ArticleCancer chemotherapy and pharmacology2013
Pharmacodynamic modeling of cell cycle and apoptotic effects of gemcitabine on pancreatic adenocarcinoma cells.
Article in Cancer chemotherapy and pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 73 citations in OpenAlex.
- Probabilistic modeling of cell cycle dynamics in response to cell cycle targeting chemotherapy drugs to guide treatment strategies.PLoS computational biology · 2025Article
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- Cytosolic Phospholipase A2 Determines Intercellular Heterogeneity of Stress Granules and Chemotherapy Response.Cancer discovery · 2025Article
- Curcumin Derivative CU4c Exhibits HDAC-Inhibitory and Anticancer Activities Against Human Lung Cancer Cells In Vitro and in Mouse Xenograft Models.Pharmaceuticals (Basel, Switzerland) · 2025Article
- A Rapid Approach for Identifying Cell Lines Lacking Functional Cytidine Deaminase.International journal of molecular sciences · 2025Article
- Design, Synthesis, and Antitumor Evaluation of an Opioid Growth Factor Bioconjugate Targeting Pancreatic Ductal Adenocarcinoma.Pharmaceutics · 2024Article
- A new technique for the analysis of metabolic pathways of cytidine analogues and cytidine deaminase activities in cells.Scientific reports · 2023Article
- circACTR2 attenuates gemcitabine chemoresiatance in pancreatic cancer through PTEN mediated PI3K/AKT signaling pathway.Biology direct · 2023Article
- Barriers and opportunities for gemcitabine in pancreatic cancer therapy.American journal of physiology. Cell physiology · 2023Review
- Review
- Circular RNA circ-MTHFD1L induces HR repair to promote gemcitabine resistance via the miR-615-3p/RPN6 axis in pancreatic ductal adenocarcinoma.Journal of experimental & clinical cancer research : CR · 2022Article
- Synergistic Pharmacodynamic Effects of Gemcitabine and Fibroblast Growth Factor Receptor Inhibitors on Pancreatic Cancer Cell Cycle Kinetics and Proliferation.The Journal of pharmacology and experimental therapeutics · 2021Article
- Improving Gemcitabine Sensitivity in Pancreatic Cancer Cells by Restoring miRNA-217 Levels.Biomolecules · 2021Article
- A quantitative systems pharmacological approach identified activation of JNK signaling pathway as a promising treatment strategy for refractory HER2 positive breast cancer.Journal of pharmacokinetics and pharmacodynamics · 2021Article
- MicroRNA-7 modulates cellular senescence to relieve gemcitabine resistance by targeting PARP1/NF-κB signaling in pancreatic cancer cells.Oncology letters · 2021Article
- Protopine/Gemcitabine Combination Induces Cytotoxic or Cytoprotective Effects in Cell Type-Specific and Dose-Dependent Manner on Human Cancer and Normal Cells.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Combination treatment of gemcitabine and sorafenib exerts a synergistic inhibitory effect on non-small cell lung cancerOncology letters · 2020Article
- Mechanistic Multiscale Pharmacokinetic Model for the Anticancer Drug 2',2'-difluorodeoxycytidine (Gemcitabine) in Pancreatic Cancer.Clinical and translational science · 2020Article
- Elaeocarpus reticulatus fruit extracts reduce viability and induce apoptosis in pancreatic cancer cells in vitro.Molecular biology reports · 2020Article
- A Severe Case of Drug-Induced Liver Injury after Gemcitabine Administration: A Highly Probable Causality Grading as Assessed by the Updated RUCAM Diagnostic Scoring System.Case reports in hepatology · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
purposeThe standard of care for treating patients with pancreatic adenocarcinomas includes gemcitabine (2',2'-difluorodeoxycytidine). Gemcitabine primarily elicits its response by stalling the DNA replication forks of cells in the S phase of the cell cycle. To provide a quantitative framework for characterizing the cell cycle and apoptotic effects of gemcitabine, we developed a pharmacodynamic model in which the activation of cell cycle checkpoints or cell death is dependent on gemcitabine exposure.
methodsThree pancreatic adenocarcinoma cell lines (AsPC-1, BxPC-3, and MiaPaca-2) were exposed to varying concentrations (0-100,000 ng/mL) of gemcitabine over a period of 96 h in order to quantify proliferation kinetics and cell distributions among the cell cycle phases. The model assumes that the drug can inhibit cycle-phase transitioning in each of the 3 phases (G1, S, and G2/M) and can cause apoptosis of cells in G1 and G2/M phases. Fitting was performed using the ADAPT5 program.
resultsThe time course of gemcitabine effects was well described by the model, and parameters were estimated with good precision. Model predictions and experimental data show that gemcitabine induces cell cycle arrest in the S phase at low concentrations, whereas higher concentrations induce arrest in all cell cycle phases. Furthermore, apoptotic effects of gemcitabine appear to be minimal and take place at later time points.
conclusionThe pharmacodynamic model developed provides a quantitative, mechanistic interpretation of gemcitabine efficacy in 3 pancreatic cancer cell lines, and provides useful insights for rational selection of chemotherapeutic agents for combination therapy.
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