ReviewFrontiers in oncology2025
Senescence-associated secretory phenotype in lung cancer: remodeling the tumor microenvironment for metastasis and immune suppression.
Review in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 2 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Inflamed Yet Immune-Evasive? A Transcriptomic Meta-Analysis Identifies Conserved Inflammatory, Developmental, and Neuronal Signatures Associated with Polyploid Giant Cancer Cells.International journal of molecular sciences · 2026Pooled it
- Senogenic-senolytic treatment strategies enhance tumor control and can improve survival in murine cancer models: a systematic review.BMC cancer · 2026Pooled it
- Senescence-associated gene signatures predict survival in lung cancer: a multi-cohort analysis.GeroScience · 2026Article
- Breast cancer radiotherapy and the risk of lung injury: Advances and perspectives.Advances in radiotherapy & nuclear medicine · 2026Article
- Targeted therapies in lung cancer: personalizing treatment across the age spectrum.Frontiers in oncology · 2026Review
- Conquering aging-related immunosenescence and tumor immune escape.Frontiers in immunology · 2026Review
- Therapy-Induced Senescence (TIS) and SASP: The p53-Mediated Interplay in Cancer Progression and Treatment.International journal of molecular sciences · 2025Review
- The controversial role of senescence-associated secretory phenotype (SASP) in cancer therapy.Molecular cancer · 2025Review
- Reprogramming cellular senescence and aging clocks for advanced cancer immunotherapy.Molecular cancer · 2025Review
- Modulating senescence-associated secretory phenotype-driven paracrine effects to overcome therapy -induced senescence: senolytic effects of hesperidin and quercetin in A549 lung adenocarcinoma cells.Molecular biology reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence exerts dual roles in lung cancer pathogenesis: initially suppressing tumorigenesis via p53/p21/p16-mediated cell cycle arrest, but promoting malignancy through the senescence-associated secretory phenotype (SASP). SASP secretes cytokines, proteases, and growth factors, reshaping the tumor microenvironment (TME) to drive immune evasion, metastasis, and therapy resistance. NF-κB activation induces APOBEC3B mutagenesis and PD-L1 overexpression, while mTOR signaling enhances glycolysis and OXPHOS to fuel tumor growth. Clinically, telomere attrition, p16/p21 expression, and SASP components serve as prognostic biomarkers. Therapeutic strategies target senescent cells and SASP. Future directions focus on single-cell multi-omics to decode senescence heterogeneity, spatially controlled drug delivery, and therapies targeting senescence-immune-metabolic crosstalk. By unraveling senescence's dual regulatory mechanisms, this review highlights precision approaches to overcome resistance and improve lung cancer outcomes.
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Identifiers
What OpenQuestion holds
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.