ArticleAnnals of surgery2004
Inflammatory mechanisms contributing to pancreatic cancer development.
Article in Annals of surgery, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 166 citations in OpenAlex.
- Pooled it
- Quantitative 3D histology reveals localized immune remodeling during early pancreatic cancer progression.Cell press blue · 2026Article
- Proteomics in pancreatic cancer.Biomarker research · 2025Review
- 3D histology reveals that immune response to pancreatic precancers is heterogeneous and depends on global pancreas structure.bioRxiv : the preprint server for biology · 2024Article
- IsTherapeutic advances in chronic disease · 2023Article
- Review
- Alpha Smooth Muscle Actin (αSMA) Immunohistochemistry Use in the Differentiation of Pancreatic Cancer from Chronic Pancreatitis.Journal of clinical medicine · 2021Article
- Development and Evaluation of Repurposed Etoricoxib Loaded Nanoemulsion for Improving Anticancer Activities against Lung Cancer Cells.International journal of molecular sciences · 2021Article
- Systemic Immune-Inflammation Index Predicts Overall Survival in Patients with Gastric Cancer: a Propensity Score-Matched Analysis.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2021Article
- S100 Proteins in Pancreatic Cancer: Current Knowledge and Future Perspectives.Frontiers in oncology · 2021Review
- Chemical Profile, Antioxidant, Anti-Inflammatory, and Anti-Cancer Effects of ItalianAntioxidants (Basel, Switzerland) · 2020Article
- Interleukin 22 Signaling Regulates Acinar Cell Plasticity to Promote Pancreatic Tumor Development in Mice.Gastroenterology · 2020Article
- Prognostic Impact of Pre- and Post-operative P-CRP Levels in Pancreatic Cancer Patients.Yonago acta medica · 2020Article
- Chronic Pancreatitis and the Development of Pancreatic Cancer.Endocrine, metabolic & immune disorders drug targets · 2020Review
- Review
- Effects of metamizole, MAA, and paracetamol on proliferation, apoptosis, and necrosis in the pancreatic cancer cell lines PaTu 8988 t and Panc-1.BMC pharmacology & toxicology · 2017Article
- The pancreatic cancer microenvironment: A true double agent.Journal of surgical oncology · 2017Review
- Inhibition of IL-8 secretion on BxPC-3 and MIA PaCa-2 cells and induction of cytotoxicity in pancreatic cancer cells with marine natural products.Anti-cancer drugs · 2017Article
- Derived neutrophil/lymphocyte ratio predicts gemcitabine therapy outcome in unresectable pancreatic cancer.Oncology letters · 2016Article
- An Overview of Genetic Changes and Risk of Pancreatic Ductal Adenocarcinoma.Journal of Cancer · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
objectivePancreatic cancer is the most deadly of all gastrointestinal (GI) malignancies, yet relatively little is known regarding mechanisms of tumor development including the role of inflammation. SUMMARY BACKGROUND DATA: Chronic pancreatitis (CP) increases the risk of developing cancer by 10- to 20-fold; mediators of the chronic inflammatory process and the surrounding fibrotic stroma likely support a transformation to malignancy, yet the exact mechanisms remain undefined. The purpose of our present study was to determine potential inflammatory components in epithelial and stromal cells that may contribute to both CP and pancreatic cancers.
methodsSpecimens of normal pancreas, CP, and pancreatic cancer were examined using laser-capture microdissection (LCM), gene array, and immunohistochemistry.
resultsGene array analysis from LCM-dissected tissues demonstrated: (i) increased expression of interleukin-8 (IL-8), an activator of the inflammatory factor nuclear factor-kappaB (NF-kappaB), and (ii) decreased expression of IkappaB (an inhibitor of NF-kappaB) in CP ductal cells compared with normal ducts. Compared with CP, cancers demonstrated: (i) increased expression of tumor related genes including S100A4, cyclin E1, and epidermal growth factor (EGF) receptor, and (ii) expression of matrix metalloproteinase 2, a pro-invasive factor for tumor cells, which was not present in the CP stroma. Increased staining of both the p50 NF-kappaB subunit and IKKalpha kinase (a protein that allows activation of NF-kappaB) was noted in CP and cancers.
conclusionsOur results demonstrate that similar inflammatory components and downstream effectors are present in CP and pancreatic cancers. Importantly, these findings suggest that a common pathway for pancreatic cancer development may be through a chronic inflammatory process including stroma formation. These findings may lead to novel strategies for pancreatic cancer prophylaxis based on inhibition of inflammatory mediators.
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.