ReviewFrontiers in oncology2019
Pancreatic Cancer Heterogeneity Can Be Explained Beyond the Genome.
Review in Frontiers in oncology, 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
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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.
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Who cites it
45 citing papers in PubMed.
- Dual-Targeting iRGD-Functionalized Pentablock Copolymer Nanosystem for miR-345-5p and Gemcitabine Delivery to Pancreatic Tumors.ACS applied materials & interfaces · 2026Article
- Single-cell transcriptomic profiling of patient-derived pancreatic ductal adenocarcinoma primary cell cultures.Scientific data · 2026Article
- Comparative Proteomic Profiling of Responses to Standard Systemic Treatment Regimens in Pancreatic Cancer.Cells · 2026Article
- Informed spatially aware patterns for multiplexed immunofluorescence data.Scientific reports · 2026Article
- Transmission electron microscopic analysis of pancreatic ductal adenocarcinoma cell spheres formed in 3D cultures.Medical molecular morphology · 2025Article
- Patient-derived tumor organoids highlight the potential of precision medicine in managing pancreatic ductal adenocarcinoma.International journal of cancer · 2025Article
- Gemcitabine-Lipid Conjugate and ONC201 Combination Therapy Effectively Treats Orthotopic Pancreatic Tumor-Bearing Mice.ACS applied materials & interfaces · 2024Article
- ITIH5 as a multifaceted player in pancreatic cancer suppression, impairing tyrosine kinase signaling, cell adhesion and migration.Molecular oncology · 2024Article
- Unveiling the Molecular Landscape of Pancreatic Ductal Adenocarcinoma: Insights into the Role of the COMPASS-like Complex.International journal of molecular sciences · 2024Review
- Smart exosomes enhance PDAC targeted therapy.Journal of controlled release : official journal of the Controlled Release Society · 2024Article
- Epigenetic priming targets tumor heterogeneity to shift transcriptomic phenotype of pancreatic ductal adenocarcinoma towards a Vitamin D susceptible state.Cell death & disease · 2024Article
- From Machine Learning to Patient Outcomes: A Comprehensive Review of AI in Pancreatic Cancer.Diagnostics (Basel, Switzerland) · 2024Review
- Combating PDAC Drug Resistance: The Role of Ref-1 Inhibitors in Accelerating Progress in Pancreatic Cancer Research.Journal of cellular signaling · 2024Article
- The value of a metabolic and immune-related gene signature and adjuvant therapeutic response in pancreatic cancer.Frontiers in genetics · 2024Article
- KMT2D links TGF-β signaling to noncanonical activin pathway and regulates pancreatic cancer cell plasticity.International journal of cancer · 2023Article
- Integrated analysis revealed hypoxia signatures and LDHA related to tumor cell dedifferentiation and unfavorable prognosis in pancreatic adenocarcinoma: Hypoxia in PDAC.Translational oncology · 2023Article
- Review
- Article
- Spatial Alignment of Organoids Tracking Subclonal Chemotherapy Resistance in Pancreatic and Ampullary Cancer.Bioengineering (Basel, Switzerland) · 2023Article
- The roles of intratumour heterogeneity in the biology and treatment of pancreatic ductal adenocarcinoma.Oncogene · 2022Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) remains a major health problem because it induces almost systematic mortality. Carcinogenesis begins with genetic aberrations which trigger epigenetic modifications. While genetic mutations initiate tumorigenesis, they are unable to explain the vast heterogeneity observed among PDAC patients. Instead, epigenetic changes drive transcriptomic alterations that can regulate the malignant phenotype. The contribution of factors from the environment and tumor microenvironment defines different epigenetic landscapes that outline two clinical subtypes: basal, with the worst prognosis, and classical. The epigenetic nature of PDAC, as a reversible phenomenon, encouraged several studies to test epidrugs. However, these drugs lack specificity and although there are epigenetic patterns shared by all PDAC tumors, there are others that are specific to each subtype. Molecular characterization of the epigenetic mechanisms underlying PDAC heterogeneity could be an invaluable tool to predict personalized therapies, stratify patients and search for novel therapies with more specific phenotype-based targets. Novel therapeutic strategies using current anticancer compounds or existing drugs used in other pathologies, alone or in combination, could be used to kill tumor cells or convert aggressive tumors into a more benign phenotype.
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Registered trials
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