ReviewFrontiers in physiology2013
Risk factors for pancreatic cancer: underlying mechanisms and potential targets.
Review in Frontiers in physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis 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
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.
- Chronic Pancreatitis and Pancreatic Cancer Risk: A Systematic Review and Meta-analysis.The American journal of gastroenterology · 2017Pooled it
- Inflammatory cytokines and combined biomarker panels in pancreatic ductal adenocarcinoma: Enhancing diagnostic accuracy.PloS one · 2019Trial
- Molecular Mechanism of Caspase-8-Dependent Interleukin-18 Activation in Pancreatic Cancer Cells Induced by 5-Fluorouracil and Nutrient Starvation.Genes to cells : devoted to molecular & cellular mechanisms · 2026Article
- Decoding Pancreatic Cancer Pain: From Tumor-Nerve Crosstalk to Targeted Analgesic Strategies.International journal of medical sciences · 2026Review
- Oncolytic viral therapy as a novel potential solution for treatment of pancreatic cancer.Gastroenterology and hepatology from bed to bench · 2025Review
- The Role of Twist1 in Chronic Pancreatitis-Associated Pancreatic Stellate Cells.The American journal of pathology · 2024Article
- Lifestyle Medicine for the Prevention and Treatment of Pancreatitis and Pancreatic Cancer.Diagnostics (Basel, Switzerland) · 2024Review
- Lipopolysaccharide (LPS) stimulation of Pancreatic Ductal Adenocarcinoma (PDAC) and macrophages activates the NLRP3 inflammasome that influences the levels of pro-inflammatory cytokines in a co-culture model.Cancer biology & therapy · 2023Article
- Pancreatic tail cancer in the setting of pancreatitis with a review of the literature: A case report.Clinical case reports · 2023Article
- Chronic pancreatitis and cancer risk in a matched cohort study using national claims data in South Korea.Scientific reports · 2022Article
- Pancreatic intraepithelial neoplasia with carcinoma in situ with repeated distally localized pancreatitis: a case report.Surgical case reports · 2022Article
- A review of physical activity in pancreatic ductal adenocarcinoma: Epidemiology, intervention, animal models, and clinical trials.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2022Review
- The role of IL-6/JAK2/STAT3 signaling pathway in cancers.Frontiers in oncology · 2022Review
- Article
- Role of Nrf2 in Pancreatic Cancer.Antioxidants (Basel, Switzerland) · 2021Review
- Nuclear factor kappa-B contributes to cigarette smoke tolerance in pancreatic ductal adenocarcinoma through cysteine metabolism.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Article
- Early screening and diagnosis strategies of pancreatic cancer: a comprehensive review.Cancer communications (London, England) · 2021Review
- Towards an updated view on the clinical management of pancreatic adenocarcinoma: Current and future perspectives.Oncology letters · 2021Review
- NF-κB and Pancreatic Cancer; Chapter and Verse.Cancers · 2021Review
- Pancreatitis and pancreatic cancer: A case of the chicken or the egg.World journal of gastroenterology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
purpose of the reviewPancreatic cancer is extremely aggressive, forming highly chemo-resistant tumors, and has one of the worst prognoses. The evolution of this cancer is multi-factorial. Repeated acute pancreatic injury and inflammation are important contributing factors in the development of pancreatic cancer. This article attempts to understand the common pathways linking pancreatitis to pancreatic cancer. RECENT
findingsIntracellular activation of both pancreatic enzymes and the transcription factor NF-κB are important mechanisms that induce acute pancreatitis (AP). Recurrent pancreatic injury due to genetic susceptibility, environmental factors such as smoking, alcohol intake, and conditions such as obesity lead to increases in oxidative stress, impaired autophagy and constitutive activation of inflammatory pathways. These processes can stimulate pancreatic stellate cells, thereby increasing fibrosis and encouraging chronic disease development. Activation of oncogenic Kras mutations through inflammation, coupled with altered levels of tumor suppressor proteins (p53 and p16) can ultimately lead to development of pancreatic cancer. SUMMARY: Although our understanding of pancreatitis and pancreatic cancer has tremendously increased over many years, much remains to be elucidated in terms of common pathways linking these conditions.
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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.