ArticleCancer research and treatment2009
Significance of cellular senescence in aging and cancer.
Article in Cancer research and treatment, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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.
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Who cites it
24 citing papers in PubMed, 50 citations in OpenAlex.
- Pre-Encoded IFN-I Sensitivity Exacerbates Memory T Cell Senescence in Solid Tumors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Development and validation of a nomogram for predicting distant metastasis and prognosis in elderly T1-T2 pancreatic ductal adenocarcinoma patients.Discover oncology · 2026Article
- Evolutionary perspectives on endometrial cancer: antagonistic pleiotropy.Molecular & cellular oncology · 2026Review
- RNA binding proteins (RBPs) on genetic stability and diseases.Global medical genetics · 2025Review
- Mitochondrial dysfunction in age-related sarcopenia: mechanistic insights, diagnostic advances, and therapeutic prospects.Frontiers in cell and developmental biology · 2025Review
- Immunotherapy: should we worry about immunosenescence?Ageing and cancer research & treatment · 2024Article
- DLL3 Is a Prognostic and Potentially Predictive Biomarker for Immunotherapy Linked to PD/PD-L Axis and NOTCH1 in Pancreatic Cancer.Biomedicines · 2023Article
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- Review
- Review
- The self-organization model reveals systematic characteristics of aging.Theoretical biology & medical modelling · 2020Article
- Atorvastatin-induced senescence of hepatocellular carcinoma is mediated by downregulation of hTERT through the suppression of the IL-6/STAT3 pathway.Cell death discovery · 2020Article
- Induction of ROS and DNA damage-dependent senescence by icaritin contributes to its antitumor activity in hepatocellular carcinoma cells.Pharmaceutical biology · 2019Article
- The OncoAge Consortium: Linking Aging and Oncology from Bench to Bedside and Back Again.Cancers · 2019Article
- Integrative analysis of methylation and transcriptional profiles to predict aging and construct aging specific cross-tissue networks.BMC systems biology · 2016Article
- Cristacarpin promotes ER stress-mediated ROS generation leading to premature senescence by activation of p21(waf-1).Age (Dordrecht, Netherlands) · 2016Article
- Protein carbamylation is a hallmark of aging.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Management of pancreatic cancer in the elderly.World journal of gastroenterology · 2016Review
- Sensitization of U937 leukemia cells to doxorubicin by the MG132 proteasome inhibitor induces an increase in apoptosis by suppressing NF-kappa B and mitochondrial membrane potential loss.Cancer cell international · 2014Article
- Genome-wide transcriptional reorganization associated with senescence-to-immortality switch during human hepatocellular carcinogenesis.PloS one · 2013Article
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 is a mechanism that induces an irreversible growth arrest in all somatic cells. Senescent cells are metabolically active but lack the capacity to replicate. Evolutionary theories suggest that cellular senescence is related to the organismal decline occurring in aging organisms. Also, such theories describe senescence as an antagonistically pleiotropic process that can have beneficial or detrimental effect on the organism. Cellular senescence is believed to be involved in the cellular changes observed as aging progresses. Accumulation of senescent cells appears to occur widely as the organism ages. Furthermore, senescence is a key element of the tumor suppressor pathways. Therefore, it is part of the natural barrier against the uncontrolled proliferation observed in cellular development of malignancies in multicellular organisms. Activation of the senescence process guarantees a limited number of cellular replications. The genetic network led by p53 is responsible for activation of senescence in response to DNA damage and genomic instability that could lead to cancer. A better comprehension of the genetic networks that control the cell cycle and induce senescence is important to analyze the association of senescence to longevity and diseases related to aging. For these reasons, experimental research both in vitro and in vivo aims to develop anticancer therapies based on senescence activation. The last decade of research on role and function of senescence in aging and cancer are discussed in this paper.
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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.