The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
Restoration of p53 function leads to tumour regression in vivo
Abstract
Tumorigenesis is a multi-step process that requires activation of oncogenes and inactivation of tumour suppressor genes. Mouse models of human cancers have recently demonstrated that continuous expression of a dominantly acting oncogene (for example, Hras, Kras and Myc) is often required for tumour maintenance; this phenotype is referred to as oncogene addiction. This concept has received clinical validation by the development of active anticancer drugs that specifically inhibit the function of oncoproteins such as BCR-ABL, c-KIT and EGFR. Identifying additional gene mutations that are required for tumour maintenance may therefore yield clinically useful targets for new cancer therapies. Although loss of p53 function is a common feature of human cancers, it is not known whether sustained inactivation of this or other tumour suppressor pathways is required for tumour maintenance. To explore this issue, we developed a Cre-loxP-based strategy to temporally control tumour suppressor gene expression in vivo. Here we show that restoring endogenous p53 expression leads to regression of autochthonous lymphomas and sarcomas in mice without affecting normal tissues. The mechanism responsible for tumour regression is dependent on the tumour type, with the main consequence of p53 restoration being apoptosis in lymphomas and suppression of cell growth with features of cellular senescence in sarcomas. These results support efforts to treat human cancers by way of pharmacological reactivation of p53.
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In the citing paper
“Interestingly, some tumor cells retain the ability to senesce in response to DNA-damaging chemotherapy or p53 reactivation; in mice, this response arrests tumor progression [ 20 – 22 ].”
From Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the p53 Tumor Suppressor (2008) · cites this paper as [21]
In the citing paper
“Recent findings show that tumors induced to senesce in mice gradually regress [ 21 , 22 ], owing perhaps to infiltration by cells of the innate immune system [ 22 ].”
From Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the p53 Tumor Suppressor (2008) · cites this paper as [21]
In the citing paper
“The tumour suppressor p53-p21 axis cell- autonomously controls the OIS response, but additionally mediates communication between senescent cells and immune cells, presumably via the SASP 144-146 .”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [144]
In the citing paper
“Specifically, restoration of Tp53 in mouse models of lymphoma and sarcoma led to tumour regression with features of cellular senescence, thereby implying that p53- mediated apoptosis and senescence- evoked immune clearance are the underlying mechanisms 144 .”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [144]
In the citing paper
“the outcome of endogenous p53 reactivation can be senescence and/or cell death depending on the tumour type 35,141,142”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [35]
In the citing paper
“This notion that p53 is able to activate different checkpoint programs in different tissues is supported by the observation that restoration of endogenous p53 function in p53 null mice activates primarily an apoptotic response to inhibit T-cell lymphomas, while inhibition of sarcomas requires activation of a cellular senescence program60.”
From Telomere dysfunction and tumour suppression: the senescence connection (2008) · cites this paper as [60]
In the citing paper
“In addition, the reactivation of p53-dependent senescence promotes the regression of established p53-deficient tumors, 186 facilitated by SASP-assisted recruitment of innate cells (natural killer [NK] cells and M4) to the tumor bed.187”
From Meta-hallmarks of aging and cancer (2023) · cites this paper as [186]
In the citing paper
“Mouse models clearly demonstrate that the inactivation of p53 promotes tumorigenesis, whereas restoration of p53 causes the regression of established tumours78–80.”
From MDM2, MDMX and p53 in oncogenesis and cancer therapy (2013) · cites this paper as [79]
In the citing paper
“Another recent surprise was the rapid in vivo clearance of tumour cells that undergo P53-triggered senescence 10, 11”
From The common biology of cancer and ageing (2007) · cites this paper as [11]
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“Discussion Knowledge of the mechanisms by which p53 chooses to initiate apoptosis or cell cycle arrest is critical to understanding tumor response on reactivation of p53 (37-39).”
BackgroundDisruption of the GH Receptor Gene in Adult Mice Increases Maximal Lifespan in Females
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Methodp53 dynamics vary between tissues and are linked with radiation sensitivity
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“The p53 gene has been identified as a multifunctional, tumorsuppressing gene and potentially useful in clinical cancer therapy [28].”
