Cited by 220Cancer-related Molecular PathwaysDNA Repair MechanismsChromatin Remodeling and Cancer

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Links between mutant p53 and genomic instability

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Hanel, Walter, Moll, Ute M.·2012·Journal of Cellular Biochemistry

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Abstract

The tumor suppressor p53 has long been known to play a central role in maintaining a stable genome in the face of toxic insults through its role in promoting cell‐cycle checkpoints, DNA repair, and apoptosis. However, p53 null cells still retain some function of certain checkpoint and repair processes, reducing the genomic changes that otherwise would occur if these mechanisms were absent. Accumulating evidence suggests that mutant forms of p53 proteins may drastically perturb these residual genome‐stabilizing mechanisms through gain‐of‐function interactions with multiple proteins leading to a higher level of genomic instability than in p53 null cells. This review summarizes the current body of evidence that mutp53 plays a role in promoting various forms of genomic instability and provides an overview of current mechanistic proposals. J. Cell. Biochem. 113: 433–439, 2012. © 2011 Wiley Periodicals, Inc.

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Genetic instabilities in human cancers
Lengauer, C., Kinzler, K. W., & Vogelstein, B. (1998) · Nature · doi:10.1038/25292 · Cited by 4,168 · cited 5×
“There are four types of genomic instability (IN): subtle sequence instabilities at the nucleotide (NIN) and mismatch (MIN) level, chromosomal instability (CIN), and amplification instability (AIN) [Lengauer et al., 1998].”
BackgroundInfluential
Trp53R172H and KrasG12D cooperate to promote chromosomal instability and widely metastatic pancreatic ductal adenocarcinoma in mice
Hingorani, S. R., Wang, L., Multani, A. S., Combs, C., Deramaudt, T. B., Hruban, R. H., Rustgi, A. K., Chang, S., & Tuveson, D. A. (2005) · Cancer Cell · doi:10.1016/j.ccr.2005.04.023 · Cited by 2,609
Distant metastasis occurs late during the genetic evolution of pancreatic cancer
Yachida, S., Jones, S., Bozic, I., Antal, T., Leary, R., Fu, B., Kamiyama, M., Hruban, R. H., Eshleman, J. R., Nowak, M. A., et al. (2010) · Nature · doi:10.1038/nature09515 · Cited by 2,502
Monoallelically Expressed Gene Related to p53 at 1p36, a Region Frequently Deleted in Neuroblastoma and Other Human Cancers
Kaghad, M., Bonnet, H., Yang, A., Créancier, L., Biscan, J.-C., Valent, A., Minty, A. J., Chalon, P., Lélias, J.-M., Dumont, X., et al. (1997) · Cell · doi:10.1016/s0092-8674(00)80540-1 · Cited by 1,659
Altered cell cycle arrest and gene amplification potential accompany loss of wild-type p53
Livingstone, L. R., White, A., Sprouse, J., Livanos, E., Jacks, T., & Tlsty, T. D. (1992) · Cell · doi:10.1016/0092-8674(92)90243-6 · Cited by 1,328
The patterns and dynamics of genomic instability in metastatic pancreatic cancer
Campbell, P. J., Yachida, S., Mudie, L. J., Stephens, P. J., Pleasance, E. D., Stebbings, L. A., Morsberger, L. A., Latimer, C., McLaren, S., Lin, M.-L., et al. (2010) · Nature · doi:10.1038/nature09460 · Cited by 1,317
Mutant p53 gain of function in two mouse models of Li-Fraumeni syndrome
