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Inside and out: the activities of senescence in cancer
Open accessAbstract
The core aspect of the senescent phenotype is a stable state of cell cycle arrest. However, this is a disguise that conceals a highly active metabolic cell state with diverse functionality. Both the cell-autonomous and the non-cell-autonomous activities of senescent cells create spatiotemporally dynamic and context-dependent tissue reactions. For example, the senescence-associated secretory phenotype (SASP) provokes not only tumour-suppressive but also tumour-promoting responses. Senescence is now increasingly considered to be an integrated and widespread component that is potentially important for tumour development, tumour suppression and the response to therapy.
Overview
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Written from the paper’s full text.
TL;DR
This review argues that senescence is more than a stable proliferative arrest: senescent cells remain metabolically active and communicate with their surroundings through secreted factors. It surveys how these cell-intrinsic and cell-extrinsic activities can suppress or promote cancer depending on context, with implications for therapy.
Key findings
- Senescence is heterogeneous and usually involves p53 and RB pathways, alongside telomere shortening/DNA damage responses, autophagy, metabolic shifts, altered secretion, and epigenetic regulation; multiple markers are needed for confident identification.
- In oncogene-induced and therapy-induced senescence, mitochondrial oxidative phosphorylation can be hyperactive. PDH activity rises in BRAF-V600E- or RAS-G12V-driven senescence; reducing PDH blocks BRAF-V600E senescence, while activating PDH is sufficient to induce senescence in normal cells. In human melanoma, roughly 10% of tumours had above-average PGC1α expression, and MITF/PGC1α-expressing melanoma cells were more resistant to oxidative stress and associated with poor prognosis.
- Autophagy is activated during senescence and can support SASP components such as IL-6 and IL-8, but its role varies by context; blocking autophagy can delay senescence, cause cell death, or exacerbate senescence depending on the model.
- The SASP can reinforce or spread senescence, recruit innate and adaptive immune cells to clear senescent cells, or promote tumorigenesis. Examples include NK-cell-mediated clearance via NKG2D–RAE1 and CD4+ T-cell-dependent senescence surveillance; stromal senescence can limit fibrosis and hepatocellular carcinoma in some models but promote hepatocellular carcinoma in an obesity/deoxycholic acid model.
Methods
- Narrative review; no primary experimental design, dataset, or statistical analysis is reported.
- The paper synthesizes published in vitro, mouse-model, and human tumour studies across pre-neoplasia, therapy-induced senescence, metabolism, autophagy, SASP, immune clearance, stromal senescence, and cytokine-mediated senescence.
- Data or sample: Not stated in the paper (no new data collected).
Limitations
- The paper states that many mechanisms remain unclear and context-dependent, including why mitochondrial dysfunction versus hyperactive respiration is observed, why stromal SASP effects differ between models, and how autophagy acts differently across tissues; further study is needed.
- Evident from the text: as a review, it does not describe a systematic search or quantitative synthesis, and its conclusions depend on heterogeneous models and contexts.
- Evident from the text: several sections contain editorial queries and incomplete figure/table formatting, which limits clarity but does not alter the scientific claims summarized.
Model-written summary. Check it against the paper before relying on it.
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Claims the paper makes
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In the paper
“senescent cells can exhibit hyperactive mitochondrial respiration (oxidative phosphorylation ) in some contexts.”
§ Inside and out; the activities of senescence in cancer > Abstract
What the sources say
- Not checked yetcites [41] Kaplon, J. et al. A key role for mitochondrial gatekeeper pyruvate dehydrogenase in oncogene-induced senescence. Nature 498, 109–112 (2013). This study established the metabolic profile of OIS cells, identifying active PDH with increased mitochondrial respiration during OIS. source
- Not checked yetcites [42] Kondoh, H. et al. Glycolytic enzymes can modulate cellular life span. Cancer Res. 65, 177–185 (2005). source
- Not checked yetcites [43] Dörr, J. R. et al. Synthetic lethal metabolic targeting of cellular senescence in cancer therapy. Nature 501, 421–425 (2013). This study shows that in a TIS model, the SASP, which provokes endoplasmic reticulum stress, is associated with increased glucose use, hyperactive mitochondrial respiration, and autophagy activation, and that TIS cells are sensitive to blocking glucose use or autophagy, which causes endoplasmic reticulum-related apoptosis. source
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“In contrast to tumour cells, which typically preferentially use glycolysis in the presence of oxygen to generate energy”
§ Inside and out; the activities of senescence in cancer > Abstract
What the sources say
- Not checked yetcites [40] Koppenol, W. H., Bounds, P. L. & Dang, C. V. Otto Warburg's contributions to current concepts of cancer metabolism. Nature Rev. Cancer 11, 325–337 (2011). source
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In the paper
“Senescent cells are metabolically active.”
§ Inside and out; the activities of senescence in cancer > Abstract
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In the paper
“recent studies have identified two distinct sub-groups in human melanoma: a conventional glycolytic group and a group characterised by high rates of oxidative phosphorylation 47,48 .”
§ Inside and out; the activities of senescence in cancer > Mitochondrial metabolism
What the sources say
- Not checked yetcites [47] Haq, R. et al. Oncogenic BRAF regulates oxidative metabolism via PGC1α and MITF. Cancer Cell 23, 302–315 (2013). source
- Not checked yetcites [48] Vazquez, F. et al. PGC1α expression defines a subset of human melanoma tumors with increased mitochondrial capacity and resistance to oxidative stress. Cancer Cell 23, 287–301 (2013). source
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In the paper
“a series of studies [22][23][24][25][26] identified senescence in several premalignant tumours, both in humans and mice.”