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“Despite the prevalence of p53mutations in cancer and clear indications that the restoration of p53 function can be therapeutic, developing drugs with this activity has proven a challenge, as evidenced by the lack of clinically available therapies that target mutant p53 (Ventura et al., 2007; Xue et al., 2007).”
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“Recent reports showed that conditional restoration of p53 in mice with hepatocarcinomas, sarcoma, or lymphoma is able to promote tumor regression (Martins et al., 2006; Xue et al., 2007; Ventura et al., 2007).”
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BackgroundValidation of MdmX as a therapeutic target for reactivating p53 in tumors
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“To analyze the effect of the targeted mutation, we first excised the LSL cassette ex vivo by adding Cre recombinase to p53 MEFs or to p53 MEFs (Ventura et al., 2007) as controls (Figures 2A and 2B).”
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“restoration of tumor suppressor function to mutant forms of p53 (75, 86).”
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Mitochondrial DNA damage induces apoptosis in senescent cells
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Bilateral inhibition of HAUSP deubiquitinase by a viral interferon regulatory factor protein
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“Several recent studies have shown that the restoration of p53 activity alone can robustly induce tumor regressio”
BackgroundChd1 is essential for the high transcriptional output and rapid growth of the mouse epiblast
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Regulation of Metabolic Activity by p53
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Role of curcumin in regulating p53 in breast cancer: an overview of the mechanism of action
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“For example, p53 restoration induces apoptosis in lymphoma, while it causes suppression of cell growth and senescence in sarcoma; these successful results support the research for treating cancer by pharmacological reactivation of p53.(65) In BC, p53 suppression increases a gene expression that encodes Burkitt lymphom…”
ResultProximity-enabled bioreactivity to generate covalent peptide inhibitors of p53–Mdm4
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“…p53 pathway in human cancers and harness its ability to induce cell cycle arrest, senescence, and apoptosis (Martins, Brown-Swigart, & Evan, 2006; Ventura et al., 2007; Xue et al., 2007). p53 activators can generally be grouped into two broad categories depending on the mechanism of action:…”
BackgroundPlasma cell dynamics in the bone marrow niche
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“, 2010), Rosa26-CreERT2 (Ventura et al., 2007), CD4-Cre (Lee et al.”
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“Although the ROSA26 promoter used in the transgene is constitutively active and ubiquitously expressed inmice (20), the presence of the loxP-stop-loxP (LSL) cassette immediately upstream prevents transcription of the MCPyV168 gene until excised by Cre recombinase (21, 22).”
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“, IL15, CSF1, MCP1, CXCL1) released by senescent tumor cells following p53 reactivation promoted tumor eradication by natural killer (NK) cells, neutrophils, and macrophages [60].”
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“E1A/H-Ras V12 transformed MEF FIP200 flox/KI cells were generated as previously described (Wei et al. 2011) and subsequently infected by MSCV.CreERT2. puro or MSCV vector alone (Kumar et al. 2009) to produce transformed FIP200 f/KI ;CreERT2 MEFs, as described previously (Ventura et al. 2007).”
Translational approaches targeting the p53 pathway for anti‐cancer therapy
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“Corroborating this assumption, wt-p53 suppresses tumour growth in a mouse model harbouring a p53 missense mutation (Wang et al., 2011), whereas full tumour regression was seen in a p53-negative tumour model (Ventura et al., 2007).”
Background杉山, 拓., Benitez, C. M., Ghodasara, A., Liu, L., McLean, G. W., Lee, J., Blauwkamp, T. A., Nusse, R., Wright, C. V. E., Gu, G., et al. (2013) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1304507110 · Cited by 76
“Mice harboring the Sox9-eGFP BAC transgene (from Mutant Mouse Regional Resource Center, University of California, Davis), a floxed allele of Ngn3, or the Rosa26CreER transgene were previously described (22, 29, 36, 37).”
BackgroundSUZ12 Promotes Human Epithelial Ovarian Cancer by Suppressing Apoptosis via Silencing HRK
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“microdissected high-grade serous primary ovarian tumor specimens as described previously (21).”
