ArticleMolecular therapy oncolytics2019
ROS/KRAS/AMPK Signaling Contributes to Gemcitabine-Induced Stem-like Cell Properties in Pancreatic Cancer.
Article in Molecular therapy oncolytics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 75 citations in OpenAlex.
- Phosphorylated STYK1 Promotes Gemcitabine Resistance via Autophagy-Mediated Cancer Stemness in Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- Deciphering RTK-RAS and MAPK Pathway Dependencies in Gemcitabine-Treated Pancreatic Ductal Adenocarcinoma Through Conversational Artificial Intelligence.International journal of molecular sciences · 2026Article
- Mesoporous Silica Nanoparticles With Customized Drug Ratio/Loading for Effective Treatment of Gemcitabine-Resistant Pancreatic Tumors.Advanced nanobiomed research · 2026Article
- Article
- Conversational Artificial Intelligence Agents-Enabled Dissection of RTK-RAS and MAPK Pathway Dependencies in Gemcitabine-Treated Pancreatic Ductal Adenocarcinoma (PDAC).medRxiv : the preprint server for health sciences · 2026Article
- c-Myc/GRPEL1 maintains fatty acid synthesis via FASN to support PDAC cell proliferation.Cell death & disease · 2026Article
- Machine learning-driven comprehensive profiling of tumor heterogeneity and sialylation in hepatocellular carcinoma.NPJ precision oncology · 2025Article
- Exploration and Application of Malignant Cell Heterogeneity Analysis with Single-Cell Transcriptome Sequencing Technology.Aging and disease · 2025Review
- KRAS inhibition reverses chemotherapy resistance promoted by therapy-induced senescence-like in pancreatic ductal adenocarcinoma.Translational oncology · 2025Article
- The role of AMPK in pancreatic cancer: from carcinogenesis to treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Encapsulation of Curcumin and Gemcitabine: Cytotoxic Effect and Mechanisms of Death in Lung Cancer.Advances in pharmacological and pharmaceutical sciences · 2025Article
- Pharmacological Insights: Mitochondrial ROS Generation by FNC (Azvudine) in Dalton's Lymphoma Cells Revealed by Super Resolution Imaging.Cell biochemistry and biophysics · 2024Article
- Cordycepin Enhanced Therapeutic Potential of Gemcitabine against Cholangiocarcinoma via Downregulating Cancer Stem-Like Properties.Biomolecules & therapeutics · 2024Article
- Review
- Improved Antitumor Efficiency ofInternational journal of nanomedicine · 2024Article
- Amurensin G Sensitized Cholangiocarcinoma to the Anti-Cancer Effect of Gemcitabine via the Downregulation of Cancer Stem-like Properties.Nutrients · 2023Article
- FTO-mediated LINC01134 stabilization to promote chemoresistance through miR-140-3p/WNT5A/WNT pathway in PDAC.Cell death & disease · 2023Article
- Review
- A Brief Review on Chemoresistance; Targeting Cancer Stem Cells as an Alternative Approach.International journal of molecular sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Poor prognosis in pancreatic cancer (PanCa) is partially due to chemoresistance to gemcitabine (GEM). Glucose metabolism has been revealed to contribute to the therapeutic resistance and pluripotent state of PanCa cells. However, few studies have focused on the effects of GEM on cancer cell metabolism, stemness of tumor cells, and molecular mechanisms that critically influence PanCa treatment. We demonstrate that GEM treatment induces metabolic reprogramming, reducing mitochondrial oxidation and upregulating aerobic glycolysis, and promotes stem-like behaviors in cancer cells. Inhibiting aerobic glycolysis suppresses cancer cell stemness and strengthens GEM's cytotoxicity. GEM-induced metabolic reprogramming is
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.