ReviewCarcinogenesis2014
The complex landscape of pancreatic cancer metabolism.
Review in Carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 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
78 citing papers in PubMed, 119 citations in OpenAlex.
- Theranostic Potential of an NAD(P)H-Activatable Fluorophore: Assessing Cancer Aggressiveness and Triggering Apoptosis.Angewandte Chemie (International ed. in English) · 2026Article
- Metabolic plasticity in pancreatic ductal adenocarcinoma progression and response to treatment.Molecular cancer · 2026Review
- Metabolic and immune crosstalk between cancer-associated fibroblasts and pancreatic cancer cells.Journal of translational medicine · 2025Review
- Review
- Reprogramming of Glucose Metabolism by Nanocarriers to Improve Cancer Immunotherapy: Recent Advances and Applications.International journal of nanomedicine · 2025Review
- Pancreatic cancer tumor organoids exhibit subtype-specific differences in metabolic profiles.Cancer & metabolism · 2024Article
- Radiopharmaceuticals for Pancreatic Cancer: A Review of Current Approaches and Future Directions.Pharmaceuticals (Basel, Switzerland) · 2024Review
- MIF/NR3C2 axis regulates glucose metabolism reprogramming in pancreatic cancer through MAPK-ERK and AP-1 pathways.Carcinogenesis · 2024Article
- Deciphering cellular plasticity in pancreatic cancer for effective treatments.Cancer metastasis reviews · 2024Review
- Regucalcin Is a Potential Regulator in Human Cancer: Aiming to Expand into Cancer Therapy.Cancers · 2023Review
- Mechanical Regulation of Redox Balance via the Induction of the PIN1/NRF2/ARE Axis in Pancreatic Cancer.International journal of molecular sciences · 2023Article
- Exploring the potential of exosomes in diagnosis and drug delivery for pancreatic ductal adenocarcinoma.International journal of cancer · 2023Review
- Review
- Harnessing bioactive nanomaterials in modulating tumor glycolysis-associated metabolism.Journal of nanobiotechnology · 2022Review
- The multifaceted role of autophagy in cancer.The EMBO journal · 2022Review
- The interactive role of inflammatory mediators and metabolic reprogramming in pancreatic cancer.Trends in cancer · 2022Review
- Limited nutrient availability in the tumor microenvironment renders pancreatic tumors sensitive to allosteric IDH1 inhibitors.Nature cancer · 2022Article
- A Serum Marker for Early Pancreatic Cancer With a Possible Link to Diabetes.Journal of the National Cancer Institute · 2022Article
- Metabolic profiling of induced acute pancreatitis and pancreatic cancer progression in a mutant Kras mouse model.Frontiers in molecular biosciences · 2022Article
- Metastatic phenotype and immunosuppressive tumour microenvironment in pancreatic ductal adenocarcinoma: Key role of the urokinase plasminogen activator (PLAU).Frontiers in immunology · 2022Article
18 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
2 authors at 2 institutions in 1 country.
Funding
Abstract
Pancreatic ductal adenocarcinomas (PDA) are extremely aggressive cancers and currently available therapies are only minimally effective in treating this disease. Tackling this devastating cancer has been a major challenge to the scientific and medical communities, in part due to its intense therapeutic resistance. One of the aspects of this tumor that contributes to its aggressive behavior is its altered cellular metabolism. Indeed, PDA cells seem to possess the ability to adapt their metabolism to the particular environment to which they are exposed, including utilizing diverse fuel sources depending on their availability. Moreover, PDA tumors are efficient at recycling various metabolic substrates through activation of different salvage pathways such as autophagy and macropinocytosis. Together, these diverse metabolic adaptations allow PDA cells to survive and thrive in harsh environments that may lack nutrients and oxygen. Not surprisingly, given its central role in the pathogenesis of this tumor, oncogenic Kras plays a critical role in much of the metabolic reprogramming seen in PDA. In this review, we discuss the metabolic landscape of PDA tumors, including the molecular underpinnings of the key regulatory nodes, and describe how such pathways can be exploited for future diagnostic and therapeutic approaches.
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.