Olive, K. P., Tuveson, D. A., Ruhe, Z. C., Yin, B., Willis, N. A., Bronson, R. T., Crowley, D., & Jacks, T. (2004) · Cell · doi:10.1016/j.cell.2004.11.004 · Cited by 1,308
Homologous recombination and non‐homologous end‐joining pathways of DNA double‐strand break repair have overlapping roles in the maintenance of chromosomal integrity in vertebrate cells
Takata, M., Sasaki, M. S., Sonoda, E., Morrison, C., Hashimoto, M., Utsumi, H., Yamaguchi‐Iwai, Y., Shinohara, A., & Takeda, S. (1998) · The EMBO Journal · doi:10.1093/emboj/17.18.5497 · Cited by 1,229
Sensing and repairing DNA double-strand breaks
Jackson, S. P. (2002) · Carcinogenesis · doi:10.1093/carcin/23.5.687 · Cited by 1,149
When mutants gain new powers: News from the mutant p53 field
Brosh, R., & Rotter, V. (2009) · Nature Reviews Cancer · doi:10.1038/nrc2693 · Cited by 1,132
Wild-type p53 restores cell cycle control and inhibits gene amplification in cells with mutant p53 alleles
Yin, Y., Tainsky, M. A., Bischoff, F. Z., Strong, L. C., & Wahl, G. M. (1992) · Cell · doi:10.1016/0092-8674(92)90244-7 · Cited by 1,090
Gain of function of a p53 hot spot mutation in a mouse model of Li-Fraumeni syndrome
Lang, G. A., Iwakuma, T., Suh, Y.-A., Liu, G., Rao, V. A., Parant, J. M., Valentin-Vega, Y. A., Terzian, T., Caldwell, L. C., Strong, L. C., et al. (2004) · Cell · doi:10.1016/j.cell.2004.11.006 · Cited by 1,069
p53 gene mutations occur in combination with 17p allelic deletions as late events in colorectal tumorigenesis.
Baker, S. J., Preisinger, A. C., Jessup, J. M., Paraskeva, C., Markowitz, S. D., Willson, J. K. V., Hamilton, S. R., & Vogelstein, B. (1990) · PubMed · Cited by 1,065
Protection of mammalian telomeres
de Lange, T. (2002) · Oncogene · doi:10.1038/sj.onc.1205080 · Cited by 942
Progression model for pancreatic cancer.
Hruban, R. H., Goggins, M., Parsons, J., & Kern, S. E. (2000) · PubMed · Cited by 872
Mutant p53 drives invasion by promoting integrin recycling
Muller, P. A. J., Caswell, P. T., Doyle, B., Iwanicki, M. P., Tan, E. H., Karim, S., Lukashchuk, N., Gillespie, D. A., Ludwig, R. L., Gosselin, P., et al. (2009) · Cell · doi:10.1016/j.cell.2009.11.026 · Cited by 796
A Mutant-p53/Smad Complex Opposes p63 to Empower TGFβ-Induced Metastasis
Adorno, M., Cordenonsi, M., Montagner, M., Dupont, S., Wong, C., Hann, B. C., Solari, A., Bobisse, S., Rondina, M. B., Guzzardo, V., et al. (2009) · Cell · doi:10.1016/j.cell.2009.01.039 · Cited by 794
Oncogenic mutations of the p53 tumor suppressor: the demons of the guardian of the genome.
Sigal, A., & Rotter, V. (2000) · PubMed · Cited by 669
Aneuploidy Affects Proliferation and Spontaneous Immortalization in Mammalian Cells
Williams, B. R., Prabhu, V. R., Hunter, K. E., Glazier, C. M., Whittaker, C. A., Housman, D. E., & Amon, A. (2008) · Science · doi:10.1126/science.1160058 · Cited by 665
The mitochondrial p53 pathway
Vaseva, A. V., & Moll, U. M. (2008) · Biochimica et Biophysica Acta (BBA) - Bioenergetics · doi:10.1016/j.bbabio.2008.10.005 · Cited by 634
Self-citation
Soft tissue sarcomas of adults: state of the translational science.
Borden, E. C., Baker, L. H., Bell, R. S., Bramwell, V. H. C., Demetri, G. D., Eisenberg, B. L., Fletcher, C. D. �., Fletcher, J. A., Ladanyi, M., Meltzer, P. S., et al. (2003) · PubMed · Cited by 612
The clinical value of somatic TP53 gene mutations in 1,794 patients with breast cancer.
