ReviewSignal transduction and targeted therapy2026
Pancreatic cancer: molecular pathogenesis and emerging therapeutic strategies.
Review in Signal transduction and targeted therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
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Who cites it
21 citing papers in PubMed.
- Expanding Synthetic Lethality in DNA Damage Response-Defective Cancers Through Stress Phenotype-Guided Kinase Targeting.International journal of molecular sciences · 2026Review
- Decoding neuro-tumor interactions in pancreatic cancer: mechanisms, immunosuppressive networks and therapeutic opportunities.Molecular biomedicine · 2026Review
- Revisiting tumor immunogenicity through the lens of mutant p53: Implications for cancer immunotherapy.Apoptosis : an international journal on programmed cell death · 2026Review
- Hypoxia Differentially Regulates Ferroptosis Sensitivity and Tumor Cell-Intrinsic Type I Interferon Signaling in Pancreatic Ductal Adenocarcinoma Cells.International journal of molecular sciences · 2026Article
- The Role of AP-1 in Cancer: Regulation, Tumor Microenvironment and Therapeutic Targeting.Biomolecules · 2026Review
- Pseudouridine synthase 7 as a context-specific therapeutic target in cancer.The Journal of pharmacology and experimental therapeutics · 2026Review
- The non-bacterial oncobiome: the role of the mycobiome and virome in tumor plasticity.Journal of the Egyptian National Cancer Institute · 2026Review
- Peptides as integrative modulators for clinical prognosis and targeted therapy in pancreatic cancer.Discover oncology · 2026Review
- UBA6 serves as a prognostic biomarker and promotes tumor progression in pancreatic ductal adenocarcinoma.Translational cancer research · 2026Article
- Explainable multi-omics modeling for risk stratification in pancreatic ductal adenocarcinoma.Gland surgery · 2026Article
- The Role of FOSL1 in Inflammatory Bowel Disease (IBD) Pathogenesis and IBD-Associated Tumorigenesis.Biomolecules · 2026Review
- Review
- Stress adaptation pathways and HA-CD44 signaling maintain the survival of pancreatic cancer cells with centrosome amplification.Cell communication and signaling : CCS · 2026Article
- Metabolic plasticity in pancreatic ductal adenocarcinoma progression and response to treatment.Molecular cancer · 2026Review
- Spatially-resolved subtype progression reveals metabolic vulnerabilities in pancreatic ductal adenocarcinoma.Molecular cancer · 2026Article
- Detection of plasma EV-associated TRAIL by nanoscale flow cytometry for liver metastasis prediction in PDAC.Advanced biotechnology · 2026Article
- Role of cancer-associated fibroblast-derived exosomes in pancreatic cancer: clinical therapeutic potential and targeting challenges.Frontiers in immunology · 2026Review
- Glycolysis and T cell-associated gene signature predicts prognosis and therapeutic responses in pancreatic cancer.Frontiers in immunology · 2026Article
- RAS signaling and remodeling of the immune microenvironment in pancreatic ductal adenocarcinoma: implications of emerging RAS-targeted therapy.Frontiers in cell and developmental biology · 2026Review
- Limited benefits of neoadjuvant therapy on R0 resection rate and overall survival in patients with resectable or locally advanced PDAC in randomized controlled trials.Frontiers in medicine · 2026Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease for which there is no effective treatment. A deep understanding of the mechanisms underlying the molecular pathogenesis, signaling pathways and risk factors leading to PDAC is of paramount importance for identifying novel targets, prognostic markers, preventive strategies, and signature markers for use in specific and personalized therapeutic procedures. Activating somatic mutations in the KRAS oncogene play a critical role in PDAC initiation and maintenance. Here, we highlight the complex interplay between KRAS signaling, the transcriptional coactivator YES1-associated protein (YAP) and Src family kinases (SFKs) in the pathogenesis of PDAC and drug sensitivity. We subsequently focused on diet-induced obesity, which has been correlated with an increased risk for developing PDAC in humans and mice and more severe clinical outcomes. Accumulating evidence also indicates that neural signals regulate critical functions of cancer cells, including their proliferation and dissemination, and that chronic stress promotes PDAC through the sympathetic nervous system via β-adrenergic receptors expressed by PDAC cells and other cells in the tumor microenvironment. Obesogenic mediators and stress neurotransmitters stimulate protein kinases, including PKA and PKD, which converge on CREB/ATF1 phosphorylation in PDAC cells. Since stress and obesity cooperate to promote the progression of PDAC, novel combinatorial strategies to prevent this devastating disease could be developed, repositioning FDA-approved drugs that are extensively used to treat cardiovascular and metabolic disorders and diseases. Finally, we review new advances in the treatment of PDAC, focusing on the discovery of novel drugs that directly inhibit KRAS and YAP function.
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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.