§ Inside and out; the activities of senescence in cancer > Senescence in pre-neoplasia
What the sources say
- Not checked yetcites [22] Braig, M. et al. Oncogene-induced senescence as an initial barrier in lymphoma development. Nature 436, 660–665 (2005). source
- Not checked yetcites [23] Chen, Z. et al. Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis. Nature 436, 725–730 (2005). source
- Not checked yetcites [24] Collado, M. et al. Tumour biology: Senescence in premalignant tumours. Nature 436, 642–642 (2005). source
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In the paper
“Senescent cells can be eliminated through a SASP-induced immune response, which can involve both innate and adaptive immunity.”
§ Inside and out; the activities of senescence in cancer > Abstract
What the sources say
- Not checked yetcites [111] Hoenicke, L. & Zender, L. Immune surveillance of senescent cells—biological significance in cancer- and non-cancer pathologies. Carcinogenesis 33, 1123–1126 (2012). source
- Not checked yetcites [112] Kang, T.-W. et al. Senescence surveillance of pre-malignant hepatocytes limits liver cancer development. Nature 479, 547–551 (2011). This is a seminal study that identifies senescence surveillance involving the adaptive immune response. source
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In the paper
“Loss of telomerase activity in mice has been shown to suppress tumorigenesis in various tumour models [13][14][15][16]”
§ Inside and out; the activities of senescence in cancer > Senescence in pre-neoplasia
What the sources say
- Not checked yetcites [13] González-Suárez, E., Samper, E., Flores, J. M. & Blasco, M. A. Telomerase-deficient mice with short telomeres are resistant to skin tumorigenesis. Nature Genet. 26, 114–117 (2000). source
- Not checked yetcites [14] Greenberg, R. A. et al. Short dysfunctional telomeres impair tumorigenesis in the INK4a(delta2/3) cancer-prone mouse. Cell 97, 515–525 (1999). source
- Not checked yetcites [15] Qi, L. et al. Short telomeres and ataxia-telangiectasia mutated deficiency cooperatively increase telomere dysfunction and suppress tumorigenesis. Cancer Res. 63, 8188–8196 (2003).
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Senescence can also be induced in response to therapy-induced genotoxic stress.”
§ Inside and out; the activities of senescence in cancer > Therapy-induced senescence
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Various triggers such as tissue damage or tumorigenesis-associated stresses can cause stromal cell senescence”
§ Inside and out; the activities of senescence in cancer > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes? Based: unclearIn the paper
“telomere attrition-induced senescence is implicated in these tumour suppressive effects 17 .”
§ Inside and out; the activities of senescence in cancer > Senescence in pre-neoplasia
What the sources say
- Not checked yetcites [17] Feldser, D. M. & Greider, C. W. Short telomeres limit tumor progression in vivo by inducing senescence. Cancer Cell 11, 461–469 (2007). source
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- Probably not a substantial claim. 8
- It may state two separate claims as one. 37
- The quote only partly states this claim. 3
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Induction of senescence, a stable state of cell cycle arrest, was originally described in normal cells, but it can also be induced in tumour cells in response to various stresses.”
§ Inside and out; the activities of senescence in cancer > Abstract
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“the long-term fate of senescent cells, which, similar to apoptotic cells, can be cleared from lesions in some contexts.”
§ Inside and out; the activities of senescence in cancer > Introduction
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In the paper
“However, the prognosis of these mice was significantly better than the Eµ-Myc; Trp53 -/-mice because the cells in the Eµ-Myc; Bcl2 lymphomas became senescent, although the Eµ-Myc; Bcl2 lymphomas also eventually progressed.”
§ Inside and out; the activities of senescence in cancer > Therapy-induced senescence
What the sources say
- Not checked yetcites [32] Schmitt, C. A. et al. A senescence program controlled by p53 and p16INK4a contributes to the outcome of cancer therapy. Cell 109, 335–346 (2002). This was the first study showing that chemotherapy-induced tumour senescence contributed to improved survival in mice, in an apoptosis defective context. source
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In the paper
“Quijano et al. 53 showed that HRAS-G12V-induced senescent HDFs exhibit reduced lipid synthesis and increased fatty acid (FA) oxidation, leading to enhanced mitochondrial oxygen consumption.”
§ Inside and out; the activities of senescence in cancer > Mitochondrial metabolism
What the sources say
- Not checked yetcites [53] Quijano, C. et al. Oncogene-induced senescence results in marked metabolic and bioenergetic alterations. Cell Cycle 11, 1383–1392 (2012). source
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Senescence has a heterogeneous phenotype in terms of cellular markers: multiple markers are required to define senescence with confidence.”
§ Inside and out; the activities of senescence in cancer > Introduction
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In the paper
“These include telomere shortening and a persistent DNA damage response, autophagy and other metabolic alterations, altered protein secretion, and epigenetic gene regulation [2][3][4] .”
§ Inside and out; the activities of senescence in cancer > Introduction
What the sources say
- Not checked yetcites [2] D'adda Di Fagagna, F. Living on a break: cellular senescence as a DNA-damage response. Nature Rev. Cancer 8, 512–522 (2008). source
- Not checked yetcites [3] Kuilman, T., Michaloglou, C., Mooi, W. J. & Peeper, D. S. The essence of senescence. Genes Dev. 24, 2463–2479 (2010). source
- Not checked yetcites [4] Salama, R., Sadaie, M., Hoare, M. & Narita, M. Cellular senescence and its effector programs. Genes Dev. 28, 99–114 (2014). source
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In the paper
“including reinforcing or inducing senescence”
§ Inside and out; the activities of senescence in cancer > Abstract
What the sources say
- Not checked yetcites [91] Kuilman, T. et al. Oncogene-induced senescence relayed by an interleukin-dependent inflammatory network. Cell 133, 1019–1031 (2008). source
- Not checked yetcites [92] Acosta, J. C. et al. Chemokine signaling via the CXCR2 receptor reinforces senescence. Cell 133, 1006–1018 (2008). References 91 and 92 describe the crucial role of pro-inflammatory cytokines and their receptors in senescence. source
- Not checked yetcites [105] Coppé, J.-P. et al. Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor. Plos Biol. 6, 2853–2868 (2008). source
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In the paper
“ME1 and ME2 expression is repressed by p53 and the MEs negatively regulate p53, thus depletion of the MEs results in p53 activation in a feed forward manner, thereby inducing senescence 50 (FIG.1).”