Olivier, M., Langer√∏d, A., Carrieri, P., Bergh, J. C. S., Klaar, S., Eyfjord, J. E., Theillet, C. G., Rodríguez, C., Lidereau, R., Bièche, I., et al. (2006) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-05-1029 · Cited by 590
Characterization of the p53-Dependent Postmitotic Checkpoint following Spindle Disruption
Lanni, J. S., & Jacks, T. (1998) · Molecular and Cellular Biology · doi:10.1128/mcb.18.2.1055 · Cited by 493
p53 and its mutants in tumor cell migration and invasion
Muller, P. A. J., Vousden, K. H., & Norman, J. C. (2011) · Journal of Cell Biology · doi:10.1083/jcb.201009059 · Cited by 463
p53 gain-of-function cancer mutants induce genetic instability by inactivating ATM
Song, H., Hollstein, M., & Xu, Y. (2007) · Nature Cell Biology · doi:10.1038/ncb1571 · Cited by 456
p53 polymorphism influences response in cancer chemotherapy via modulation of p73-dependent apoptosis
Bergamaschi, D., Gasco, M., Hiller, L., Sullivan, A., Syed, N., Trigiante, G., Yuluğ, I. G., Merlano, M. C., Numico, G., Comino, A., et al. (2003) · Cancer Cell · doi:10.1016/s1535-6108(03)00079-5 · Cited by 445
Tetraploid State Induces p53-dependent Arrest of Nontransformed Mammalian Cells in G1
Andreassen, P. R., Lohez, O. D., Lacroix, F., & Margolis, R. L. (2001) · Molecular Biology of the Cell · doi:10.1091/mbc.12.5.1315 · Cited by 440
TAp73 knockout shows genomic instability with infertility and tumor suppressor functionsPreprint
Tomasini, R., Tsuchihara, K., Wilhelm, M., Fujitani, M., Rufini, A., Cheung, C. C., Khan, F., Itie-YouTen, A., Wakeham, A. C., Tsao, M., et al. (2008) · Genes & Development · doi:10.1101/gad.1695308 · Cited by 440
Mutant p53 gain of function: differential effects of different p53 mutants on resistance of cultured cells to chemotherapy
Blandino, G., Levine, A. J., & Oren, M. (1999) · Oncogene · doi:10.1038/sj.onc.1202314 · Cited by 439
TAp63 suppresses metastasis through coordinate regulation of Dicer and miRNAs
Su, X., Chakravarti, D., Cho, M. S., Liu, L.-Z., Gi, Y. J., Lin, Y.-L., Leung, M. L., El‐Naggar, A. K., Creighton, C. J., Suraokar, M. B., et al. (2010) · Nature · doi:10.1038/nature09459 · Cited by 429
Unrepaired DNA Breaks in p53-Deficient Cells Lead to Oncogenic Gene Amplification Subsequent to Translocations
Zhu, C., Mills, K. D., Ferguson, D. O., Lee, C., Manis, J., Fleming, J., Gao, Y., Morton, C. C., & Alt, F. W. (2002) · Cell · doi:10.1016/s0092-8674(02)00770-5 · Cited by 421 · cited 1×
“Moreover, enhanced double strand breaks followed by improper repair can also result in gene amplification, particularly in NHEJ deficient cells [Zhu et al., 2002].”
Background
Gain of function of mutant p53: The mutant p53/NF-Y protein complex reveals an aberrant transcriptional mechanism of cell cycle regulation
Di Agostino, S., Strano, S., Emiliozzi, V., Zerbini, V., Mottolese, M., Sacchi, A., Blandino, G., & Piaggio, G. (2006) · Cancer Cell · doi:10.1016/j.ccr.2006.08.013 · Cited by 418
Chemosensitivity linked to p73 function
Irwin, M. S., Kondo, K., Marín, M. C., Cheng, L. S., Hahn, W. C., & Kaelin, W. G. (2003) · Cancer Cell · doi:10.1016/s1535-6108(03)00078-3 · Cited by 406
DNA Ligase IV-Dependent NHEJ of Deprotected Mammalian Telomeres in G1 and G2
Smogorzewska, A., Karlseder, J., Holtgreve-Grez, H., Jauch, A. S., & de Lange, T. (2002) · Current Biology · doi:10.1016/s0960-9822(02)01179-x · Cited by 392