BackgroundRenner, G., Janoušková, H., Noulet, F., Koenig, V., Guérin, É., Bär, S., Nüesch, J. P. F., Rechenmacher, F., Neubauer, S., Kessler, H., et al. (2015) · Cell Death and Differentiation · doi:10.1038/cdd.2015.131 · Cited by 80
“The consequences of p53 activation in tumor cells are variable ranging from cell cycle arrest/senescence and/or apoptosis and the balance between these outcomes determines the tumor regression in a tumor type-dependent way.(22,23) As apoptosis may be preferred over cell cycle arrest/senescence upon p53 reactivation, i…”
BackgroundSox2 Suppresses Gastric Tumorigenesis in Mice
Sarkar, A., Huebner, A. J., Sulahian, R., Anselmo, A. N., Xu, X., Flattery, K., Desai, N., Sebastián, C., Yram, M. A., Arnold, K., et al. (2016) · Cell Reports · doi:10.1016/j.celrep.2016.07.034 · Cited by 76
“RosaCreER (Ventura et al., 2007), Sox2CreER (Arnold et al., 2011), Lgr5GFP-Ires-CreERT2 (Barker et al., 2010), and Apcfl/fl (Colnot et al., 2004) mice have been previously described and were obtained from Jackson Laboratories or provided by K. Haigis.”
Cancer’s Achilles’ Heel: Apoptosis and Necroptosis to the Rescue
Dasgupta, A., Nomura, M., Shuck, R. L., & Yustein, J. T. (2016) · International Journal of Molecular Sciences · doi:10.3390/ijms18010023 · Cited by 78
Regulation of cilia abundance in multiciliated cells
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Pharmacological reactivation of p53 as a strategy to treat cancer
Zawacka‐Pankau, J., & Selivanova, G. (2015) · Journal of Internal Medicine · doi:10.1111/joim.12336 · Cited by 82
The long non-coding RNA MIR31HG regulates the senescence associated secretory phenotype
Montes, M., Lubas, M., Arendrup, F. S., Mentz, B., Rohatgi, N., Tumas, S., Harder, L. M., Skanderup, A. J., Andersen, J., & Lund, A. H. (2021) · Nature Communications · doi:10.1038/s41467-021-22746-4 · Cited by 76
Shumliakivska, M., Luxán, G., Hemmerling, I., Scheller, M., Li, X., Müller-Tidow, C., Schuhmacher, B., Sun, Z., Dendorfer, A., Debes, A., et al. (2024) · Nature Communications · doi:10.1038/s41467-023-43003-w · Cited by 76
Crescenzi, E., Pacifico, F., Lavorgna, A., Palma, R. D., D’Aiuto, E., Palumbo, G. A., Formisano, S., & Leonardi, A. (2011) · Oncogene · doi:10.1038/onc.2011.1 · Cited by 76
“For instance, restoration of endogenous p53 expression in hepatocarcinoma and sarcomas leads to induction of a senescence program that triggers an innate-immune response and in vivo tumor clearance (Ventura et al., 2007; Xue et al., 2007).”
Backgroundp53 DNA Binding Cooperativity Is Essential for Apoptosis and Tumor Suppression In Vivo
Timofeev, O. N., Schlereth, K., Wanzel, M., Braun, A., Nieswandt, B., Pagenstecher, A., Rosenwald, A., Elsässer, H., & Stiewe, T. (2013) · Cell Reports · doi:10.1016/j.celrep.2013.04.008 · Cited by 82
“Reactivation of thewild-type p53 protein in establishedMyc-driven B cell lymphomas led to tumor regression due to apoptosis (Martins et al., 2006; Ventura et al., 2007), whereas in sarcomas and hepatic carcinomas, p53 caused senescence-mediated cessation of tumor growth followed by tumor clearance…”
BackgroundInfluentialDNA damage response to the Mdm2 inhibitor Nutlin-3
Verma, R., Rigatti, M. J., Belinsky, G. S., Godman, C. A., & Giardina, C. A. (2009) · Biochemical Pharmacology · doi:10.1016/j.bcp.2009.09.020 · Cited by 77
Di, X. M., Shiu, R. P. C., Newsham, I., & Gewirtz, D. A. (2009) · Biochemical Pharmacology · doi:10.1016/j.bcp.2008.12.016 · Cited by 76
Advances in the treatment of ovarian cancer: a potential role of antiinflammatory phytochemicals.
