The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.
Tumour suppression by p53: the importance of apoptosis and cellular senescence
Abstract
p53 is regarded as a central player in tumour suppression, as it controls programmed cell death (apoptosis) as well as cellular senescence. While apoptosis eliminates cells at high risk for oncogenic transformation, senescence acts as a barrier to tumourigenesis by imposing irreversible cell cycle arrest. p53 can act directly or indirectly at multiple levels of the tumour suppression network by invoking a myriad of mechanisms. p53 induces the extrinsic and intrinsic apoptotic pathways at multiple steps to ensure an efficient death response. This response involves transcriptional activation or repression of target genes, as well as the recently identified microRNAs, and transcription‐independent functions. Importantly, p53 loss of function is required for tumour maintenance. Therefore, therapeutic strategies aimed at reactivation of p53 in tumours emerge as a promising approach for the treatment of cancer patients. Copyright © 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
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
“DNA damage triggers senescence, a process often referred to as stress-induced premature senescence.83”
From Targeting p53 pathways: mechanisms, structures, and advances in therapy (2023) · cites this paper as [83]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997) · Cell · doi:10.1016/s0092-8674(00)81902-9 · Cited by 5,218 · cited 3×
“Notably, it seems that certain oncogenes, such as Myc, preferentially induce ARF–p53-dependent apoptosis, whereas Ras is a prototypical mediator of senescence in primary fibroblasts [62,89].”
BackgroundIn Vivo Activation of the p53 Pathway by Small-Molecule Antagonists of MDM2
Vassilev, L. T., Vu, B. T., Graves, B., Carvajal, D., Podlaski, F., Filipovic, Z., Kong, N., Kammlott, U., Lukacs, C., Klein, C., et al. (2004) · Science · doi:10.1126/science.1092472 · Cited by 4,661
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A. (1992) · Nature · doi:10.1038/356215a0 · Cited by 4,649
Cellular senescence: when bad things happen to good cells
Campisi, J., & d'Adda di Fagagna, F. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2233 · Cited by 4,441
Blinded by the Light: The Growing Complexity of p53
Vousden, K. H., & Prives, C. (2009) · Cell · doi:10.1016/j.cell.2009.04.037 · Cited by 3,163
A DNA damage checkpoint response in telomere-initiated senescence
Fagagna, F. D. D., Reaper, P. M., Clay-Farrace, L., Fiegler, H., Carr, P., von Zglinicki, T., Saretzki, G., Carter, N. P., & Jackson, S. P. (2003) · Nature · doi:10.1038/nature02118 · Cited by 2,917 · cited 1×
“It is conjectured that telomere erosion beyond a certain limit triggers a DNA damage response and subsequent activation of the ATM/ATR–p53 pathway, resulting in growth arrest [11,12].”
BackgroundSenescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas
Xue, W., Zender, L., Miething, C., Dickins, R. A., Hernando, E., Krizhanovsky, V., Cordon-Cardo, C., & Lowe, S. W. (2007) · Nature · doi:10.1038/nature05529 · Cited by 2,473
Transcriptional control of human p53-regulated genes
Riley, T., Sontag, E., Chen, P., & Levine, A. (2008) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2395 · Cited by 1,921
Restoration of p53 function leads to tumour regression in vivo
Ventura, A., Kirsch, D. G., McLaughlin, M. E., Tuveson, D. A., Grimm, J., Lintault, L., Newman, J., Reczek, E. E., Weissleder, R., & Jacks, T. (2007) · Nature · doi:10.1038/nature05541 · Cited by 1,820 · cited 3×
“Interestingly, restoration of p53 in two types of solid tumour, radiation-induced sarcomas and hepatocellular carcinoma, led to cellular senescence and tumour clearance [105,106].”
BackgroundHerbig, U., Jobling, W. A., Chen, B. P. C., Chen, D. J., & Sedivy, J. M. (2004) · Molecular Cell · doi:10.1016/s1097-2765(04)00256-4 · Cited by 1,344 · cited 1×
“It is conjectured that telomere erosion beyond a certain limit triggers a DNA damage response and subsequent activation of the ATM/ATR–p53 pathway, resulting in growth arrest [11,12].”
