ReviewMolecular cancer2025
The controversial role of senescence-associated secretory phenotype (SASP) in cancer therapy.
Review in Molecular cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed.
- Orthogonal Light- and Enzyme-Triggered and-Gate Prodrugs for Senolytic Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- MnOMaterials today. Bio · 2026Article
- Article
- Review
- DHCR24 promotes endometrial carcinoma progression and is associated with cellular senescence regulation.Medical oncology (Northwood, London, England) · 2026Article
- The Gut Microbiome as a Mechanistic Link Between the Planetary Health Diet and Healthy Aging.Nutrients · 2026Review
- Pharmacological targeting of the senescence-associated secretory phenotype in atherosclerosis: therapeutic potential of senolytics and senomorphics.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Article
- Cellular senescence and aging: molecular mechanisms and convergent pathways.Cellular and molecular life sciences : CMLS · 2026Review
- p16 Beyond Senescence: Cancer Biology Lessons Applied to Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Engineering Extracellular Vesicles for Anti-Aging Therapy: Mechanisms, Applications, and Perspectives.Aging cell · 2026Review
- Fate Bifurcation of Cellular Senescence: Dynamic Regulation from Tumor Suppression to Recurrence Risk.Cells · 2026Review
- The Aging Microenvironment Shapes Angiogenic Remodeling in IBD-Associated Colorectal Carcinogenesis.Aging cell · 2026Review
- TP53, HIF1A, and CDKN2A in Hepatocellular Carcinoma: Roles in Senescence, Ferroptosis, and Prognosis.Clinical and translational gastroenterology · 2026Article
- Regenerative Approaches to Enhance the Skin Microenvironment and Boost Aesthetic Efficacy: A Narrative Review.International journal of molecular sciences · 2026Review
- Exploring the prognostic role of senescence-related genes in gastric cancer through multi-omics integration and machine learning.Human genomics · 2026Article
- Article
- Osteocytes in the Metastatic Bone Niche: Mechanistic Pathways and Therapeutic Targets.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Exercise, Cellular Senescence, and Cancer: Novel Perspectives on Functional Aging Through Block Strength Training in Older Adults-A Narrative Review.Biomedicines · 2026Review
- Radiation-Induced Salivary Gland Fibrosis: Mechanisms, Emerging Therapies, and Gelatin-Based Bioengineered Models.Gels (Basel, Switzerland) · 2026Review
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.
Funding
Abstract
Cellular senescence, characterized by partially irreversible cell cycle arrest, has a dual role in cancer progression via the senescence-associated secretory phenotype (SASP). SASP encompasses a wide range of bioactive chemicals, including cytokines, chemokines, growth factors, and proteases, all of which can have a significant impact on the tumor microenvironment (TME). Initially, SASP can enhance tumor suppression by attracting immune cells and inhibiting cancer cell proliferation, but its long-term presence at TME can promote tumor growth, metastasis, and treatment resistance. Moreover, therapy-induced senescence, a common side effect of cancer treatments, can result in an increase of senescent cells and pro-tumorigenic SASP. Therefore, recent research has highlighted the potential of targeting SASP to improve cancer therapy. Among the therapeutic strategies, senolytic therapies selectively eliminate senescent cells, whereas senomorphic drugs decrease SASP without cytotoxicity, and there is also combined therapy targeting SASP for oncotherapy. Therefore, it is of crucial importance to develop more specific senotherapeutics and investigate the clinical applications of SASP modulation, such as using SASP components as biomarkers for therapy monitoring and personalized medicine. Taken together, understanding the molecular processes of SASP induction and their function in TME, including its heterogeneity across cell types and tissues, and designing personalized treatment are critical for optimizing cancer therapy and improving patient outcomes.
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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.