ReviewCancers2019
Glucose Metabolism in Pancreatic Cancer.
Review in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05132244 (Pancreatic Cancer Glucose Assessment and Regulation Study), which is not on this map. Cited by 76 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.
Pancreatic Cancer Glucose Assessment and Regulation Study
Who cites it
76 citing papers in PubMed, 122 citations in OpenAlex.
- Mitochondrial metabolite transporters at the crossroads of metabolic reprogramming, epigenetic regulation and therapeutic vulnerabilities in colorectal cancer.Molecular biology reports · 2026Review
- A BioactivatedMolecules (Basel, Switzerland) · 2026Article
- Spiky Magnetic Titania Particles for Integrated Exosome Capture and Metabolic Profiling Toward Cancer Diagnosis.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- SGLT2 inhibition induces autophagic flux blockade and sensitizes pancreatic cancer to EGFR-targeted therapy.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Metabolotheranostics of pancreatic cancer by targeting choline, glutamine, and glucose transporters with photoimmunotherapy.Npj imaging · 2026Article
- Dynamic evaluation of the glycolytic determinants LDH-A and GLUT-1 enhances prognostic significance and their inhibition affects the growth of mesothelioma spheroids.Molecular metabolism · 2026Article
- Diagnostic Biomarkers for Pancreatic Ductal Adenocarcinoma Using Non-Targeted Metabolomic Analysis.Cancers · 2026Article
- Research progress and trends on PET/CT imaging of pancreatic cancer: a bibliometric analysis.Discover oncology · 2026Article
- Melatonin Rescues Heat Stress-Induced Suppression of TCA Cycle and Mitochondrial Damage in Goat Sertoli Cells.International journal of molecular sciences · 2025Article
- Network pharmacology and experimental study on the inhibition of glycolysis by amentoflavone in pancreatic cancer.Discover oncology · 2025Article
- PI5P4Kα promotes glucose and iron acquisition to support metabolic fitness in pancreatic cancer.Cell reports · 2025Article
- Survival mechanism of pancreatic tumor bacteria and their ability to metabolize chemotherapy drugs.Microbiology spectrum · 2025Article
- Spatiotemporal Heterogeneity of Tumor Glucose Metabolism Reprogramming: From Single-Cell Mechanisms to Precision Interventions.International journal of molecular sciences · 2025Review
- Molecular Imaging: Unveiling Metabolic Abnormalities in Pancreatic Cancer.International journal of molecular sciences · 2025Review
- Simulated Microgravity-Induced Alterations in PDAC Cells: A Potential Role for Trichostatin A in Restoring Cellular Phenotype.International journal of molecular sciences · 2025Article
- Article
- Reprogramming of glucose metabolism in pancreatic cancer: mechanisms, implications, and therapeutic perspectives.Frontiers in immunology · 2025Review
- Recent Update of Natural Compounds as HIF-1α Inhibitors in Colorectal Carcinoma.Drug design, development and therapy · 2025Review
- Targeting Perineural Invasion in Pancreatic Cancer.Cancers · 2024Review
- DeepGR: a deep-learning prognostic model based on glycolytic radiomics for non-small cell lung cancer.Translational lung cancer research · 2024Article
16 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
4 authors at 1 institution in 1 country.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive and lethal cancers, with a five-year survival rate of around 5% to 8%. To date, very few available drugs have been successfully used to treat PDAC due to the poor understanding of the tumor-specific features. One of the hallmarks of pancreatic cancer cells is the deregulated cellular energetics characterized by the "Warburg effect". It has been known for decades that cancer cells have a dramatically increased glycolytic flux even in the presence of oxygen and normal mitochondrial function. Glycolytic flux is the central carbon metabolism process in all cells, which not only produces adenosine triphosphate (ATP) but also provides biomass for anabolic processes that support cell proliferation. Expression levels of glucose transporters and rate-limiting enzymes regulate the rate of glycolytic flux. Intermediates that branch out from glycolysis are responsible for redox homeostasis, glycosylation, and biosynthesis. Beyond enhanced glycolytic flux, pancreatic cancer cells activate nutrient salvage pathways, which includes autophagy and micropinocytosis, from which the generated sugars, amino acids, and fatty acids are used to buffer the stresses induced by nutrient deprivation. Further, PDAC is characterized by extensive metabolic crosstalk between tumor cells and cells in the tumor microenvironment (TME). In this review, we will give an overview on recent progresses made in understanding glucose metabolism-related deregulations in PDAC.
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.