Background
Research works printed but not linked: 102
- 10.1038/nature03098 · DOI · Paper page
- 10.1016/S0092-8674(04)01252-8 · DOI · Paper page
- 10.1038/sj.cdd.4401913 · DOI · Paper page
- 10.1038/sj.onc.1202314 · DOI · Paper page
- 10.1016/j.cell.2004.11.006 · DOI · Paper page
- 10.1038/nrm2147 · DOI · Paper page
- 10.1016/S0959-437X(99)00047-7 · DOI · Paper page
- 10.1016/j.ccr.2007.02.026 · DOI · Paper page
- 10.1126/science.1116801 · DOI · Paper page
- 10.1016/j.tcb.2007.07.012 · DOI
- 10.1038/ncb1024 · DOI · Paper page
- 10.1016/S0959-437X(01)00271-4 · DOI
- 10.1016/j.ccr.2005.05.025 · DOI · Paper page
- Harvey M, 1993, In vitro growth characteristics of embryo fibroblasts isolated from p53‐deficient mice, Oncogene, 8, 2457
- 10.1016/S1097-2765(00)80264-6 · DOI · Paper page
- 10.1038/sj.onc.1206439 · DOI
- Roninson IB, 2003, Tumor cell senescence in cancer treatment, Cancer Res, 63, 2705
- 10.1128/MCB.22.10.3497-3508.2002 · DOI · Paper page
- 10.1128/MCB.20.1.273-285.2000 · DOI · Paper page
- 10.1038/sj.onc.1207729 · DOI
- 10.1038/onc.2009.101 · DOI
- 10.1042/bj3320043 · DOI · Paper page
- 10.1016/j.febslet.2007.05.036 · DOI
- 10.4161/cc.2.2.337 · DOI
- 10.1101/gad.14.16.2015 · DOI · Paper page
- 10.1038/35018127 · DOI · Paper page
- 10.1016/S1097-2765(04)00062-0 · DOI · Paper page
- 10.1038/sj.cdd.4401910 · DOI · Paper page
- 10.1126/science.277.5331.1501 · DOI · Paper page
- 10.1074/jbc.M000284200 · DOI · Paper page
- 10.1038/sj.onc.1202667 · DOI · Paper page
- 10.1038/sj.onc.1209989 · DOI
- 10.1016/j.molcel.2004.11.002 · DOI · Paper page
- 10.1111/j.1582-4934.2008.00616.x · DOI
- 10.1038/sj.emboj.7600769 · DOI
- 10.1038/sj.onc.1210148 · DOI
- 10.1074/jbc.M710268200 · DOI
- 10.1002/jcp.1041650324 · DOI
- 10.1038/sj.cdd.4401908 · DOI · Paper page
- 10.2174/156800908783769337 · DOI · Paper page
- 10.1016/j.bbabio.2008.10.005 · DOI · Paper page
- 10.1128/MCB.00738-07 · DOI
- 10.1074/jbc.M802940200 · DOI · Paper page
- 10.1128/MCB.00959-05 · DOI
- 10.4161/cbt.7.12.7460 · DOI
- Maecker HL, 2000, p53 promotes selection for Fas‐mediated apoptotic resistance, Cancer Res, 60, 4638
- 10.1038/38525 · DOI · Paper page
- 10.1016/j.ceb.2005.09.007 · DOI · Paper page
- 10.1074/jbc.275.21.16202 · DOI · Paper page
- 10.1016/S1097-2765(03)00050-9 · DOI · Paper page
- 10.1038/sj.onc.1209641 · DOI
- 10.1158/0008-5472.CAN-05-1084 · DOI
- 10.1128/MCB.24.15.6728-6741.2004 · DOI · Paper page
- 10.1038/ng1093 · DOI · Paper page
- 10.1038/nrc2232 · DOI · Paper page
- 10.1016/j.ccr.2007.10.028 · DOI · Paper page
- 10.1158/0008-5472.CAN-05-3830 · DOI · Paper page
- 10.1038/sj.cdd.4402083 · DOI
- 10.1038/ng2003 · DOI · Paper page
- 10.1038/onc.2008.37 · DOI
- 10.4161/cc.7.2.5236 · DOI
- 10.1016/j.molcel.2006.11.021 · DOI · Paper page
- 10.1093/emboj/18.23.6845 · DOI · Paper page
- 10.1038/ncb714 · DOI · Paper page
- 10.4161/cc.5.23.3526 · DOI
- 10.1016/j.molcel.2007.02.007 · DOI · Paper page
- 10.1038/nsmb1306 · DOI
- 10.1083/jcb.200512059 · DOI · Paper page
- 10.1016/j.cell.2006.09.031 · DOI · Paper page
- 10.1158/0008-5472.CAN-08-0865 · DOI
- 10.1038/443159a · DOI