§ Inside and out; the activities of senescence in cancer > Mitochondrial metabolism
What the sources say
- Not checked yetcites [50] Jiang, P., Du, W., Mancuso, A., Wellen, K. E. & Yang, X. Reciprocal regulation of p53 and malic enzymes modulates metabolism and senescence. Nature 493, 689–693 (2013). This study shows that malic enzymes and p53 reciprocally repress each other and that depletion of ME1 or ME2 induces senescence in both normal and tumour cells. source
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In the paper
“Autophagy is dynamically activated during OIS and facilitates the synthesis of interleukin 6 (IL-6) and IL-8, major components of the SASP 58,59 .”
§ Inside and out; the activities of senescence in cancer > Autophagy
What the sources say
- Not checked yetcites [58] Narita, M. et al. Spatial coupling of mTOR and autophagy augments secretory phenotypes. Science 332, 966–970 (2011). source
- Not checked yetcites [59] Young, A. R. J. et al. Autophagy mediates the mitotic senescence transition. Genes Dev. 23, 798–803 (2009). This study shows that autophagy is activated during senescence and that the inhibition of autophagy delays the onset of senescence and the SASP. source
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In the paper
“activation of PDH in mutant BRAF-driven human melanoma cells not only blocks tumorigenesis but also sensitises them to the BRAF inhibitor PLX4720 (an analogue of vemurafenib), eliminating treatment-resistant cell populations 41 .”
§ Inside and out; the activities of senescence in cancer > Mitochondrial metabolism
What the sources say
- Not checked yetcites [41] Kaplon, J. et al. A key role for mitochondrial gatekeeper pyruvate dehydrogenase in oncogene-induced senescence. Nature 498, 109–112 (2013). This study established the metabolic profile of OIS cells, identifying active PDH with increased mitochondrial respiration during OIS. source
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Senescence typically depends on the p53 and RB pathways, but other effector programs confer additional layers of regulation.”
§ Inside and out; the activities of senescence in cancer > Introduction
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In the paper
“In this model, autophagy deficient mice exhibit a marked but transient accumulation of early PanIN accompanied by increased rates of apoptotic cell death, and these lesions never progress to late stage PanINs or PDA 87 .”
§ Inside and out; the activities of senescence in cancer > Autophagy
What the sources say
- Not checked yetcites [87] Rosenfeldt, M. T. et al. p53 status determines the role of autophagy in pancreatic tumour development. Nature 504, 296–300 (2014). source
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In the paper
“some SASP components not only reinforce the senescence response in cells that are already primed for senescence, but also induce senescence in normal neighbouring cells in a paracrine fashion 93,106”
§ Inside and out; the activities of senescence in cancer > Cytokine-mediated senescence
What the sources say
- Not checked yetcites [93] Acosta, J. C. et al. A complex secretory program orchestrated by the inflammasome controls paracrine senescence. Nature Cell Biol. 15, 978–990 (2013). This study identified the inflammasome as a critical regulator of the SASP. source
- Not checked yetcites [106] Hubackova, S. et al. IL1- and TGFβ-Nox4 signaling, oxidative stress and DNA damage response are shared features of replicative, oncogene-induced, and drug-induced paracrine 'bystander senescence'. Aging 4, 932–951 (2012). source
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In the paper
“In an Eµ-Myc lymphoma model, p53induced apoptosis of lymphoma cells led to the activation of macrophages to secrete TGFß1, which in turn induced senescence in lymphoma cells 36”
§ Inside and out; the activities of senescence in cancer > Cytokine-mediated senescence
What the sources say
- Not checked yetcites [36] Reimann, M. et al. Tumor stroma-derived TGF-b limits Myc-Driven lymphomagenesisvia Suv39h1-dependent senescence. Cancer Cell 17, 262–272 (2010). source
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These data indicate that senescence in the context of some forms of tissue damage involves the spatio-temporal control of secreted protein levels as well as the content of SASP, which in turn modulates the senescence phenotype and dynamically regulates the surrounding tissue integrity; eventually contributing to the resolution of the lesion.”
§ Inside and out; the activities of senescence in cancer > Senescence in the stroma
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In the paper
“Treatment of mice with Tag-T H 1 cells in this model induces a cell proliferation arrest in the tumors and improves the survival of these mice 128”
§ Inside and out; the activities of senescence in cancer > Cytokine-mediated senescence
What the sources say
- Not checked yetcites [128] Müller-Hermelink, N. et al. TNFR1 signaling and IFN-γ signaling determine whether T cells induce tumor dormancy or promote multistage carcinogenesis. Cancer Cell 13, 507–518 (2008). source
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In the paper
“pancreatic acinar cells, in which Kras-G12V is activated during adulthood, exhibit a low frequency of PanIN development and resistance to transformation, at least in part due to OIS 118”
§ Inside and out; the activities of senescence in cancer > Clearance of senescent cells through an immune response
What the sources say
- Not checked yetcites [118] Guerra, C. et al. Pancreatitis-induced inflammation contributes to pancreatic cancer by inhibiting oncogene-induced senescence. Cancer Cell 19, 728–739 (2011). source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“activated HSCs become senescent, exhibiting a typical SASP, including the expression of extracellular matrix degrading enzymes and proinflammatory cytokines.”
