ReviewCancers2017
Pancreatic Cancer Chemoresistance to Gemcitabine.
Review in Cancers, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 278 papers, 1 of them a synthesis that pooled it.
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
278 citing papers in PubMed, 1 synthesis or guideline pooled it, 445 citations in OpenAlex.
- Role of N6-Methyladenosine Methylation Regulators in the Drug Therapy of Digestive System Tumours.Frontiers in pharmacology · 2022Pooled it
- Stress-specific 14-3-3-client modules in digestive cancers: an evidence-graded review of adaptive survival and therapy resistance.Cancer biology & therapy · 2026Review
- Actinomycetota-Derived Metabolites in Pancreatic Cancer: Chemical Diversity, Metabolic Vulnerability, and Translational Barriers.Current oncology reports · 2026Review
- Aporphine AlkaloidPharmaceuticals (Basel, Switzerland) · 2026Article
- Parameter-Dependent Electroporation and Cellular Responses Induced by Microsecond Pulsed Electric Fields: Different Sensitivity of Two Pancreatic Ductal Adenocarcinoma Cell Lines.Bioengineering (Basel, Switzerland) · 2026Article
- Nucleotide Metabolism in Health and Disease.MedComm · 2026Review
- All-trans retinoic acid destabilizes ADAR1 protein through retinoylation-mediated USP7 dissociation and improves immunotherapy in pancreatic cancer.Nature communications · 2026Article
- GelMA Versus Agarose Hydrogels in Pancreatic Cancer 3D Spheroid Modeling: Effects on Morphology, HIF-1α Expression, and Gemcitabine Response.Gels (Basel, Switzerland) · 2026Article
- Gemcitabine-induced β4 integrin drives cancer progression and gemcitabine resistance in pancreatic cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- Mesoporous Silica Nanoparticles With Customized Drug Ratio/Loading for Effective Treatment of Gemcitabine-Resistant Pancreatic Tumors.Advanced nanobiomed research · 2026Article
- Dual Inhibition of KRAS G12D and PI3K/BRD4 signaling overcomes therapeutic resistance in pancreatic cancer.Acta biomaterialia · 2026Article
- A humanized LIF-targeting antibody synergistically enhances chemo- and immunotherapy in pancreatic cancer.Journal of translational medicine · 2026Article
- Integrating machine learning and physics-based modeling for predictive design of gemcitabine-loaded nanocomposites.Scientific reports · 2026Article
- Article
- Loss of Regulator of G Protein Signaling 11 Promotes Protumorigenic Features in Pancreatic Cancer.Molecular cancer research : MCR · 2026Article
- Targeting the gut-pancreatic axis: microbial modulation of immunotherapy in pancreatic cancer.Frontiers in immunology · 2026Review
- Developments & Potential of Nanotechnology for the Detection and Treatment of Pancreatic Cancer.International journal of nanomedicine · 2026Review
- Computational study on QSAR modeling, molecular docking, and ADMET profiling of pyrazole-modified catalpol derivatives as prospective dual inhibitors of VEGFR-2/BRAF V600E.Journal of computer-aided molecular design · 2025Article
- Targeting PAK1 or PAK4 Uncovers Different Mechanisms of Vascular Reprogramming in Pancreatic Cancer.Cells · 2025Article
- Extracellular Vesicle-Mediated Regulation of H3C14 Contributes to Gemcitabine Resistance in Bladder Cancer.Journal of extracellular vesicles · 2025Article
218 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
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC), commonly referred to as pancreatic cancer, ranks among the leading causes of cancer-related deaths in the Western world due to disease presentation at an advanced stage, early metastasis and generally a very limited response to chemotherapy or radiotherapy. Gemcitabine remains a cornerstone of PDAC treatment in all stages of the disease despite suboptimal clinical effects primarily caused by molecular mechanisms limiting its cellular uptake and activation and overall efficacy, as well as the development of chemoresistance within weeks of treatment initiation. To circumvent gemcitabine resistance in PDAC, several novel therapeutic approaches, including chemical modifications of the gemcitabine molecule generating numerous new prodrugs, as well as new entrapment designs of gemcitabine in colloidal systems such as nanoparticles and liposomes, are currently being investigated. Many of these approaches are reported to be more efficient than the parent gemcitabine molecule when tested in cellular systems and in vivo in murine tumor model systems; however, although promising, their translation to clinical use is still in a very early phase. This review discusses gemcitabine metabolism, activation and chemoresistance entities in the gemcitabine cytotoxicity pathway and provides an overview of approaches to override chemoresistance in pancreatic cancer.
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.