ArticleGut2022
Senolytic elimination of Cox2-expressing senescent cells inhibits the growth of premalignant pancreatic lesions.
Article in Gut, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.
- Comprehensive analysis of regulated cell death pathways: intrinsic disorder, protein-protein interactions, and cross-pathway communication.Apoptosis : an international journal on programmed cell death · 2025Pooled it
- Epigenetic dynamics of cellular senescence: From mechanistic insights to precision senotherapy.Chinese medical journal · 2026Review
- Dissecting oral premalignant carcinogenesis: spatial omics mechanisms and nanomedicine-driven therapeutic innovation.Molecular cancer · 2026Review
- Extracellular vesicles from chemotherapy-induced senescent tumor cells reprogram hepatic phospholipid metabolism to promote pancreatic cancer liver metastasis.Journal of experimental & clinical cancer research : CR · 2026Article
- Spliceosome induction is a druggable dependency of RAS-driven senescence and cancer.Nature communications · 2026Article
- Signaling pathways and targeted interventions for precancers.Signal transduction and targeted therapy · 2026Review
- The Implications of Radiotherapy-Induced Cellular Senescence for Cancer Treatment and Tumor Microenvironment Modulation.International journal of biological sciences · 2026Review
- Senescent macrophages in tumor: phenotypes, roles, and interventions.Cell death & disease · 2025Review
- Stromal senescence contributes to age-related increases in cancer.Nature reviews. Cancer · 2025Review
- CD4 T cells acquire Eomesodermin to modulate cellular senescence and aging.Nature aging · 2025Article
- Senescent Microglia Mediate Neuroinflammation-Induced Cognitive Dysfunction by Selective Elimination of Excitatory Synapses in the Hippocampal CA1.Aging cell · 2025Article
- The rise of RAS: how gradual oncogene activation shapes the OIS spectrum.Genes & development · 2025Review
- Senescence-associated lysosomal dysfunction impairs cystine deprivation-induced lipid peroxidation and ferroptosis.Nature communications · 2025Article
- Mesothelin-Associated Anti-Senescence Through P53 in Pancreatic Ductal Adenocarcinoma.Cancers · 2025Article
- Targeting Senescence: A Review of Senolytics and Senomorphics in Anti-Aging Interventions.Biomolecules · 2025Review
- Oncogene-Induced Senescence Transcriptomes Signify Premalignant Colorectal Adenomas.Current issues in molecular biology · 2025Article
- The complex interplay between aging and cancer.Nature aging · 2025Review
- A BCL-xL/BCL-2 PROTAC effectively clears senescent cells in the liver and reduces MASH-driven hepatocellular carcinoma in mice.Nature aging · 2025Article
- Immune therapeutic strategies for the senescent tumor microenvironment.British journal of cancer · 2025Review
- Resolution of oncogene-induced senescence markers in HPV-infected cervical cancer tissue.BMC cancer · 2025Article
Corrections and comments
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Authors and funding
24 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveCellular senescence limits tumourigenesis by blocking the proliferation of premalignant cells. Additionally, however, senescent cells can exert paracrine effects influencing tumour growth. Senescent cells are present in premalignant pancreatic intraepithelial neoplasia (PanIN) lesions, yet their effects on the disease are poorly characterised. It is currently unknown whether senolytic drugs, aimed at eliminating senescent cells from lesions, could be beneficial in blocking tumour development.
designTo uncover the functions of senescent cells and their potential contribution to early pancreatic tumourigenesis, we isolated and characterised senescent cells from PanINs formed in a Kras-driven mouse model, and tested the consequences of their targeted elimination through senolytic treatment.
resultsWe found that senescent PanIN cells exert a tumour-promoting effect through expression of a proinflammatory signature that includes high Cox2 levels. Senolytic treatment with the Bcl2-family inhibitor ABT-737 eliminated Cox2-expressing senescent cells, and an intermittent short-duration treatment course dramatically reduced PanIN development and progression to pancreatic ductal adenocarcinoma.
conclusionsThese findings reveal that senescent PanIN cells support tumour growth and progression, and provide a first indication that elimination of senescent cells may be effective as preventive therapy for the progression of precancerous lesions.
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Registered trials
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