§ Inside and out; the activities of senescence in cancer > Senescence in the stroma
What the sources say
- Not checked yetcites [94] Lujambio, A. et al. Non-cell-autonomous tumor suppression by p53. Cell 153, 449–460 (2013). source
- Not checked yetcites [120] Krizhanovsky, V. et al. Senescence of activated stellate cells limits liver fibrosis. Cell 134, 657–667 (2008). This was the first study to show that HSC senescence controls fibrosis through the SASP. source
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In the paper
“Although Tag binds both RB and p53, it attenuates, rather than fully inactivates, their activity, thus their residual activities allow the RIP-Tag2 mice to exhibit progressive tumorigenesis with only a small portion of islets developing invasive pancreatic cancer 127,129”
§ Inside and out; the activities of senescence in cancer > Cytokine-mediated senescence
What the sources say
- Not checked yetcites [127] Bergers, G., Javaherian, K., Lo, K. M., Folkman, J. & Hanahan, D. Effects of angiogenesis inhibitors on multistage carcinogenesis in mice. Science 284, 808–812 (1999). source
- Not checked yetcites [129] Casanovas, O., Hager, J. H., Chun, M. G. H. & Hanahan, D. Incomplete inhibition of the Rb tumor suppressor pathway in the context of inactivated p53 is sufficient for pancreatic islet tumorigenesis. Oncogene 24, 6597–6604 (2005). source
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In the paper
“in contrast to the pancreas model, autophagy deficiency (by autophagy related 7 (Atg7) knockout) suppresses Kras G12D -driven lung cancer development even in the absence of Trp53; presumably this is partially due to mitochondrial dysfunction.”
§ Inside and out; the activities of senescence in cancer > Autophagy
What the sources say
- Not checked yetcites [88] Guo, J. Y. et al. Autophagy suppresses progression of K-ras-induced lung tumors to oncocytomas and maintains lipid homeostasis. Genes Dev. 27, 1447–1461 (2013). source
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In the paper
“CCN1 can also promote myofibroblast senescence, which is associated with the expression of antifibrotic genes in the skin, thus CCN1 mediated stromal senescence might be involved in wound healing 123”
§ Inside and out; the activities of senescence in cancer > Senescence in the stroma
What the sources say
- Not checked yetcites [123] Jun, J.-I. & Lau, L. F. The matricellular protein CCN1 induces fibroblast senescence and restricts fibrosis in cutaneous wound healing. Nature Cell Biol. 12, 676–685 (2010). source
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“The senescence phenotype is dependent on the p16-RB pathway, thus unlike the aforementioned Tag-driven hepatoma model, the residual RB activity seems to be sufficient for senescence induction in this model 129”
§ Inside and out; the activities of senescence in cancer > Cytokine-mediated senescence
What the sources say
- Not checked yetcites [129] Casanovas, O., Hager, J. H., Chun, M. G. H. & Hanahan, D. Incomplete inhibition of the Rb tumor suppressor pathway in the context of inactivated p53 is sufficient for pancreatic islet tumorigenesis. Oncogene 24, 6597–6604 (2005). source
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“human melanocytic naevi (an OIS model), remain non-proliferative for decades without transformation into malignant melanoma 25”
§ Inside and out; the activities of senescence in cancer > Clearance of senescent cells through an immune response
What the sources say
- Not checked yetcites [25] Michaloglou, C. et al. BRAFE600-associated senescence-like cell cycle arrest of human naevi. Nature 436, 720–724 (2005). This is a seminal study that identified OIS of human melanocytic naevi. source
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None of the sources cited for this claim have been checked yet.
In the paper
“these same factors can facilitate senescence in a cell-autonomous fashion, thus amplifying the phenotype 91,92,105”
§ Inside and out; the activities of senescence in cancer > Senescence-associated secretory phenotype (SASP)
What the sources say
- Not checked yetcites [91] Kuilman, T. et al. Oncogene-induced senescence relayed by an interleukin-dependent inflammatory network. Cell 133, 1019–1031 (2008). source
- Not checked yetcites [92] Acosta, J. C. et al. Chemokine signaling via the CXCR2 receptor reinforces senescence. Cell 133, 1006–1018 (2008). References 91 and 92 describe the crucial role of pro-inflammatory cytokines and their receptors in senescence. source
- Not checked yetcites [105] Coppé, J.-P. et al. Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor. Plos Biol. 6, 2853–2868 (2008). source
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In the paper
“Re-expression of endogenous p53 induced senescence and the elimination of the senescent tumour cells was mediated by innate immune cells, including macrophages, neutrophils and natural killer (NK) cells, albeit in mice lacking an adaptive immune system.”