Monoallelic TP53 inactivation is associated with poor prognosis in chronic lymphocytic leukemia: results from a detailed genetic characterization with long-term follow-up
Zenz, T., Kröber, A., Scherer, K., Häbe, S., Bühler, A., Benner, A., Denzel, T., Winkler, D. F. H., Edelmann, J., Schwänen, C., et al. (2008) · Blood · doi:10.1182/blood-2008-04-154070 · Cited by 383
Mre11 Nuclease Activity Has Essential Roles in DNA Repair and Genomic Stability Distinct from ATM Activation
Buis, J. M., Wu, Y., Deng, Y., Leddon, J. L., Westfield, G., Eckersdorff, M., Sekiguchi, J., Chang, S. S., & Ferguson, D. O. (2008) · Cell · doi:10.1016/j.cell.2008.08.015 · Cited by 357
A Pin1/Mutant p53 Axis Promotes Aggressiveness in Breast Cancer
Girardini, J. E., Napoli, M., Piazza, S., Rustighi, A., Marotta, C., Radaelli, E., Capaci, V., Jordan, L. B., Quinlan, P., Thompson, A., et al. (2011) · Cancer Cell · doi:10.1016/j.ccr.2011.06.004 · Cited by 290
Multiple stages and genetic alterations in immortalization, malignant transformation, and tumor progression of human skin keratinocytes
Fusenig, N. E., & Boukamp, P. (1998) · Molecular Carcinogenesis · doi:10.1002/(sici)1098-2744(199811)23:3 · Cited by 287
Centrosome hyperamplification in human cancer: chromosome instability induced by p53 mutation and/or Mdm2 overexpression
Carroll, P. E., Okuda, M., Horn, H. F., Biddinger, P., Stambrook, P. J., Gleich, L. L., Li, Y.-Q., Tarapore, P., & Fukasawa, K. (1999) · Oncogene · doi:10.1038/sj.onc.1202515 · Cited by 279
Homologous and non‐homologous recombination differentially affect DNA damage repair in mice
Essers, J., STEEG, H. V., de Wit, J., Swagemakers, S. M. A., Vermeij, M., Hoeijmakers, J. H. J., & Kanaar, R. (2000) · The EMBO Journal · doi:10.1093/emboj/19.7.1703 · Cited by 247
p73 induction after DNA damage is regulated by checkpoint kinases Chk1 and Chk2Preprint
Urist, M. J., Tanaka, T., Poyurovsky, M. V., & Prives, C. L. (2004) · Genes & Development · doi:10.1101/gad.1221004 · Cited by 245
An oncogenic form of p53 confers a dominant, gain-of-function phenotype that disrupts spindle checkpoint control
Gualberto, A., Aldape, K., Kozakiewicz, K., & Tlsty, T. D. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.9.5166 · Cited by 241
DeltaNp63alpha and TAp63alpha regulate transcription of genes with distinct biological functions in cancer and development.
Wu, G., Nomoto, S., Hoque, M. O., Dracheva, T., Osada, M., Lee, C. R., Dong, S. M., Guo, Z., Benoit, N. E., Cohen, Y., et al. (2003) · PubMed · Cited by 221
Mutant p53 gain of function: reduction of tumor malignancy of human cancer cell lines through abrogation of mutant p53 expression
Bossi, G., Lapi, E., Strano, S., Rinaldo, C., Blandino, G., & Sacchi, A. (2005) · Oncogene · doi:10.1038/sj.onc.1209026 · Cited by 202
The presence of p53 mutations in human osteosarcomas correlates with high levels of genomic instability
Overholtzer, M., Rao, P. H., Favis, R., Lu, X.-Y., Elowitz, M. B., Barany, F., Ladanyi, M., Gorlick, R., & Levine, A. J. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1934852100 · Cited by 193
Loss of p53 and centrosome hyperamplification
Tarapore, P., & Fukasawa, K. (2002) · Oncogene · doi:10.1038/sj.onc.1205707 · Cited by 193
Are interactions with p63 and p73 involved in mutant p53 gain of oncogenic function?
