important mediator of tumor-derived angiogenesis and that it may serve as a survival factor for pancreatic cancer. Blockade of either CXCL5 or CXCR2 may be a critical adjunct antiangiogenic therapy against pancreatic cancer.
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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.