§ Inside and out; the activities of senescence in cancer > Clearance of senescent cells through an immune response
What the sources say
- Not checked yetcites [34] Xue, W. et al. Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas. Nature 445, 656–660 (2007). This was the first study to show that the innate immune response eliminates the senescent cells induced in tumours in mice. source
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In the paper
“episodic pancreatitis induced by caerulein, a decapeptide analog of the gastrointestinal peptide hormone cholecystokinin, inhibited the OIS program, thus facilitating malignant transformation in this model 118”
§ Inside and out; the activities of senescence in cancer > Clearance of senescent cells through an immune response
What the sources say
- Not checked yetcites [118] Guerra, C. et al. Pancreatitis-induced inflammation contributes to pancreatic cancer by inhibiting oncogene-induced senescence. Cancer Cell 19, 728–739 (2011). source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“the depletion of MYC in a mouse subcutaneous transplantation model of T cell acute lymphoblastic lymphoma (T-ALL), which carries tetracycline regulated MYC transgene, results in sustained tumour regression associated with senescence and apoptosis, where an adaptive immune response (involving CD4 + T cells in particular) was required for senescence induction and sustained tumour regression, but not”
§ Inside and out; the activities of senescence in cancer > Clearance of senescent cells through an immune response
What the sources say
- Not checked yetcites [116] Rakhra, K. et al. CD4(+) T cells contribute to the remodeling of the microenvironment required for sustained tumor regression upon oncogene inactivation. Cancer Cell 18, 485–498 (2010). source
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In the paper
“The SASP also attracts innate immune cells that in turn eliminate the senescent HSCs and facilitate the resolution of fibrosis 94,120”
§ Inside and out; the activities of senescence in cancer > Senescence in the stroma
What the sources say
- Not checked yetcites [94] Lujambio, A. et al. Non-cell-autonomous tumor suppression by p53. Cell 153, 449–460 (2013). source
- Not checked yetcites [120] Krizhanovsky, V. et al. Senescence of activated stellate cells limits liver fibrosis. Cell 134, 657–667 (2008). This was the first study to show that HSC senescence controls fibrosis through the SASP. source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“The TAA-expressing islets treated with Tag-T H 1 cells are functional (i.e. they produce insulin), thus appeared to be in a state of tumour dormancy 128”
§ Inside and out; the activities of senescence in cancer > Cytokine-mediated senescence
What the sources say
- Not checked yetcites [128] Müller-Hermelink, N. et al. TNFR1 signaling and IFN-γ signaling determine whether T cells induce tumor dormancy or promote multistage carcinogenesis. Cancer Cell 13, 507–518 (2008). source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“| | LSL-Kras G12V ; RERTn +/ERT | Cdk4 ablation | development | 158 | | | |”
- Also stated in: § Additional information · plain
“| | | | | | Suppression of non-small cell lung carcinoma | | |”
§ Inside and out; the activities of senescence in cancer > Additional information
What the sources say
- Not checked yetcites [158] Puyol, M. et al. A synthetic lethal interaction between K-Ras oncogenes and Cdk4 unveils a therapeutic strategy for non-small cell lung carcinoma. Cancer Cell 18, 63–73 (2010). source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe quote only partly states this claim.
- Also stated in: § Additional information · plain
In the paper
“This is a seminal study that identified OIS of human melanocytic naevi.”
§ Inside and out; the activities of senescence in cancer > References
What the sources say
- Not checked yetcites [25] Michaloglou, C. et al. BRAFE600-associated senescence-like cell cycle arrest of human naevi. Nature 436, 720–724 (2005). This is a seminal study that identified OIS of human melanocytic naevi. source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“This seminal paper established the concept of OIS.”
§ Inside and out; the activities of senescence in cancer > References
What the sources say
- Not checked yetcites [19] Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D. & Lowe, S. W. Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a. Cell 88, 593–602 (1997). This seminal paper established the concept of OIS. source
Strength:boosted· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Embryonic cell senescence is p21, but not p53, dependent, is accompanied by the SASP, and these cells are eliminated by macrophages 149,150”
§ Inside and out; the activities of senescence in cancer > Embryogenesis:
What the sources say
- Not checked yetcites [149] Muñoz-Espín, D. et al. Programmed cell senescence during mammalian embryonic development. Cell 155, 1104–1118 (2013). source
- Not checked yetcites [150] Storer, M. et al. Senescence is a developmental mechanism that contributes to embryonic growth and patterning. Cell 155, 1119–1130 (2013). source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“| CDK4 inhibitor | LSL-Kras G12V ; RERTn +/ERT | PD0332991 | development | 158 | | | |”
- Also stated in: § Additional information · plain
“| | | | | | Suppression of non-small cell lung carcinoma | | |”
§ Inside and out; the activities of senescence in cancer > Additional information
What the sources say
- Not checked yetcites [158] Puyol, M. et al. A synthetic lethal interaction between K-Ras oncogenes and Cdk4 unveils a therapeutic strategy for non-small cell lung carcinoma. Cancer Cell 18, 63–73 (2010). source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe quote only partly states this claim.
- Also stated in: § Additional information · plain
None of the sources cited for this claim have been checked yet.
In the paper
“The partial induction of senescence in tumours could eradicate or exacerbate the tumours 110,113”
§ Inside and out; the activities of senescence in cancer > Concluding remarks
What the sources say
- Not checked yetcites [110] Jackson, J. G. et al. p53-mediated senescence impairs the apoptotic response to chemotherapy and clinical outcome in breast cancer. Cancer Cell 21, 793–806 (2012). source
- Not checked yetcites [113] Iannello, A., Thompson, T. W., Ardolino, M., Lowe, S. W. & Raulet, D. H. p53-dependent chemokine production by senescent tumor cells supports NKG2D-dependent tumor elimination by natural killer cells. J. Exp. Med. 210, 2057–2069 (2013). This study suggests that NK cells that are recruited to the tumour lesion by the SASP of senescent tumour cells may also kill non-senescent tumour cells. source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“This study established the metabolomics profile of OIS cells, identifying active PDH with increased mitochondrial respiration during OIS.”
