ReviewBMB reports2019
Cellular senescence: a promising strategy for cancer therapy.
Review in BMB reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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
68 citing papers in PubMed, 114 citations in OpenAlex.
- Integrated profiling identifies NCOA3 as a prognostic factor in patients with glioma.Functional & integrative genomics · 2026Article
- Protodioscin enhances Methotrexate-induced senescence and senolytic activity in HepG2 liver cancer spheroids by modulating cell cycle regulators and the TGF-β/p-Smad2-4 signaling pathway.Scientific reports · 2025Article
- Cellular senescence in cancer: Unveiling dual roles, tumor microenvironment dynamics and therapeutic innovations (Review).Oncology letters · 2025Review
- Single-Cell Fluorescence Imaging Reveals Heterogeneity in Senescence Biomarkers and Identifies Rapamycin-Responsive Sub-Populations.Aging cell · 2025Article
- Establishment of a chemoresistant laryngeal cancer cell model to study chemoresistance and chemosensitization responses via transcriptomic analysis and a tumor-on-a-chip platform.Bioengineering & translational medicine · 2025Article
- c-Myc inhibition and p21 modulation contribute to unsymmetrical bisacridines-induced apoptosis and senescence in pancreatic cancer cells.Pharmacological reports : PR · 2025Article
- The Common Hallmarks and Interconnected Pathways of Aging, Circadian Rhythms, and Cancer: Implications for Therapeutic Strategies.Research (Washington, D.C.) · 2025Review
- Functional circuits of LYL1 controlled by supraphysiological androgen in prostate cancer cells to regulate cell senescence.Cell communication and signaling : CCS · 2024Article
- Methods to Investigate the Secretome of Senescent Cells.Methods and protocols · 2024Review
- A review for the impacts of circadian disturbance on urological cancers.Sleep and biological rhythms · 2024Review
- LncRNA PCAT6 is a predictor of poor prognosis of colorectal cancer.Journal of gastrointestinal oncology · 2024Article
- The multifaceted role of Fragile X-Related Protein 1 (FXR1) in cellular processes: an updated review on cancer and clinical applications.Cell death & disease · 2024Review
- Article
- Therapy-induced senescent tumor cells in cancer relapse.Journal of the National Cancer Center · 2023Review
- YPEL3 expression induces cellular senescence via the Hippo signaling pathway in human breast cancer cells.Toxicological research · 2023Article
- Inhibition of protein kinase C delta leads to cellular senescence to induce anti-tumor effects in colorectal cancer.Cancer science · 2023Article
- Metabolic Flux Analysis Reveals the Roles of Stearate and Oleate on CPT1C-mediated Tumor Cell Senescence.International journal of biological sciences · 2023Article
- A predictive molecular signature consisting of lncRNAs associated with cellular senescence for the prognosis of lung adenocarcinoma.PloS one · 2023Article
- Basic and translational research on carbon-ion radiobiology.American journal of cancer research · 2023Review
- Protective roles of cytoplasmic p21Cell proliferation · 2022Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence, a permanent state of cell cycle arrest, is believed to have originally evolved to limit the proliferation of old or damaged cells. However, it has been recently shown that cellular senescence is a physiological and pathological program contributing to embryogenesis, immune response, and wound repair, as well as aging and age-related diseases. Unlike replicative senescence associated with telomere attrition, premature senescence rapidly occurs in response to various intrinsic and extrinsic insults. Thus, cellular senescence has also been considered suppressive mechanism of tumorigenesis. Current studies have revealed that therapy-induced senescence (TIS), a type of senescence caused by traditional cancer therapy, could play a critical role in cancer treatment. In this review, we outline the key features and the molecular pathways of cellular senescence. Better understanding of cellular senescence will provide insights into the development of powerful strategies to control cellular senescence for therapeutic benefit. Lastly, we discuss existing strategies for the induction of cancer cell senescence to improve efficacy of anticancer therapy. [BMB Reports 2019; 52(1): 35-41].
Indexed as
Identifiers
30526771PMC6386234W2913103261What 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.