ReviewCells2021
The Jekyll and Hyde of Cellular Senescence in Cancer.
Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed.
- The Relationship Between Immunogenic Cell Death and Cellular Senescence in Cancer Immunotherapy.Life (Basel, Switzerland) · 2026Review
- Terpenoids as modulators of autophagy-senescence crosstalk in lung cancer.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Review
- Review
- Cyclin-Dependent Kinases 4 and 6 Inhibitors: An Emerging Therapeutic Framework from Growth Suppression to Tumor Clearance.ACS pharmacology & translational science · 2026Review
- Multi-omics integration constructs a senescence-based prognostic model and identifies EIF4EBP1 as a therapeutic target in clear cell renal cell carcinoma.Discover oncology · 2026Article
- Decoding cancer dormancy: integrative genomic, phenotypic and live-cell imaging analysis to reveal the hidden cancer cell reservoir.Molecular cancer · 2025Review
- Oxidative Stress-Driven Cellular Senescence: Mechanistic Crosstalk and Therapeutic Horizons.Antioxidants (Basel, Switzerland) · 2025Review
- Unveiling the therapeutic potential of senescence-related IQGAP2 in pancreatic Cancer through post-GWAS genomic and scRNA-seq analyses.Discover oncology · 2025Article
- Tumor Immunosenescence Driven by Chronic Inflammation: Mechanisms, Microenvironment Remodeling and Therapeutic Strategies.Aging and disease · 2025Review
- Cellular senescence in the tumor with a bone niche microenvironment: friend or foe?Clinical and experimental medicine · 2025Review
- Resistance to spindle inhibitors in glioblastoma depends on STAT3 and therapy induced senescence.iScience · 2024Article
- Cellular senescence in Alzheimer's disease: from physiology to pathology.Translational neurodegeneration · 2024Review
- The Senolytic Effect of Indole-3-Carbinol (I3C) on Mouse Embryonic (MEF) and Human Fibroblast Cell Lines.International journal of molecular sciences · 2024Article
- Furan-rich, biobased transfection agents as potential oligomeric candidates for intracellular plasmid DNA delivery.RSC advances · 2024Article
- Targeting senescence-associated secretory phenotypes to remodel the tumour microenvironment and modulate tumour outcomes.Clinical and translational medicine · 2024Review
- Senescence Promotes the Recovery of Stemness among Cancer Cells via Reprograming.Biomolecules · 2024Review
- Hepatitis B virus X protein and TGF-β: partners in the carcinogenic journey of hepatocellular carcinoma.Frontiers in oncology · 2024Review
- MicroRNA miR-214-5p induces senescence of microvascular endothelial cells by targeting the JAG1/Notch signaling pathway.Non-coding RNA research · 2023Article
- Review
- Cellular senescence-related long noncoding ribonucleic acids: Predicting prognosis in hepatocellular carcinoma.Cancer reports (Hoboken, N.J.) · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Cellular senescence is a state of stable cell cycle arrest that can be triggered in response to various insults and is characterized by distinct morphological hallmarks, gene expression profiles, and the senescence-associated secretory phenotype (SASP). Importantly, cellular senescence is a key component of normal physiology with tumor suppressive functions. In the last few decades, novel cancer treatment strategies exploiting pro-senescence therapies have attracted considerable interest. Recent insight, however, suggests that therapy-induced senescence (TIS) elicits cell-autonomous and non-cell-autonomous implications that potentially entail detrimental consequences, reflecting the Jekyll and Hyde nature of cancer cell senescence. In essence, the undesirable manifestations that generally culminate in inflammation, cancer stemness, senescence reversal, therapy resistance, and disease recurrence are dictated by the persistent accumulation of senescent cells and the SASP. Thus, mitigating these pro-tumorigenic effects by eliminating these cells or inhibiting their SASP production holds great promise for developing innovative therapeutic strategies. In this review, we describe the fundamental aspects and dynamics of cancer cell senescence and summarize the comprehensive research on the adverse outcomes of TIS. Furthermore, we underline the rationale and motivation of emerging senotherapeutic modalities surrounding the removal of senescent cells and the SASP to help maximize the overall efficacy of cancer therapies.
Indexed as
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.