§ Inside and out; the activities of senescence in cancer > References
What the sources say
- Not checked yetcites [41] Kaplon, J. et al. A key role for mitochondrial gatekeeper pyruvate dehydrogenase in oncogene-induced senescence. Nature 498, 109–112 (2013). This study established the metabolic profile of OIS cells, identifying active PDH with increased mitochondrial respiration during OIS. source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“age-dependent accumulation of p16-positive cells in tissue stem cell or progenitor cell compartments contributes to tissue degeneration, and p16 depletion attenuates some age-dependent phenotypes [145][146][147]”
§ Inside and out; the activities of senescence in cancer > Box 1: Consequences of cellular senescence: aging and development
What the sources say
- Not checked yetcites [145][146][147]
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Much like dormant cells, senescent cells are resistant to apoptosis or mitotic catastrophe upon chemotherapy, thus if senescent tumour cells are not eliminated, the sustained expression of pro-tumorigenic cytokines can lead to a worse outcome 110”
§ Inside and out; the activities of senescence in cancer > Concluding remarks
What the sources say
- Not checked yetcites [110] Jackson, J. G. et al. p53-mediated senescence impairs the apoptotic response to chemotherapy and clinical outcome in breast cancer. Cancer Cell 21, 793–806 (2012). source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“| SKP2 inhibitor | xenografts | | | SKP2 Inhibitor#25 | Tumour growth inhibition | 159 |”
- Also stated in: § Additional information · plain
“| | Human lung and prostate cancer | | | | | | |”
§ Inside and out; the activities of senescence in cancer > Additional information
What the sources say
- Not checked yetcites [159] Chan, C.-H. et al. Pharmacological inactivation of Skp2 SCF ubiquitin ligase restricts cancer stem cell traits and cancer progression. Cell 154, 556–568 (2013). source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe quote only partly states this claim.
- Also stated in: § Additional information · plain
None of the sources cited for this claim have been checked yet.
In the paper
“the majority of prostate cancer patients at presentation have lost one allele of PTEN while maintaining intact TP53; whereas TP53 mutations and the complete loss of PTEN are both associated with advanced stage prostate cancer 153,154”
§ Inside and out; the activities of senescence in cancer > Box 2: PTEN loss-induced cellular senescence (PICS)
What the sources say
- Not checked yetcites [153] Schlomm, T. et al. Clinical significance of p53 alterations in surgically treated prostate cancers. Mod. Pathol. 21, 1371–1378 (2008). source
- Not checked yetcites [154] Song, M. S., Salmena, L. & Pandolfi, P. P. The functions and regulation of the PTEN tumour suppressor. Nature Rev. Mol. Cell. Biol. 13, 283–296 (2012). source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Pten heterozygosity promotes tumour initiation and proliferation in the prostate, but paradoxically, the complete loss of Pten can oppose prostate tumorigenesis by triggering a powerful p53-dependent cellular senescence response 38”
§ Inside and out; the activities of senescence in cancer > Box 2: PTEN loss-induced cellular senescence (PICS)
What the sources say
- Not checked yetcites [38] Nardella, C., Clohessy, J. G., Alimonti, A. & Pandolfi, P. P. Pro-senescence therapy for cancer treatment. Nature Rev. Cancer 11, 503–511 (2011). source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“| | haematopoietic system | MYC suppression | lymphoma | 116 | | | |”
§ Inside and out; the activities of senescence in cancer > Additional information
What the sources say
- Not checked yetcites [116] Rakhra, K. et al. CD4(+) T cells contribute to the remodeling of the microenvironment required for sustained tumor regression upon oncogene inactivation. Cancer Cell 18, 485–498 (2010). source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✗ Asserted: fails✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The authors may not put it forward as true. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“unlike p16-ablation, elimination of p16-expressing cells does not facilitate tumorigenesis in this model.”
§ Inside and out; the activities of senescence in cancer > Box 1: Consequences of cellular senescence: aging and development
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“This study suggests that NK cells recruited to the tumour lesion by the SASP of senescent tumour cells may also kill non-senescent tumour cells.”
§ Inside and out; the activities of senescence in cancer > References
What the sources say
- Not checked yetcites [113] Iannello, A., Thompson, T. W., Ardolino, M., Lowe, S. W. & Raulet, D. H. p53-dependent chemokine production by senescent tumor cells supports NKG2D-dependent tumor elimination by natural killer cells. J. Exp. Med. 210, 2057–2069 (2013). This study suggests that NK cells that are recruited to the tumour lesion by the SASP of senescent tumour cells may also kill non-senescent tumour cells. source
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“This study shows that in a TIS model the SASP, which provokes endoplasmic reticulum (ER) stress, is associated with increased glucose use, hyperactive mitochondrial respiration, and autophagy activation”
§ Inside and out; the activities of senescence in cancer > References
What the sources say
- Not checked yetcites [43] Dörr, J. R. et al. Synthetic lethal metabolic targeting of cellular senescence in cancer therapy. Nature 501, 421–425 (2013). This study shows that in a TIS model, the SASP, which provokes endoplasmic reticulum stress, is associated with increased glucose use, hyperactive mitochondrial respiration, and autophagy activation, and that TIS cells are sensitive to blocking glucose use or autophagy, which causes endoplasmic reticulum-related apoptosis. source
Strength:boosted· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“This study shows that Malic enzymes (MEs) and p53 reciprocally repress each other”
§ Inside and out; the activities of senescence in cancer > References
What the sources say
- Not checked yetcites [50] Jiang, P., Du, W., Mancuso, A., Wellen, K. E. & Yang, X. Reciprocal regulation of p53 and malic enzymes modulates metabolism and senescence. Nature 493, 689–693 (2013). This study shows that malic enzymes and p53 reciprocally repress each other and that depletion of ME1 or ME2 induces senescence in both normal and tumour cells. source
Strength:boosted· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“In fact, senescent cells secrete an array of inflammatory proteins, growth factors, and metalloproteases that collectively constitute the SASP (senescence-associated secretory phenotype).”
From Integrin Beta 3 Regulates Cellular Senescence by Activating the TGF-β Pathway (2017) · cites this paper as Pérez-Mancera et al., 2014
In the citing paper
“However, the deleterious consequences that result from ineffective clearance of senescent cells and their over-accumulation in tissues can promote age-related diseases and cancer.2,26–30”
From Paracrine roles of cellular senescence in promoting tumourigenesis (2018) · cites this paper as [30]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Lung cancer model has two different KRAS mutations
MinorThe same discussion identifies the autophagy-inhibition lung model as KRAS-G12V-driven and then as KRAS-G12D-driven. These are different mutations, so the model is described inconsistently.
