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Senescence in tumours: evidence from mice and humans
Open accessAbstract
The importance of cellular senescence, which is a stress response that stably blocks proliferation, is increasingly being recognized. Senescence is prevalent in pre-malignant tumours, and progression to malignancy requires evading senescence. Malignant tumours, however, may still undergo senescence owing to interventions that restore tumour suppressor function or inactivate oncogenes. Senescent tumour cells can be cleared by immune cells, which may result in efficient tumour regression. Standard chemotherapy also has the potential to induce senescence, which may partly underlie its therapeutic activity. Although these concepts are well supported in mouse models, translating them to clinical oncology remains a challenge.
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“There is little doubt that the senescence growth arrest suppresses the development of cancer (8, 48, 136).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [136]
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In the citing paper
“Other senescence markers have been shown to be overexpressed or activated in cancer152.”
From Guidelines for minimal information on cellular senescence experimentation in vivo (2024) · cites this paper as [152]
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In the citing paper
“Whatever the case, the examples above, and a growing list of similar studies (Collado and Serrano, 2010), argue that cellular senescence restrains cancer by imposing a cell-autonomous block to the proliferation of oncogenically damaged/stressed cells (Fig. 2).”
From Four faces of cellular senescence (2011) · cites this paper as Collado and Serrano, 2010
In the citing paper
“A SASP profile can be further determined by the activation of molecular cascades linked to p53/p21 (due to persistent double strands breaks/telomere shortening)”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [24]
In the citing paper
“but also to p16/Rb (due to epigenetic modifications) [3,22,24,25,26]”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [24]
In the citing paper
“It is believed that senescence is a key mechanism by which p53 suppresses tumorigenesis (Braig and Schmitt, 2006; Collado and Serrano, 2010).”
From p53-dependent chemokine production by senescent tumor cells supports NKG2D-dependent tumor elimination by natural killer cells (2013) · cites this paper as Collado and Serrano, 2010
In the citing paper
“Therefore, it has been proposed that senescence escape is required for tumor progression to overt malignancy [18,21].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [21]
In the citing paper
“However, senescence has also been implicated both in promoting carcinogenesis 15 and in age-related pathologies 16,17 through its autocrine and paracrine effects, known as the senescence-associated secretory phenotype (SASP) originally described by the Campisi group.18,19”
From Senescence from G2 arrest, revisited (2015) · cites this paper as [15]
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“However, for a tumor as a cell community, the happening of tumor cell senescence may have controversial effects on tumor development (Collado and Serrano, 2010).”
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BackgroundRamotar, D., & Nepveu, A. (2018) · Journal of Radiation and Cancer Research · doi:10.4103/jrcr.jrcr_8_18 · Cited by 4
Słotwiński, R., Lech, G., & Słotwińska, S. M. (2021) · Central European Journal of Immunology · doi:10.5114/ceji.2021.107027 · Cited by 4
“Senescence has been proposed to be an important tumor-suppressive mechanism [63, 64] and a selective fibroblast growth factor receptor 4 (FGFR4) inhibitor (BLU9931) reduced PDAC cell proliferation and invasion while promoting their senescence [65].”
BackgroundLiu, L., Luo, X., YU, H.-M., Feng, Y., Ren, Y., Yin, Y.-F., Shang, H., & He, Z. (2015) · Molecular Medicine Reports · doi:10.3892/mmr.2015.4412 · Cited by 4
“Studies have demonstrated that various forms of oxidative stress can induce senescence, including exposure to reactive oxygen species (45-47).”
Cellular Senescence and Stem Cell Niche
Krause, A., Conboy, M. J., & Conboy, I. M. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-802734-9.00012-3 · Cited by 4
Yamaguchi, M., Kajiya, H., Egashira, R., Yasunaga, M., 萩尾, 佳., Sato, A., Toshimitsu, T., Naito, T., & Ohno, J. (2018) · Journal of Hard Tissue Biology · doi:10.2485/jhtb.27.199 · Cited by 5
Malumbres, M. (2014) · Elsevier eBooks · doi:10.1016/b978-1-4557-2865-7.00004-7 · Cited by 5
Autophagy in Cell Fate and Diseases
Grasso, D., Ropolo, A., & Vaccaro, M. I. (2015) · InTech eBooks · doi:10.5772/61553 · Cited by 6
“Then, the so-called oncogene-induced senescence is a potent tumor suppressor mechanism against cellular transformation [91-94] and it is the first option that cells have against oncogene activation.”
BackgroundCell Death Mechanisms of the Promising Anticancer Compound Gallotannin
Houssein, M., & Gali‐Muhtasib, H. U. (2019) · IntechOpen eBooks · doi:10.5772/intechopen.90187 · Cited by 4
“This senescence response was thought to have an antitumorigenic role in cancer-predisposed tissues [27].”