Chen, S. S., Michael, A., & Butler-Manuel, S. A. (2012) · PubMed · Cited by 76
Reactivation of mutant p53 by capsaicin, the major constituent of peppers
Garufi, A., Pistritto, G., Cirone, M., & D’Orazi, G. (2016) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-016-0417-9 · Cited by 76
Roles of tumor heterogeneity in the development of drug resistance: A call for precision therapy
Wu, D., Wang, D. C., Cheng, Y., Qian, M., Zhang, M., Shen, Q., & Wang, X. (2016) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2016.11.006 · Cited by 77
Lgr5+ stem and progenitor cells reside at the apex of a heterogeneous embryonic hepatoblast pool
Prior, N., Hindley, C. J., Rost, F., Esteban, E. M., Lau, W. W. Y., Göttgens, B., Rulands, S., Simons, B. D., & Huch, M. (2019) · Development · doi:10.1242/dev.174557 · Cited by 77
Fitz, J., Neumann, T., & Pavri, R. (2018) · The EMBO Journal · doi:10.15252/embj.201797965 · Cited by 74
“We crossed Supt5h Fl/ (cid:1) mouse lines (generated as described in Materials and Methods) with mice expressing Cre-ERT2 constitutively from the Rosa26 locus (Ventura et al , 2007) to generate Supt5h Fl/ (cid:1) Rosa26 Cre-ERT2/+ mice (Fig EV1A).”
Ahamed, M., Alhadlaq, H. A., Khan, M. A. M., & Akhtar, M. J. (2012) · Journal of Nanoparticle Research · doi:10.1007/s11051-012-1225-6 · Cited by 75
“Sophisticated animal models have shown that activation of the p53 response in even advanced tumors can be curative (Ventura et al. 2007; Xue et al. 2007).”
Interaction of the oncogenic miR-21 microRNA and the p53 tumor suppressor pathway
Ma, X., Choudhury, S. N., Xiang, H., Dai, Z., & Li, Y. (2013) · Carcinogenesis · doi:10.1093/carcin/bgt044 · Cited by 76
Targeting protein neddylation: a novel therapeutic strategy for the treatment of cancer
Wang, M., Medeiros, B. C., Erba, H. P., DeAngelo, D. J., Giles, F. J., & Swords, R. T. (2011) · Expert Opinion on Therapeutic Targets · doi:10.1517/14728222.2011.550877 · Cited by 74
“It is well recognized in p53-deficient mice that restoration of activity leads to increased senescence and apoptosis [41-43].”
Background30 years and a long way into p53 research
Hainaut, P. L., & Wiman, K. G. (2009) · The Lancet Oncology · doi:10.1016/s1470-2045(09)70198-6 · Cited by 80
Scheller, M., Ludwig, A. K., Göllner, S., Rohde, C., Krämer, S., Stäble, S., Janssen, M., Müller, J.-A., He, L., Bäumer, N., et al. (2021) · Nature Cancer · doi:10.1038/s43018-021-00213-9 · Cited by 73
Therapeutic targeting of replicative immortality
Yaswen, P., MacKenzie, K. L., Keith, W. N., Hentosh, P., Rodier, F., Zhu, J., Firestone, G. L., Matheu, A., Carnero, A., Bilsland, A. E., et al. (2015) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2015.03.007 · Cited by 82
“Simlar work by others using a mouse osteosarcoma model has also hown that re-expression of endogenous p53 leads to a senescenceike cell-cycle arrest and complete tumor regression [140].”