“Interestingly, the effect of autophagy inhibition in Kras G12V -driven lung tumorigenesis (another OIS model 24 ) is distinct from the pancreas model.”
“Thus, in contrast to the pancreas model, autophagy deficiency (by autophagy related 7 (Atg7) knockout) suppresses Kras G12D -driven lung cancer development even in the absence of Trp53; presumably this is partially due to mitochondrial dysfunction.”
Citations
Cites
1 retracted
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Items 401–468 of 468
The rise of RAS: how gradual oncogene activation shapes the OIS spectrumPreprint
Zhu, H., Chan, A. S. L., & Narita, M. (2025) · Genes & Development · doi:10.1101/gad.352761.125 · Cited by 2
“…between senescent cells and immune cells: OIS hepatocytes trigger an immune response through the inflammatory SASP, and within 12 – 30 days after oncogenic RAS introduction, the senescent cells are eliminated by the immune cells (Kang et al. 2011; Pérez-Mancera et al. 2014; Yin et al. 2022).”
Self-citationGonzález-Meljem, J. M., Haston, S., Gallage, S., & Innes, A. J. (2018) · Springer eBooks · doi:10.1007/978-3-319-95387-8_3 · Cited by 1
Noureen, N., & Kang, M. H. (2025) · Computational and Structural Biotechnology Journal · doi:10.1016/j.csbj.2025.11.020 · Cited by 1
Stress factor – dependent differences in molecular mechanisms of premature cell senescence
Petrova, N. V., Velichko, A. K., Petrova, N. V., Razin, S. V., & Kantidze, O. L. (2015) · Biopolymers and Cell · doi:10.7124/bc.0008f4 · Cited by 1
“to eliminate cells with signs of senescence from the tissues [30].”
BackgroundAlive failures behind the windows of cancer therapy
Islam, M. T. (2017) · International Journal of Medicine · doi:10.14419/ijm.v5i2.7035 · Cited by 1
Cyclin D1, Metabolism, and the Autophagy-Senescence Balance
Valenzuela, C. A., & Brown, N. E. (2017) · Current cancer research · doi:10.1007/978-3-319-64451-6_5 · Cited by 2
Repurposing Drugs Modulating Autophagy: Toward a New Era for the Treatment of Cancer
Al‐Bari, M. A. A. (2023) · Springer eBooks · doi:10.1007/978-3-030-80962-1_284-1 · Cited by 1
Lompardía, S. L., Pibuel, M. A., Díaz, M., Poodts, D., & Hajos, S. E. (2022) · Glycobiology · doi:10.1093/glycob/cwac028 · Cited by 1
Morphological and Metabolic Features of Brain Aging in MammalsPreprint
Lepore, G., Succu, S., Cappai, M. G., Frau, A., Senes, A., Zedda, M., Farina, V., & Gadau, S. D. (2024) · Preprints.org · doi:10.20944/preprints202408.1405.v1 · Cited by 1
Cabral, J. E., Lin, S., Zhou, H., Wu, A., Lackner, A., Pham, M. A., Chi, F., & McNulty, R. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.03.07.642110 · Cited by 1
“Senescent cells remain metabolically active but exhibit altered gene expression(33), resistance to apoptosis(34), and secretion of pro-inflammatory cytokines, growth factors, and matrix-remodeling enzymes known as the senescence-associated secretory phenotype (SASP)(12).”
Midha, A. (2015) · cIRcle (University of British Columbia) · doi:10.14288/1.0166529
“agents such as doxorubicin and cyclophosphamide (133).”
Effects of Ageing on Adaptive Immune Responses
Henson, S. M. (2016) · Springer eBooks · doi:10.1007/978-3-319-43365-3_2
“The importance of understanding this interplay is underscored by highly differentiated T cells being found in high numbers not only during ageing but in chronic viral infections [92, 93], malignancies [94] and autoimmunity [31, 95].”
BackgroundUsing [U-13C6]-Glucose Tracer to Study Metabolic Changes in Oncogene-Induced Senescence Fibroblasts
Leonova, K. I., & Scott, D. A. (2016) · Methods in molecular biology · doi:10.1007/978-1-4939-6670-7_11
Basic Principles of DNA Repair in Toxicology
Dutta, A. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-801238-3.65423-5
Wassmer, G., Hmitti, Z., Voisin, L., & Perfettini, J. (2018) · médecine/sciences · doi:10.1051/medsci/20183401011
Zytokin-induzierte Seneszenz: eine experimentelle Therapie peritonealer Tumoren
Wieder, T., Brenner, E., Braumüller, H., & Röcken, M. (2018) · Springer eBooks · doi:10.1007/978-3-662-54500-3_14
Apoptosis Pathways and Chemotherapy in Brain Tumors
Venere, M., De, K., Yoo, J. Y., & Kaur, B. (2018) · Elsevier eBooks · doi:10.1016/b978-0-12-812100-9.00020-6
Role Of Cellular Senescence in Age-Related Intervertebral Disc Degeneration
Patil, P. R. (2019) · D-Scholarship@Pitt (University of Pittsburgh)
The Molecular Physiology of Ageing: New Targets for Regenerative Medicine
Macip, S., & Althubiti, M. (2019) · Springer eBooks · doi:10.1007/978-3-030-15458-5_3
Cytokine-Induced Senescence: An Experimental Treatment of Peritoneal Tumors
Wieder, T., Brenner, E., Braumüller, H., Garg, P. K., & Röcken, M. (2021) · Springer eBooks · doi:10.1007/978-3-030-62640-2_14
Targeting MDM2, the antagonist of the tumor suppressor p53
Sriraman, A. (2018) · eDiss (Georg-August-Universität Göttingen) · doi:10.53846/goediss-7056
Faculty Opinions recommendation of Revisiting the hallmarks of cancer.