BackgroundCan hypoxic exercise retard cellular senescence? A narrative review
Huang, T., Tsang, C. S. L., & Huang, T. (2024) · European Review of Aging and Physical Activity · doi:10.1186/s11556-024-00352-9 · Cited by 3
Cellular Senescence in Cancer: Mechanisms, Roles in Tumor Progression, and Therapeutic Implications
Yan, J., Zhang, Y., Mao, G., Yu, J., Zhou, T., & Hao, J. (2025) · MedComm – Oncology · doi:10.1002/mog2.70029 · Cited by 3
Limitations of the p16-3MR mouse model for detecting and eliminating senescent cells
Hori, N., Kawamoto, S., Uemura, K., Kinugasa‐Katayama, Y., Okumura, Y., Tanaka, K., Park, J. H., Wakita, M., Motooka, D., Ohtani, N., et al. (2026) · EMBO Reports · doi:10.1038/s44319-026-00802-8 · Cited by 3
“Consequently, cellular senescence has long been regarded as an important tumor suppression mechanism (Campisi and d ’ Adda di Fagagna, 2007; Collado and Serrano, 2010; He and Sharpless, 2017).”
Moderate stem-cell telomere shortening rate postpones cancer onset in a stochastic model
Holbek, S., Bendtsen, K. M., & Juul, J. (2013) · Physical Review E · doi:10.1103/physreve.88.042706 · Cited by 3
Mishra, K., Puthli, A., & Tiwari, R. (2016) · Journal of Radiation and Cancer Research · doi:10.4103/jrcr.jrcr_7_17 · Cited by 3
Advancing Single-Cell Detection of Senescent Cells: Laboratory Methods and Clinical Applications
Lung, S. H., & Lung, T. (2025) · OBM Geriatrics · doi:10.21926/obm.geriatr.2502307 · Cited by 3
Zedoary Turmeric Oil Induces Senescence and Apoptosis in Human Colon Cancer HCT116 Cells
Su, M.-Q., Zhou, Y., Li, C., Wang, Z., Wang, Y.-L., Shen, B., & Dou, J. (2018) · Natural Product Communications · doi:10.1177/1934578x1801300731 · Cited by 3
“Senescence also presents in tumor cells[14], and the induction of tumor cell senescence benefits tumor suppression[15].”
BackgroundDevelopment of Water Melon (Citrullus vulgaris L.) Red Wine
DARMAN, D. R., Ngang, J. J. E., & Etoa, F. X. (2010) · Notulae Botanicae Horti Agrobotanici Cluj-Napoca · doi:10.15835/nbha3824818 · Cited by 3
“It has to be mentioned that the usual amount of Ginkgo-biloba used in human therapeutic (disorders of the senescence) is 3 to 6 ml /day (Collado and Serrano 2010; Vidal, 1998, David, 1995).”
Coates, P. J. (2013) · The Journal of Pathology · doi:10.1002/path.4182 · Cited by 3
Cancers in Children Ages 8 to 12 Are Injury-Related
Walen, K. H. (2015) · Journal of Cancer Therapy · doi:10.4236/jct.2015.62020 · Cited by 3
Oncogene‐induced cellular senescence elicits an anti‐ W arburg effect
Banks, R. E. (2013) · PROTEOMICS · doi:10.1002/pmic.201300335 · Cited by 3
“One that is now recognized is oncogene-induced senescence (OIS) where the initial proliferative burst seen after activation of oncogenes such as BRAF, HRAS, and KRAS is followed by a largely irreversible arrest of cell proliferation, essentially halting tumor progression [1, 2].”
Endometrial cellular senescence contributes to preterm birth
Hirota, Y. (2014) · Inflammation and Regeneration · doi:10.2492/inflammregen.34.064 · Cited by 3
Hua, D., Qi, S., Li, H., Zhang, Z., & Fu, L. (2012) · Journal of Biomedical Optics · doi:10.1117/1.jbo.17.6.066002 · Cited by 3
L’implantation trophoblastique, modèle de l’implantation tumorale et métastatique
Piechowski, J. (2015) · Bulletin du Cancer · doi:10.1016/j.bulcan.2015.06.003 · Cited by 3
Zelluläre Seneszenz im kolorektalen Karzinom
Foersch, S. (2017) · Der Pathologe · doi:10.1007/s00292-017-0357-y · Cited by 3
Quantitative Identification of Senescent Cells in Cancer
Biran, A., Porat, Z., & Krizhanovsky, V. (2018) · Methods in molecular biology · doi:10.1007/978-1-4939-8885-3_18 · Cited by 3
Quantification of beta-galactosidase activity as a marker of radiation-driven cellular senescence
Klapp, V., Bloy, N., Petroni, G., & Martino, M. D. (2022) · Methods in cell biology · doi:10.1016/bs.mcb.2022.10.001 · Cited by 3
A bibliometric study of the top 100 most cited papers on aging and cancer
Zhang, Y., Guo, Y., & Zhang, C. (2023) · Medicine · doi:10.1097/md.0000000000034428 · Cited by 3
“Checkpoint activation and stable cell cycle arrest serve as precise and powerful barriers to avoid cancer genesis.[16,17] Cellular senescence suppresses cancer by blocking cell division and arresting cell proliferation in response to oncogenic stimuli including genotoxic stress.”
