ArticleMolecules and cells2014
Comparative proteomic profiling of pancreatic ductal adenocarcinoma cell lines.
Article in Molecules and cells, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 50 citations in OpenAlex.
- Characterization of carcinogenesis resistance in Anatolian blind mole-rat mesenchymal stem cells and assessment of transcriptomic signatures.Stem cells (Dayton, Ohio) · 2026Article
- Article
- Co-treatment of ticagrelor and anti-PD-1 immunotherapy in tumor-associated macrophages reduces pancreatic cancer cell growth and migration through the TGF-β1/Smad2 pathway.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
- Simulating tumor complexity: 3D pancreatic tumor spheroid model for improved drug screening.Human cell · 2025Article
- Proteomics in pancreatic cancer.Biomarker research · 2025Review
- Mapping Tumor-Stroma-ECM Interactions in Spatially Advanced 3D Models of Pancreatic Cancer.ACS applied materials & interfaces · 2025Article
- Integrative single-cell RNA sequencing and bulk RNA sequencing reveals the characteristics of glutathione metabolism and protective role of GSTA4 gene in pancreatic cancer.Frontiers in immunology · 2025Article
- Metabolomic Approach to Identify Potential Biomarkers in KRAS-Mutant Pancreatic Cancer Cells.Biomedicines · 2024Article
- Novel Pt (II) Complexes With Anticancer Activity Against Pancreatic Ductal Adenocarcinoma Cells.Bioinorganic chemistry and applications · 2024Article
- Proteomics-Driven Biomarkers in Pancreatic Cancer.Proteomes · 2023Review
- Systemic deuteration of SCID mice using the water-isotopologue deuterium oxide (DMolecular carcinogenesis · 2023Article
- Counteracting gemcitabine+nab-paclitaxel induced dysbiosis in KRAS wild type and KRASCell death discovery · 2023Article
- FOLFIRINOX Pharmacodynamic Interactions in 2D and 3D Pancreatic Cancer Cell Cultures.The AAPS journal · 2022Article
- Transcriptomics and Metabolomics Analysis of the Ovaries of High and Low Egg Production Chickens.Animals : an open access journal from MDPI · 2022Article
- Cancer Associated Fibroblast (CAF) Regulation of PDAC Parenchymal (CPC) and CSC Phenotypes Is Modulated by ECM Composition.Cancers · 2022Article
- Article
- Article
- Article
- Role of epithelial-mesenchymal transition in chemoresistance in pancreatic ductal adenocarcinoma.World journal of clinical cases · 2021Review
- Mechanistic Actions betweenMolecules (Basel, Switzerland) · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic cancer is one of the most fatal cancers and is associated with limited diagnostic and therapeutic modalities. Currently, gemcitabine is the only effective drug and represents the preferred first-line treatment for chemotherapy. However, a high level of intrinsic or acquired resistance of pancreatic cancer to gemcitabine can contribute to the failure of gemcitabine treatment. To investigate the underlying molecular mechanisms for gemcitabine resistance in pancreatic cancer, we performed label-free quantification of protein expression in intrinsic gemcitabine-resistant and - sensitive human pancreatic adenocarcinoma cell lines using our improved proteomic strategy, combined with filter-aided sample preparation, single-shot liquid chromatography-mass spectrometry, enhanced spectral counting, and a statistical method based on a power law global error model. We identified 1931 proteins and quantified 787 differentially expressed proteins in the BxPC3, PANC-1, and HPDE cell lines. Bioinformatics analysis identified 15 epithelial to mesenchymal transition (EMT) markers and 13 EMT-related proteins that were closely associated with drug resistance were differentially expressed. Interestingly, 8 of these proteins were involved in glutathione and cysteine/methionine metabolism. These results suggest that proteins related to the EMT and glutathione metabolism play important roles in the development of intrinsic gemcitabine resistance by pancreatic cancer cell lines.
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.