Li, Y., & Prives, C. L. (2007) · Oncogene · doi:10.1038/sj.onc.1210311 · Cited by 174
DNA Damage Detection and Repair Pathways—Recent Advances with Inhibitors of Checkpoint Kinases in Cancer Therapy
Ashwell, S., & Zabludoff, S. (2008) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-07-5138 · Cited by 165
p73 in Cancer
Rufini, A., Agostini, M., Grespi, F., Tomasini, R., Sayan, B. S., Niklison-Chirou, M. V., Conforti, F., Velletri, T., Mastino, A., Mak, T. W., et al. (2011) · Genes & Cancer · doi:10.1177/1947601911408890 · Cited by 151
An inducible mouse model for skin cancer reveals distinct roles for gain- and loss-of-function p53 mutations
Caulı́n, C., Nguyen, T., Lang, G. A., Goepfert, T. M., Brinkley, B. R., Cai, W., Lozano, G., & Roop, D. R. (2007) · Journal of Clinical Investigation · doi:10.1172/jci31721 · Cited by 141
TAp73 regulates the spindle assembly checkpoint by modulating BubR1 activity
Tomasini, R., Tsuchihara, K., Tsuda, C., Lau, S. K., Wilhelm, M., Rufini, A., Tsao, M., Iovanna, J., Jurisicova, A., Melino, G., et al. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0812096106 · Cited by 132
Mre11: roles in DNA repair beyond homologous recombination
Zha, S., Boboilă, C., & Alt, F. W. (2009) · Nature Structural & Molecular Biology · doi:10.1038/nsmb0809-798 · Cited by 102
Quantitative analysis of chromosomal CGH in human breast tumors associates copy number abnormalities with p53 status and patient survival
Jain, A. N., Chin, K., Børresen‐Dale, A., Erikstein, B., Lønning, P. E., Kaaresen, R., & Gray, J. W. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.151241198 · Cited by 93
A gain of function p53 mutant promotes both genomic instability and cell survival in a novel p53‐null mammary epithelial cell mode .
Murphy, K. L., Dennis, A. P., & Rosen, J. M. (2000) · The FASEB Journal · doi:10.1096/fj.00-0128com · Cited by 91
The interaction between p53 and DNA topoisomerase I is regulated differently in cells with wild-type and mutant p53
Gobert, C., Składanowski, A., & Larsen, A. K. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.18.10355 · Cited by 90
A transgenic mouse model for mammary carcinogenesis
Li, B., Murphy, K. L., Laucirica, R., Kittrell, F. S., Medina, D., & Rosen, J. M. (1998) · Oncogene · doi:10.1038/sj.onc.1201621 · Cited by 89
Centrosome amplification as a possible mechanism for numerical chromosome aberrations in cerebral primitive neuroectodermal tumors with TP53 mutations
Weber, R. G., Bridger, J. M., Benner, A., Weisenberger, D., Ehemann, V., Reifenberger, G., & Lichter, P. (1998) · Cytogenetic and Genome Research · doi:10.1159/000015168 · Cited by 88
p53 mutation and loss have different effects on tumourigenesis in a novel mouse model of pleomorphic rhabdomyosarcoma
Doyle, B. J., Morton, J. P., Delaney, D., Ridgway, R. A., Wilkins, J. A., & Sansom, O. J. (2010) · The Journal of Pathology · doi:10.1002/path.2748 · Cited by 88
Transcriptional Control of BubR1 by p53 and Suppression of Centrosome Amplification by BubR1
Oikawa, T., Okuda, M., Ma, Z., Goorha, R. M., Tsujimoto, H., INOKUMA, H., & Fukasawa, K. (2005) · Molecular and Cellular Biology · doi:10.1128/mcb.25.10.4046-4061.2005 · Cited by 68
Cyclin-dependent Kinases Phosphorylate p73 at Threonine 86 in a Cell Cycle-dependent Manner and Negatively Regulate p73
Gaiddon, C., Lokshin, M., Groß, I., Levasseur, D., Taya, Y., Loeffler, J., & Prives, C. L. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m300251200 · Cited by 63
Gain-of-function p53 mutations enhance alteration of the T-cell receptor following X-irradiation, independently of the cell cycle and cell survival.
Iwamoto, K. S., Mizuno, T., Ito, T., Tsuyama, N., Kyoizumi, S., & Seyama, T. (1996) · PubMed · Cited by 57
Induction of gene amplification as a gain-of-function phenotype of mutant p53 proteins.
