ReviewInternational journal of molecular sciences2021
Pancreatic Cancer and Cellular Senescence: Tumor Microenvironment under the Spotlight.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 56 citations in OpenAlex.
- Chemotherapy-induced senescence promotes stroma stiffness and antioxidant adaptation to promote chemoresistance in pancreatic ductal adenocarcinoma.Nature communications · 2026Article
- The mediating role of biological age acceleration in the associations between lifestyle factors and incident digestive system cancers: A Prospective Cohort Study from the UK Biobank.The journal of nutrition, health & aging · 2026Article
- Pancreatic ductal adenocarcinoma: integrating molecular insights for targeted interventions.Signal transduction and targeted therapy · 2026Review
- Loop of N2-polarized neutrophils and exhausted CD8 + T cells induces immunotherapy resistance in NSCLC.Molecular and cellular biochemistry · 2026Article
- USP7 Stabilizes MESP1 To Promote the Malignant Progression of Non-Small Cell Lung Cancer.Applied biochemistry and biotechnology · 2026Article
- Cellular Senescence as a Risk Factor in Head and Neck Cancer-Diagnostic and Therapeutic Perspective.Cancers · 2025Review
- PRRX2 Regulates GLI2 to Promote Proliferation, Invasion, and Metastasis by Inhibiting Senescence via Hedgehog Signaling.Cancer science · 2025Article
- Sciellin inhibits senescence and promotes pancreatic cancer progress by activating the notch signaling pathway.Scientific reports · 2025Article
- Berberine Derivative B68 Promotes Tumor Immune Clearance by Dual-Targeting BMI1 for Senescence Induction and CSN5 for PD-L1 Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- c-Myc inhibition and p21 modulation contribute to unsymmetrical bisacridines-induced apoptosis and senescence in pancreatic cancer cells.Pharmacological reports : PR · 2025Article
- Revealing the role of cancer-associated fibroblast senescence in prognosis and immune landscape in pancreatic cancer.iScience · 2025Article
- Growth Hormone Receptor Antagonist Markedly Improves Gemcitabine Response in a Mouse Xenograft Model of Human Pancreatic Cancer.International journal of molecular sciences · 2024Article
- Review
- Mitochondrial energy metabolism-related gene signature as a prognostic indicator for pancreatic adenocarcinoma.Frontiers in pharmacology · 2024Article
- Pancreatic cancer tumor microenvironment is a major therapeutic barrier and target.Frontiers in immunology · 2024Review
- CXCL5 Promotes the Malignant Phenotype of Pancreatic Cancer and Is Associated With Immune Infiltration.Clinical Medicine Insights. Oncology · 2024Article
- Pancreatic index: A prognostic factor of upfront surgery for body or tail pancreatic ductal adenocarcinoma with vascular involvement-A retrospective study.Cancer medicine · 2023Article
- Detection of HHV-6 Virus in specimen of a ductal pancreatic adenocarcinoma with comparison in tumor and normal tissue.Diagnostic pathology · 2023Article
- Advanced glycation end product (AGE) targeting antibody SIWA318H is efficacious in preclinical models for pancreatic cancer.Scientific reports · 2023Article
- Senescence program and its reprogramming in pancreatic premalignancy.Cell death & disease · 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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) has one of the most dismal prognoses of all cancers due to its late manifestation and resistance to current therapies. Accumulating evidence has suggested that the malignant behavior of this cancer is mainly influenced by the associated strongly immunosuppressive, desmoplastic microenvironment and by the relatively low mutational burden. PDAC develops and progresses through a multi-step process. Early in tumorigenesis, cancer cells must evade the effects of cellular senescence, which slows proliferation and promotes the immune-mediated elimination of pre-malignant cells. The role of senescence as a tumor suppressor has been well-established; however, recent evidence has revealed novel pro-tumorigenic paracrine functions of senescent cells towards their microenvironment. Understanding the interactions between tumors and their microenvironment is a growing research field, with evidence having been provided that non-tumoral cells composing the tumor microenvironment (TME) influence tumor proliferation, metabolism, cell death, and therapeutic resistance. Simultaneously, cancer cells shape a tumor-supportive and immunosuppressive environment, influencing both non-tumoral neighboring and distant cells. The overall intention of this review is to provide an overview of the interplay that occurs between senescent and non-senescent cell types and to describe how such interplay may have an impact on PDAC progression. Specifically, the effects and the molecular changes occurring in non-cancerous cells during senescence, and how these may contribute to a tumor-permissive microenvironment, will be discussed. Finally, senescence targeting strategies will be briefly introduced, highlighting their potential in the treatment of PDAC.
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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.