ReviewAmerican journal of cancer research2022
Glycolysis in the progression of pancreatic cancer.
Review in American journal of cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed, 36 citations in OpenAlex.
- FGD5 regulates PGK1 ubiquitination to synergize with 2-deoxy-D-glucose in pancreatic ductal adenocarcinoma.Oncogene · 2026Article
- Detection of Pancreatic Cancer via Specific Metabolite Markers: A Metabolomics Approach.Health science reports · 2026Article
- The dual role of AMPK in cancer metabolic reprogramming.Molecular biology reports · 2026Review
- Targeting mitochondrial α-ketoglutarate sequestration disables dual oncogenic drivers and metabolic adaptability in pancreatic ductal adenocarcinoma.Cell death & disease · 2026Article
- Mitochondrial inhibition enhances the sensitivity of pancreatic ductal adenocarcinoma cells to oncolytic adenovirus.Molecular therapy. Oncology · 2026Article
- Emerging role of protein arginine methyltransferase 5 in gastrointestinal cancer (Review).Oncology letters · 2026Review
- Identification of prognostic genes and development of a risk model for pancreatic cancer based on hypoxia- and lipid metabolism-related genes.Discover oncology · 2026Article
- Metabolic plasticity in pancreatic ductal adenocarcinoma progression and response to treatment.Molecular cancer · 2026Review
- Expression of glycolytic markers in cancer and stromal cells of treatment-naïve and neoadjuvantly treated pancreatic ductal adenocarcinoma.Virchows Archiv : an international journal of pathology · 2026Article
- A TXNIP-driven bioluminescent reporter for high-throughput discovery of glycolytic inhibitors against renal cell carcinoma.BMC biotechnology · 2026Article
- The Multi-Target lncRNA-miRNA-mRNA TRIAD in Pancreatic Cancer Diagnosis and Therapy.International journal of molecular sciences · 2026Review
- Dual molecular and clinical machine-learning prognostic modeling in pancreatic ductal adenocarcinoma: a chaperone-mediated autophagy-based framework integrating multi-cohort molecular signatures and a single-center clinical nomogram.Frontiers in cell and developmental biology · 2026Article
- The CLIC1-PKM2 axis orchestrates glycolytic metabolism to accelerate gastric cancer progression.Journal of translational medicine · 2025Article
- PI5P4Kα promotes glucose and iron acquisition to support metabolic fitness in pancreatic cancer.Cell reports · 2025Article
- Menin regulates YBX1 nucleus translocation to boost the HKDC1 transcription and affects pancreatic cancer glycolysis.iScience · 2025Article
- The Multifaceted Role of p53 in Cancer Molecular Biology: Insights for Precision Diagnosis and Therapeutic Breakthroughs.Biomolecules · 2025Review
- Multi-omics integration and machine learning uncover molecular basal-like subtype of pancreatic cancer and implicate A2ML1 in promoting tumor epithelial-mesenchymal transition.Journal of translational medicine · 2025Article
- Article
- The emerging role of glycolysis and immune evasion in ovarian cancer.Cancer cell international · 2025Review
- Nanotechnology-driven EGCG: bridging antioxidant and therapeutic roles in metabolic and cancer pathways.Nanomedicine (London, England) · 2025Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic reprogramming, as a key hallmark of cancers, leads to the malignant behavior of pancreatic cancer, which is closely related to tumor development and progression, as well as the supportive tumor microenvironments. Although cells produce adenosine triphosphate (ATP) from glucose by glycolysis when lacking oxygen, pancreatic cancer cells elicit metabolic conversion from oxide phosphorylation to glycolysis, which is well-known as "Warburg effect". Glycolysis is critical for cancer cells to maintain their robust biosynthesis and energy requirement, and it could promote tumor initiation, invasion, angiogenesis, and metastasis to distant organs. Multiple pathways are involved in the alternation of glycolysis for pancreatic cancer cells, including UHRF1/SIRT4 axis, PRMT5/FBW7/cMyc axis, JWA/AMPK/FOXO3a/FAK axis, KRAS/TP53/TIGAR axis, etc. These signaling pathways play an important role in glycolysis and are potential targets for the treatment of pancreatic cancer. Mutations in glycolytic enzymes (such as LDH, PKM2, and PGK1) also contribute to the early diagnosis and monitoring of pancreatic cancer. In this review, we summarized the recent advances on the mechanisms for glycolysis in pancreatic cancer and the function of glycolysis in the progression of pancreatic cancer, which suggested new targets for cancer diagnosis and treatment.
Indexed as
Identifiers
35261808PMC8900001W4226437693What 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.