ArticleAge (Dordrecht, Netherlands)2014
A comparison of oncogene-induced senescence and replicative senescence: implications for tumor suppression and aging.
Article in Age (Dordrecht, Netherlands), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 49 citations in OpenAlex.
- Single-Cell Transcriptomic Profiling Reveals Superficial Zone Chondrocytes as a Catabolic and Senescent Focus in Osteoarthritis Cartilage.Cartilage · 2026Article
- Neuroendocrine-associated epigenetic factors in cellular senescence: mechanisms and therapeutic implications.Biogerontology · 2026Review
- Machine learning-based morphological quantification of replicative senescence in human fibroblasts.GeroScience · 2024Article
- Branched-Chain Amino Acid Accumulation Fuels the Senescence-Associated Secretory Phenotype.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Systematic transcriptomic analysis and temporal modelling of human fibroblast senescence.Frontiers in aging · 2024Article
- Aging microenvironment and antitumor immunity for geriatric oncology: the landscape and future implications.Journal of hematology & oncology · 2023Review
- Unveiling E2F4, TEAD1 and AP-1 as regulatory transcription factors of the replicative senescence program by multi-omics analysis.Protein & cell · 2022Article
- Nuclear morphology is a deep learning biomarker of cellular senescence.Nature aging · 2022Article
- Genome-nanosurface interaction of titania nanotube arrays: evaluation of telomere, telomerase and NF-κB activities on an epithelial cell model.RSC advances · 2022Article
- Radiation-Induced Senescence in p16+/LUC Mouse Lung Compared to Bone Marrow Multilineage Hematopoietic Progenitor Cells.Radiation research · 2021Article
- Possibility of inducing tumor cell senescence during therapy.Oncology letters · 2021Review
- Simple Detection Methods for Senescent Cells: Opportunities and Challenges.Frontiers in aging · 2021Review
- Normal Aging and Its Role in Cancer Metastasis.Cold Spring Harbor perspectives in medicine · 2020Review
- Review
- How the ageing microenvironment influences tumour progression.Nature reviews. Cancer · 2020Review
- Involvement of condensin in cellular senescence through gene regulation and compartmental reorganization.Nature communications · 2019Article
- mRNA methylation in cell senescence.Wiley interdisciplinary reviews. RNA · 2019Review
- Biological Hallmarks of Cancer in Alzheimer's Disease.Molecular neurobiology · 2019Review
- A prospect of cell immortalization combined with matrix microenvironmental optimization strategy for tissue engineering and regeneration.Cell & bioscience · 2019Review
- Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Cellular senescence is a stable proliferation arrest associated with an altered secretory pathway, the senescence-associated secretory phenotype. However, cellular senescence is initiated by diverse molecular triggers, such as activated oncogenes and shortened telomeres, and is associated with varied and complex physiological endpoints, such as tumor suppression and tissue aging. The extent to which distinct triggers activate divergent modes of senescence that might be associated with different physiological endpoints is largely unknown. To begin to address this, we performed gene expression profiling to compare the senescence programs associated with two different modes of senescence, oncogene-induced senescence (OIS) and replicative senescence (RS [in part caused by shortened telomeres]). While both OIS and RS are associated with many common changes in gene expression compared to control proliferating cells, they also exhibit substantial differences. These results are discussed in light of potential physiological consequences, tumor suppression and aging.
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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.