Vecchio, G., & Melillo, R. M. (2019) · Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · doi:10.3410/f.727685941.793556548
Cell biology and carcinogenesis in older people
Fülöp, T., Anisimov, V. N., Rodier, F., & Extermann, M. (2017) · Oxford University Press eBooks · doi:10.1093/med/9780198701590.003.0090
Diosgenin Inhibits Prostate Cancer Progression by Inducing UHRF1 Protein DegradationPreprint
Tang, R., Peng, Y., Ding, L., Liu, Y., Yin, L., Fu, Y., Deng, T., & Li, X. (2022) · doi:10.22541/au.165237524.42526501/v1
An Overview of the Role of Senescence in Cancer
Al-Janabi, I. I. (2022) · Al-Rafidain Journal of Medical Sciences · doi:10.54133/ajms.v3i.77
“Tumor mass often exhibits a mixed phenotype of cells following chemotherapy with some showing senescence and others showing apoptosis [60].”
BackgroundSun, Z., Wang, Z., & Zheng, X. S. (2022) · Research Square · doi:10.21203/rs.3.rs-2291800/v1
Data from Glioblastomas Require Integrin αvβ3/PAK4 Signaling to Escape Senescence
Franovic, A., Elliott, K. C., Seguin, L., Camargo, M. F., Weis, S. M., & Cheresh, D. A. (2023) · doi:10.1158/0008-5472.c.6507503.v1
Data from Female Immunity Protects from Cutaneous Squamous Cell Carcinoma
Budden, T., Gaudy‐Marqueste, C., Craig, S., Hu, Y., Earnshaw, C. H., Gurung, S., Ra, A., Akhras, V., Shenjere, P., Green, R., et al. (2023) · doi:10.1158/1078-0432.c.6529916
Data from Female Immunity Protects from Cutaneous Squamous Cell Carcinoma
Budden, T., Gaudy‐Marqueste, C., Craig, S., Hu, Y., Earnshaw, C. H., Gurung, S., Ra, A., Akhras, V., Shenjere, P., Green, R., et al. (2023) · doi:10.1158/1078-0432.c.6529916.v1
Li, W., Kawaguchi, K., Tanaka, S., He, C., Maeshima, Y., Suzuki, E., & Toi, M. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.04.08.536098
Role of Circulating microRNA as a Potential Biomarker in Metastatic Breast Cancer
Kendarini, N. P. Y., Mahadewa, T. G. B., & Maratni, N. P. T. (2023) · International Journal of Health Sciences and Research · doi:10.52403/ijhsr.20230719
Field Cancerization: A Malignant Transformation
Saw, P. E., & Song, E. (2023) · Springer eBooks · doi:10.1007/978-981-99-1183-7_10
Wang, Z. (2023) · Journal of Clinical Images and Medical Case Reports · doi:10.52768/2766-7820/2459
“Beneficial to the elimination of senescent or diseased cells [143].”
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WANG, J., Yi, L., HUANG, K., Wang, Y., WANG, H., & Zhai, Z. (2024) · Biocell · doi:10.32604/biocell.2024.047871
“Cellular senescence is a state of stress-responsive cell-cycle arrest and is known to play a vital role in tumor suppression [11,12].”
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Basic Principles of DNA Repair in Toxicology
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Molecular drivers in primary brain tumor formation
Richard, H. (2025) · Advances in cancer research · doi:10.1016/bs.acr.2025.04.006
Hsu, T.-W., Li, S., Ho, Y.-J., Zhang, X., Malik, I., Bessel, D., Ji, L., Edwards, C., Capistrano, K. J., Vougiouklakis, T., et al. (2025) · SSRN Electronic Journal · doi:10.2139/ssrn.5265216
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Repurposing Drugs Modulating Autophagy: Toward a New Era for the Treatment of Cancer
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Menjivar, N. G., Gad, A., Thompson, R. E., Meyers, M. A., Hollinshead, F., & Tesfaye, D. (2024) · Figshare · doi:10.6084/m9.figshare.26632998
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Targeted Supramolecular Senolytics by Enzyme-Responsive Disassembly and Intracellular Polymerization
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“During this screening, induction of the PRCC-TFE3 fusion triggered a robust oncogene-induced senescence (OIS) program [16,17] in HK-2 human proximal tubular epithelial cells.”
Cell death pathways and chemotherapy in brain tumors
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Metadata
- Authors
- Pérez-Mancera, P. A., Young, A. R. J., & Narita, M.
- Affiliations
- University of Cambridge (GB)
- Corresponding author
- Narita, Masashi
- Venue
- Nature Reviews Cancer
- Published
- 2014-07-17
- Volume
- 14
- Issue
- 8
- Pages
- 547-558
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- OpenAlex
- W1963704214
- Semantic Scholar
- 34d61b9672e8adfeea27bec14cd0bfbd47df2729
- Cited by
- 462
- References
- 161
- Citations by year
- 2026: 9 · 2025: 26 · 2024: 32 · 2023: 35 · 2022: 41 · 2021: 39 · 2020: 34 · 2019: 41 · 2018: 48 · 2017: 58 · 2016: 55 · 2015: 39 · 2014: 5
- FWCI
- 6.14
- Type
- journal article
- Language
- en
- Open access
- Locations
- Nature reviews. Cancer (publishedVersion)
- PubMed (publishedVersion)
- Apollo (University of Cambridge) (submittedVersion)
- Funders
- Cancer Research UK (15890)
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Keywords
- cellular senescence, senescence-associated secretory phenotype, carcinogenesis, tumor progression, tumor suppression, tumor promotion, cell cycle arrest, non-cell-autonomous effects, cancer therapy response
- MeSH terms
- Animals, Humans, Neoplasms, Precancerous Conditions, Signal Transduction, Cellular Senescence, Tumor Microenvironment
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