- 10.1016/j.cell.2007.02.022 · DOI
- 10.1038/sj.bjc.6604098 · DOI
- 10.1097/01.cad.0000217422.52208.fa · DOI
- 10.1016/S0076-6879(05)99041-1 · DOI
- 10.1074/jbc.M410233200 · DOI · Paper page
- 10.1038/nature05194 · DOI · Paper page
- 10.1158/0008-5472.CAN-07-0200 · DOI · Paper page
- 10.1158/0008-5472.CAN-07-2780 · DOI · Paper page
- 10.1158/1541-7786.MCR-07-0161 · DOI
- 10.1158/0008-5472.CAN-06-2710 · DOI · Paper page
- 10.4161/cc.8.11.8596 · DOI
- 10.1038/nm1146 · DOI · Paper page
- 10.1186/1742-4682-2-38 · DOI
- 10.1038/sj.cdd.4402301 · DOI
- 10.1126/science.286.5449.2507 · DOI · Paper page
- 10.1128/MCB.23.6.2171-2181.2003 · DOI · Paper page
- 10.1073/pnas.0604507103 · DOI
- 10.1172/JCI32481 · DOI · Paper page
- 10.1016/S1535-6108(03)00078-3 · DOI · Paper page
- 10.1073/pnas.0802091105 · DOI · Paper page
- 10.1172/JCI28920 · DOI
- 10.1016/S0065-2660(05)54010-0 · DOI
- 10.1089/hum.2005.16.1016 · DOI · Paper page
- 10.1038/cgt.2008.69 · DOI · Paper page
- 10.1215/15228517-2008-015 · DOI
- 10.1158/1535-7163.MCT-07-0395 · DOI
- 10.4161/cc.7.16.6070 · DOI
- 10.4161/cbt.5.11.3300 · doi:10.4161/cbt.5.11.3300
- 10.1016/j.cell.2005.04.032 · DOI
- 10.1101/gad.1162404 · DOI · Paper page
- 10.1016/j.ejca.2006.10.019 · DOI
Cited by
Targeting p53 pathways: mechanisms, structures, and advances in therapy
Wang, H., Guo, M., Wei, H., & Chen, Y. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01347-1 · Cited by 1,016
Interleukin-22 induces hepatic stellate cell senescence and restricts liver fibrosis in mice
Kong, X., Feng, D., Wang, H., Hong, F., Bertola, A., Wang, F.-S., & Gao, B. (2012) · Hepatology · doi:10.1002/hep.25744 · Cited by 448
Programmed cell death in aging
Tower, J. (2015) · Ageing Research Reviews · doi:10.1016/j.arr.2015.04.002 · Cited by 426
MicroRNAs in apoptosis, autophagy and necroptosis
Su, Z., Yang, Z., Xu, Y., Chen, Y., & Yu, Q. (2015) · Oncotarget · doi:10.18632/oncotarget.3523 · Cited by 342
MicroRNA regulation of core apoptosis pathways in cancer
Lima, R. T., Busacca, S., Almeida, G. M., Gaudino, G., Fennell, D. A., & Vasconcelos, M. H. (2011) · European Journal of Cancer · doi:10.1016/j.ejca.2010.11.005 · Cited by 260
Jiang, C., Liu, G., Luckhardt, T., Antony, V., Zhou, Y., Carter, A. B., Thannickal, V. J., & Liu, R. (2017) · Aging Cell · doi:10.1111/acel.12643 · Cited by 234
Apoptosis and aging: increased resistance to apoptosis enhances the aging process
Salminen, A., Ojala, J., & Kaarniranta, K. (2011) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-010-0597-y · Cited by 158
Myeloid-derived suppressor cells (MDSC): an important partner in cellular/tissue senescence
Salminen, A., Kauppinen, A., & Kaarniranta, K. (2018) · Biogerontology · doi:10.1007/s10522-018-9762-8 · Cited by 84
Metadata
- Authors
- Zuckerman, V., Wolyniec, K., Sionov, R. V., Haupt, S., & Haupt, Y.
- Venue
- The Journal of Pathology
- Publisher
- Wiley
- Published
- 2009-06-26
- Volume
- 219
- Issue
- 1
- Pages
- 3-15
- ISSN
- 0022-3417
- 1096-9896
- Cited by
- 170
- References
- 43
- Language
- en
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.