ReviewWorld journal of gastroenterology2016
Peroxisome proliferator activated receptors at the crossroad of obesity, diabetes, and pancreatic cancer.
Review in World journal of gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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
48 citing papers in PubMed, 83 citations in OpenAlex.
- Prognostic value of body composition on early recurrence and long-term survival of resectable pancreatic ductal adenocarcinoma.European radiology · 2026Article
- Carvacrol Selectively Induces Mitochondria-Related Apoptotic Signaling in Primary Breast Cancer-Associated Fibroblasts.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Mitochondria-immunometabolism in sepsis-induced liver injury: mechanisms, biomarkers, and therapeutic opportunities.Frontiers in cellular and infection microbiology · 2026Review
- Transcriptomic analysis on pancreatic adenocarcinoma patients uncovers KRAS-mediated PPAR pathway alteration.Frontiers in oncology · 2025Article
- Bile Acids in Pancreatic Carcinogenesis.Metabolites · 2024Review
- Next-Cell Hypothesis: Mechanism of Obesity-Associated Carcinogenesis.Advances in experimental medicine and biology · 2024Review
- Alteration in the expression of the chemotherapy resistance‑related genes in response to chronic and acute hypoxia in pancreatic cancer.Biomedical reports · 2023Article
- What Dietary Patterns and Nutrients are Associated with Pancreatic Cancer? Literature Review.Cancer management and research · 2023Review
- Article
- The Role of PPARs in Breast Cancer.Cells · 2022Review
- Review
- Isoforms of the orphan nuclear receptor COUP‑TFII differentially modulate pancreatic cancer progression.International journal of oncology · 2022Article
- Qihuang Zhuyu Formula Attenuates Atherosclerosis via Targeting PPAROxidative medicine and cellular longevity · 2022Article
- Article
- Coffee BioactiveBiomolecules · 2021Article
- Diabetes and pancreatic cancer: Exploring the two-way traffic.World journal of gastroenterology · 2021Review
- Contribution of RAGE axis activation to the association between metabolic syndrome and cancer.Molecular and cellular biochemistry · 2021Review
- Study on <em>CCDC69</em> interfering with the prognosis of patients with breast cancer through PPAR signal pathway.European journal of histochemistry : EJH · 2021Article
- Construction of miRNA-mRNA-TF Regulatory Network for Diagnosis of Gastric Cancer.BioMed research international · 2021Article
- Nobiletin Attenuates Pathological Cardiac Remodeling after Myocardial Infarction via Activating PPARPPAR research · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is the fourth cause of cancer death with an overall survival of 5% at five years. The development of PDAC is characteristically associated to the accumulation of distinctive genetic mutations and is preceded by the exposure to several risk factors. Epidemiology has demonstrated that PDAC risk factors may be non-modifiable risks (sex, age, presence of genetic mutations, ethnicity) and modifiable and co-morbidity factors related to the specific habits and lifestyle. Recently it has become evident that obesity and diabetes are two important modifiable risk factors for PDAC. Obesity and diabetes are complex systemic and intertwined diseases and, over the years, experimental evidence indicate that insulin-resistance, alteration of adipokines, especially leptin and adiponectin, oxidative stress and inflammation may play a role in PDAC. Peroxisome proliferator activated receptor-γ (PPARγ) is a nuclear receptor transcription factor that is implicated in the regulation of metabolism, differentiation and inflammation. PPARγ is a key regulator of adipocytes differentiation, regulates insulin and adipokines production and secretion, may modulate inflammation, and it is implicated in PDAC. PPARγ agonists are used in the treatment of diabetes and oxidative stress-associated diseases and have been evaluated for the treatment of PDAC. PPARγ is at the cross-road of diabetes, obesity, and PDAC and it is an interesting target to pharmacologically prevent PDAC in obese and diabetic patients.
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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.