BackgroundEpidemiology, Risk Factors, and Survival in CUP: Pointers to Disease Mechanisms
Hemminki, K. (2015) · Springer eBooks · doi:10.1007/978-3-319-22581-4_2 · Cited by 3
NUAK1 links genomic instability and senescence
Bernard, D., & Augert, A. (2010) · Aging · doi:10.18632/aging.100153 · Cited by 3
“With the development of adequate mouse models of cancer susceptibility and new tools to detect senescence in vivo, it has become possible do demonstrate its effectiveness in blocking malignant transformation [11].”
BackgroundTesei, A., Arienti, C., Bossi, G., Santi, S., Santis, I. D., Bevilacqua, A., Zanoni, M., Pignatta, S., Cortesi, M., Zamagni, A., et al. (2020) · Research Square · doi:10.21203/rs.3.rs-125316/v1 · Cited by 3
Silva‐Álvarez, S. D., & Collado, M. (2015) · Elsevier eBooks · doi:10.1016/b978-0-12-394447-4.30066-9 · Cited by 4
Self-citationSilva‐Álvarez, S. D., & Collado, M. (2022) · Elsevier eBooks · doi:10.1016/b978-0-12-821618-7.00219-4 · Cited by 3
Self-citationDelgado‐Calle, J., Adhikari, M., Kaur, J., Sabol, H. M., Anloague, A., Khan, S., Kurihara, N., Diaz‐delCastillo, M., Andreasen, C. M., Barnes, C. L., et al. (2024) · Research Square · doi:10.21203/rs.3.rs-4047486/v1 · Cited by 3
“The absence of an anti-tumor effect can be attributed to either the dose of senolytic therapy used in our studies or the inability of malignant tumors to undergo spontaneous senescence without external interventions such as chemotherapy or radiation therapy (53).”
BackgroundNew insights in cellular senescence: The pituitary model
Herbstein, F., Rosmino, J., Guitelman, M. A., Cagliero, J., Gonilski‐Pacin, D., del Giudice, N. C., Fiz, M., Fuertes, M., & ARZT, E. S. (2025) · Journal of Neuroendocrinology · doi:10.1111/jne.70008 · Cited by 3
“64 It exhibits the classical hallmarks of senescence, including the upregulation of cell cycle inhibitors such as p16 and p53, as well as persistent DNA damage that remains unresolved.”
Extracellular Vesicles in the Aging Male Reproductive System: Progresses and Perspectives
Li, W., Yu, Z., Xu, S., Zheng, L., & Xia, W. (2025) · Advances in experimental medicine and biology · doi:10.1007/978-3-031-82990-1_16 · Cited by 2
Makulyte, G., Safwan‐Zaiter, H., Goehrig, D., Huna, A., Mangelinck, A., Mikawa, T., Palazzo, A., Moudombi, L., Médard, J., Chanal, M., et al. (2025) · Aging Cell · doi:10.1111/acel.70307 · Cited by 2
“Cellular senescence acts as a fail-safe program in order to inhibit tumorigenesis by stopping the proliferation of damaged cells and by inducing their clearance through the SASP (Collado and Serrano 2010; Collado et al. 2005).”
Redox metabolism in cell senescence: focusing on contributions from the metabolomic field
Chacón, E., Grünwaldt, G., Marmisolle, I., Martínez, J., & Quijano, C. (2026) · Frontiers in Molecular Biosciences · doi:10.3389/fmolb.2025.1754469 · Cited by 2
c-Myc: Central regulator of autophagy and senescence in cancer
Ji, S., Sun, T., Zhang, Q., Wu, M., Cao, Y., Gao, R., Wang, L., Nicot, C., & Sethi, G. (2026) · Cancer Letters · doi:10.1016/j.canlet.2026.218315 · Cited by 2
Metadata
- Authors
- Collado, M., & Serrano, M.
- Affiliations
- Spanish National Cancer Research Centre (ES)
- Venue
- Nature Reviews Cancer
- Published
- 2010-01
- Volume
- 10
- Issue
- 1
- Pages
- 51-57
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- PMC
- PMC3672965
- OpenAlex
- W2087999409
- Cited by
- 1,124
- References
- 58
- Citations by year
- 2026: 34 · 2025: 40 · 2024: 56 · 2023: 73 · 2022: 60 · 2021: 64 · 2020: 47 · 2019: 67 · 2018: 66 · 2017: 66 · 2016: 73 · 2015: 81 · 2014: 104 · 2013: 102 · 2012: 82
- FWCI
- 6.97
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Cancer (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- oncogene-induced senescence, cellular senescence, tumor suppressor function, tumor regression, chemotherapy-induced senescence, senescence therapy, mouse tumor model
- MeSH terms
- Animals, Disease Models, Animal, Humans, Neoplasms, Cellular Senescence, Mice
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