El-Hizawi, S., Lagowski, J. P., Kulesz-Martin, M. F., & Albor, A. (2002) · PubMed · Cited by 56
p53 Activation in Response to Mitotic Spindle Damage Requires Signaling via BubR1-Mediated Phosphorylation
Ha, G., Baek, K., Kim, H. S., Jeong, S.-J., Kim, C., McKeon, F., & Lee, C. (2007) · Cancer Research · doi:10.1158/0008-5472.can-06-3392 · Cited by 54
Difference in the centrosome duplication regulatory activity among p53 ‘hot spot’ mutants: potential role of Ser 315 phosphorylation-dependent centrosome binding of p53
Tarapore, P., Tokuyama, Y., Horn, H. F., & Fukasawa, K. (2001) · Oncogene · doi:10.1038/sj.onc.1204848 · Cited by 52
Loss of atm sensitises p53-deficient cells to topoisomerase poisons and antimetabolites
Fedier, A., Schlamminger, M., Schwarz, V. A., Haller, U., Howell, S. B., & Fink, D. A. (2003) · Annals of Oncology · doi:10.1093/annonc/mdg240 · Cited by 45
Interference with the p53 family network contributes to the gain of oncogenic function of mutant p53 in hepatocellular carcinoma
Schilling, T., Kairat, A., Melino, G., Krammer, P. H., Stremmel, W., Oren, M., & Müller, M. (2010) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2010.03.082 · Cited by 36
Chromosomal comparative genomic hybridization abnormalities in early- and late-onset human breast cancers: correlation with disease progression and TP53 mutations
Jong, Y.-J., Li, L.-H., Tsou, M.-H., Chen, Y.-J., Cheng, S. H., Wang‐Wuu, S., Tsai, S., Chen, C.-M., Huang, A. T., Hsu, M., et al. (2003) · Cancer Genetics and Cytogenetics · doi:10.1016/s0165-4608(03)00205-x · Cited by 30
Cell cycle and genetic background dependence of the effect of loss of BRCA2 on ionizing radiation sensitivity
Tutt, A. N. J., Connor, F., Bertwistle, D., Kerr, P., Peacock, J., Ross, G., & Ashworth, A. (2003) · Oncogene · doi:10.1038/sj.onc.1206522 · Cited by 30
Transcriptional Regulation by p53 and p73Preprint
Lokshin, M., Tanaka, T., & Prives, C. L. (2005) · Cold Spring Harbor Symposia on Quantitative Biology · doi:10.1101/sqb.2005.70.046 · Cited by 23
p53 mutations indicate a changing clonal evolution in a portion of chronic myelocytic leukemia patients [letter; comment]
Guinn, B., Padua, R. A., Burnett, A. K., & Mills, K. (1994) · Blood · doi:10.1182/blood.v84.10.3591.3591 · Cited by 4

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Authors: Hanel, W., & Moll, U. M.
Affiliations: Stony Brook University (US)
Corresponding author: Moll, Ute M.
ORCID: Hanel, Walter
Moll, Ute M.
Venue: Journal of Cellular Biochemistry
Publisher: Wiley
Published: 2012-01-05
Volume: 113
Issue: 2
Pages: 433-439
ISSN: 0730-2312 (ISSN-L)
1097-4644
DOI: 10.1002/jcb.23400
PMC: PMC4407809
OpenAlex: W1984372257
Cited by: 216
References: 70
Citations by year: 2026: 15 · 2025: 7 · 2024: 14 · 2023: 15 · 2022: 22 · 2021: 12 · 2020: 17 · 2019: 18 · 2018: 22 · 2017: 10 · 2016: 16 · 2015: 14 · 2014: 17 · 2013: 10 · 2012: 7
FWCI: 1.00
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Journal of Cellular Biochemistry (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Cancer Institute (R01CA060664)
National Institute of General Medical Sciences (T32GM008444)
Topics: Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
Keywords: mutant p53, gain-of-function p53, genomic instability, p53 tumor suppressor, cell cycle checkpoints, DNA repair, apoptosis, p53-null cells
MeSH terms: Aneuploidy, Animals, Cell Survival, DNA Damage, Gene Amplification, Humans, Mutation, Neoplasms, Translocation, Genetic, Tumor Suppressor Protein p53, Genomic Instability

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Links between mutant p53 and genomic instability

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