BackgroundTal, P., Eizenberger, S., Cohen, E., Goldfinger, N., Pietrokovski, S., Oren, M., & Rotter, V. (2016) · Oncotarget · doi:10.18632/oncotarget.7857 · Cited by 73
“Reactivation of p53 has been recently demonstrated as effective and specific for the elimination of tumors [17]: p53ERTAM knock-in (KI) mice reproduce a classical p53 knockout phenotype with a high incidence of spontaneous tumors.”
BackgroundYPEL3, a p53-Regulated Gene that Induces Cellular Senescence
Kelley, K. D., Miller, K. R., Todd, A., Kelley, A. R., Tuttle, R., & Berberich, S. J. (2010) · Cancer Research · doi:10.1158/0008-5472.can-09-3219 · Cited by 73
“Although p53 transcriptional and nontranscriptional mechanisms to induce apoptosis have been linked to tumor inhibition (3), recent in vivo studies have shown that p53dependent cellular senescence represents an important mechanism to block tumor development (4, 5).”
BackgroundThe a“MAZE”ing World of Lung-Specific Transgenic Mice
Rawlins, E. L., & Perl, A. T. (2011) · American Journal of Respiratory Cell and Molecular Biology · doi:10.1165/rcmb.2011-0372ps · Cited by 72
The senescence journey in cancer immunoediting
Zingoni, A., Antonangeli, F., Sozzani, S., Santoni, A., Cippitelli, M., & Soriani, A. (2024) · Molecular Cancer · doi:10.1186/s12943-024-01973-5 · Cited by 77
“Similar findings were reported by others in sarcomas [30].”
ResultCellular senescence: a hitchhiker’s guide
Aravinthan, A. D. (2015) · Human Cell · doi:10.1007/s13577-015-0110-x · Cited by 83
“p16 and p53 are the genes inactivated most commonly in human tumours [192, 193], and induction of senescence through reactivation of p53 in p53-deficient tumours [164, 194] highlights the pivotal role of cellular senescence in tumour suppression.”
Backgroundp53 family members in cancer diagnosis and treatment
Machado-Silva, A., Perrier, S., & Bourdon, J. (2010) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2010.02.005 · Cited by 73
Novel roles of Skp2 E3 ligase in cellular senescence, cancer progression, and metastasis
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Hasegawa, H., Yamada, Y., Iha, H., Tsukasaki, K., Nagai, K., Atogami, S., Sugahara, K., Tsuruda, K., Ishizaki, A., & Kamihira, S. (2009) · Leukemia · doi:10.1038/leu.2009.171 · Cited by 75
UBXN3B positively regulates STING-mediated antiviral immune responses
Yang, L., Wang, L., Ketkar, H., Ma, J., Yang, G., Cui, S., Geng, T., Mordue, D. G., Fujimoto, T., Cheng, G., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-04759-8 · Cited by 73
“We obtained Ubxn3b fl ox/ fl ox (exon 1, homologous recombination) from our collaborator 24 and crossed it with a tamoxifen-inducible Cre mouse line 25,26 , to generate a Cre + / − Ubxn3b fl ox/ fl ox mouse.”
Zhou, Q., Yu, M., Tirado-Magallanes, R., Li, B., Kong, L., Guo, M., Tan, Z. H., Lee, S., Chai, L., Numata, A., et al. (2021) · Nature Communications · doi:10.1038/s41467-020-20282-1 · Cited by 79
Scleraxis is required for the growth of adult tendons in response to mechanical loading
Gumucio, J. P., Schonk, M. M., Kharaz, Y. A., Comerford, E. J., & Mendias, C. L. (2020) · JCI Insight · doi:10.1172/jci.insight.138295 · Cited by 72
The emerging role of p53 in stem cells
Bonizzi, G., Cicalese, A., Insinga, A., & Pelicci, P. G. (2011) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2011.08.002 · Cited by 74
Puzio‐Kuter, A. M., Xu, L., McBrayer, M. K., Dominique, R., Li, H. H., Fahr, B. J., Brown, A. M., Wiebesiek, A. E., Russo, B. M., Mulligan, C. L., et al. (2025) · Cancer Discovery · doi:10.1158/2159-8290.cd-24-1421 · Cited by 75
Beyond effector caspase inhibition
Stegh, A. H., & DePinho, R. A. (2011) · Cell Cycle · doi:10.4161/cc.10.1.14365 · Cited by 72
Aylon, Y., Yabuta, N., Besserglick, H., Buganim, Y., Rotter, V., Nojima, H., & Oren, M. (2009) · Oncogene · doi:10.1038/onc.2009.270 · Cited by 71
Lian, X. J., & Gallouzi, I. (2009) · Journal of Biological Chemistry · doi:10.1074/jbc.m806372200 · Cited by 71
Yanagi, S., Tsubouchi, H., Miura, A., Matsuo, A., Matsumoto, N., & Nakazato, M. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18030503 · Cited by 74
Altered compensatory cytokine signaling underlies the discrepancy between Flt3–/– and Flt3l–/– mice
Durai, V., Bagadia, P., Briseño, C. G., Theisen, D. J., Iwata, A., Davidson, J. T., Gargaro, M., Fremont, D. H., Murphy, T. L., & MURPHY, K. M. M. (2018) · The Journal of Experimental Medicine · doi:10.1084/jem.20171784 · Cited by 70
“, 2006) in WT and Flt3−/− mice using a tamoxifen-inducible Cre recombinase (Ventura et al., 2007).”
MethodLessons from senescence: Chromatin maintenance in non-proliferating cells
Singh, T., & Adams, P. D. (2011) · Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms · doi:10.1016/j.bbagrm.2011.07.014 · Cited by 80
Co-delivery of genes and drugs with nanostructured calcium carbonate for cancer therapy
Chen, S., Zhao, D. M., Li, F., Zhuo, R., & Cheng, S. (2012) · RSC Advances · doi:10.1039/c1ra00527h · Cited by 69
Wu, P., Hong, S., Veeranki, S., Karkhanis, M. S., Starenki, D., Plaza, J. A., & Park, J. (2013) · Molecular and Cellular Biology · doi:10.1128/mcb.00021-13 · Cited by 71
“Inactivation of p53 is a hallmark of cancer, and its reactivation has been proposed as a novel therapeutic strategy (47, 48).”
BackgroundRegulation of tumor suppressor p53 at the RNA level
Vilborg, A., Wilhelm, M., & Wiman, K. G. (2010) · Journal of Molecular Medicine · doi:10.1007/s00109-010-0609-2 · Cited by 74
“Importantly, restoration of wild-type p53 expression in p53deficient mouse tumors triggers rapid elimination of the tumor through cell cycle arrest, senescence, and/or apoptosis [15, 16 ], supporting the idea that pharmacological p53 reactivation should eradicate tumors with minimal effects on normal cells.”
Background
Metadata
- Authors
- Ventura, A., Kirsch, D. G., McLaughlin, M. E., Tuveson, D. A., Grimm, J., Lintault, L., Newman, J., Reczek, E. E., Weissleder, R., & Jacks, T.
- Affiliations
- Massachusetts Institute of Technology (US)
- Massachusetts General Hospital (US)
- Harvard University (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Jacks, Tyler
- ORCID
- Venue
- Nature
- Published
- 2007-01-24
- Volume
- 445
- Issue
- 7128
- Pages
- 661-665
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2154799239
- Cited by
- 1,820
- References
- 31
- Citations by year
- 2026: 44 · 2025: 78 · 2024: 83 · 2023: 77 · 2022: 96 · 2021: 94 · 2020: 78 · 2019: 83 · 2018: 80 · 2017: 100 · 2016: 95 · 2015: 99 · 2014: 113 · 2013: 108 · 2012: 104
- FWCI
- 60.89
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- p53 reactivation, tumor regression, tumor suppressor, cellular senescence, innate immune response, tumor clearance, oncogene addiction, sarcoma, apoptosis
- MeSH terms
- Alleles, Animals, Cell Division, Disease Models, Animal, Humans, Lymphoma, Neoplasms, Organ Specificity, Sarcoma, Tumor Suppressor Protein p53, Cellular Senescence, Apoptosis, Mice
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