The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Allele-specific silencing of mutant p53 attenuates dominant-negative and gain-of-function activities
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
“a specific deoxyribozyme (DZ-249A) has been designed to target the mutation site of TP53 to degrade the mRNA of mutant TP53, thereby reducing the expression of the mutant p53 protein.551,552”
From Targeting p53 pathways: mechanisms, structures, and advances in therapy (2023) · cites this paper as [552]
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
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
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
Mutant p53 Drives Pancreatic Cancer Metastasis through Cell-Autonomous PDGF Receptor β Signaling
Weissmueller, S., Manchado, E., Saborowski, M., Morris, J. P., Wagenblast, E., Davis, C. A., Moon, S.-H., Pfister, N. T., Tschaharganeh, D. F., Kitzing, T., et al. (2014) · Cell · doi:10.1016/j.cell.2014.01.066 · Cited by 466 · cited 2×
“These p53 mutants frequently show oncogenic gain-of-function (GOF) activities, such as enhanced metastatic potential and drug resistance [5-8].”
BackgroundTranslating p53 into the clinic
Cheok, C. F., Verma, C. S., Baselga, J., & Lane, D. P. (2011) · Nature Reviews Clinical Oncology · doi:10.1038/nrclinonc.2010.174 · Cited by 381
Martinez, L. A., Naguibneva, I., Lehrmann, H., Vervisch, A., Tchénio, T., Lozano, G., & Harel-Bellan, A. (2002) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.222406899 · Cited by 210
Self-citationLipid Nanoparticle Delivery of siRNA to Silence Neuronal Gene Expression in the Brain
Rungta, R. L., Choi, H. B., Lin, P. J., Ko, R. W., Ashby, D., Nair, J., Manoharan, M., Cullis, P. R., & MacVicar, B. A. (2013) · Molecular Therapy—Nucleic Acids · doi:10.1038/mtna.2013.65 · Cited by 165 · cited 1×
“Methodologies that specifically deliver siRNAs into tumors in vivo, such as surface-modified nanoparticle-mediated siRNA delivery, should be further developed to improve the efficacy and specificity of targeted cancer therapies by siRNAs [48-51].”
BackgroundVikhanskaya, F., Lee, M. K., Mazzoletti, M., Broggini, M., & Sabapathy, K. (2007) · Nucleic Acids Research · doi:10.1093/nar/gkm099 · Cited by 145
Resistance acquisition to MDM2 inhibitors
Cinatl, J., Speidel, D., Hardcastle, I., & Michaelis, M. (2014) · Biochemical Society Transactions · doi:10.1042/bst20140035 · Cited by 30
Research works printed but not linked: 48
- McCormick, 2011, Cancer therapy based on oncogene addiction, J Surg Oncol, 103, 464, 10.1002/jso.21749 · DOI
- Boyes, 2014, Oncogene dependency and the potential of targeted RNAi-based anti-cancer therapy, Biochem J, 461, 1, 10.1042/BJ20140173 · DOI
- Levine, 2000, Surfing the p53 network, Nature, 408, 307, 10.1038/35042675 · DOI · Paper page
- Epstein, 1995, The spectrum of mutations at the p53 locus. Evidence for tissue-specific mutagenesis, selection of mutant alleles, and a “gain of function” phenotype, Ann N Y Acad Sci, 768, 111, 10.1111/j.1749-6632.1995.tb12115.x · DOI
- Iwakuma, 2009, Mutant p53 gain of oncogenic function:evidence, mechanism of action and its clinical implications, Fukuoka Igaku Zasshi, 100, 217
- Xie, 2013, Silencing of mutant p53 by siRNA induces cell cycle arrest and apoptosis in human bladder cancer cells, World J Surg Oncol, 11, 22, 10.1186/1477-7819-11-22 · DOI
- Lozano, 2008, The inherent instability of mutant p53 is alleviated by Mdm2 or p16INK4a loss, Genes Dev, 22, 1337, 10.1101/gad.1662908 · DOI · Paper page
- Sacchi, 2006, Mutant p53 gain of function: reduction of tumor malignancy of human cancer cell lines through abrogation of mutant p53 expression, Oncogene, 25, 304, 10.1038/sj.onc.1209026 · DOI · Paper page
- Leong, 2009, Mutant p53 mediates survival of breast cancer cells, Br J Cancer, 101, 1606, 10.1038/sj.bjc.6605335 · DOI · Paper page
- Chen, 2008, Suppression of inhibitor of differentiation 2, a target of mutant p53, is required for gain-of-function mutations, Cancer Res, 68, 6789, 10.1158/0008-5472.CAN-08-0810 · DOI
- Kwok, 2007, p53-R273H gains new function in induction of drug resistance through down-regulation of procaspase-3, Mol Cancer Ther, 6, 1054, 10.1158/1535-7163.MCT-06-0336 · DOI · Paper page
- Watanabe, 2014, V843I, a lung cancer predisposing EGFR mutation, is responsible for resistance to EGFR tyrosine kinase inhibitors, Journal of thoracic oncology, 9, 1377, 10.1097/JTO.0000000000000241 · DOI
- Kaspar, 2008, Single-nucleotide-specific siRNA targeting in a dominant-negative skin model, J Invest Dermatol, 128, 594, 10.1038/sj.jid.5701060 · DOI
- Moore, 2014, Development of allele-specific gene-silencing siRNAs for TGFBI Arg124Cys in lattice corneal dystrophy type I, Invest Ophthalmol Vis Sci, 55, 977, 10.1167/iovs.13-13279 · doi:10.1167/iovs.13-13279
- Paulson, 2003, Allele-specific silencing of dominant disease genes, Proc Natl Acad Sci U S A, 100, 7195, 10.1073/pnas.1231012100 · DOI · Paper page
- Agami, 2002, Stable suppression of tumorigenicity by virus-mediated RNA interference, Cancer Cell, 2, 243, 10.1016/S1535-6108(02)00122-8 · DOI · Paper page
- Lozano, 2004, Gain of function of a p53 hot spot mutation in a mouse model of Li-Fraumeni syndrome, Cell, 119, 861, 10.1016/j.cell.2004.11.006 · DOI · Paper page
- Rangarajan, 2014, Identification of a novel AMPK-PEA15 axis in the anoikis-resistant growth of mammary cells, Breast Cancer Res, 16, 420, 10.1186/s13058-014-0420-z · DOI
- Ayuso-Sacido, 2012, Genomic instability of surgical sample and cancer-initiating cell lines from human glioblastoma, Front Biosci (Landmark Ed), 17, 1469, 10.2741/3998 · DOI
- Birch, 1997, A detailed study of loss of heterozygosity on chromosome 17 in tumours from Li-Fraumeni patients carrying a mutation to the TP53 gene, Oncogene, 14, 865, 10.1038/sj.onc.1201041 · DOI
- Donehower, 2014, Effects of TP53 mutational status on gene expression patterns across 10 human cancer types, J Pathol, 232, 522, 10.1002/path.4321 · DOI
- Donehower, 1998, Retention of wild-type p53 in tumors from p53 heterozygous mice: reduction of p53 dosage can promote cancer formation, EMBO J, 17, 4657, 10.1093/emboj/17.16.4657 · DOI · Paper page
- Vogelstein, 1990, p53 gene mutations occur in combination with 17p allelic deletions as late events in colorectal tumorigenesis, Cancer Res, 50, 7717
- Marks, 1991, Maintenance of p53 alterations throughout breast cancer progression, Cancer Res, 51, 2605
- Iglehart, 1991, p53 alterations in all stages of breast cancer, J Surg Oncol, 48, 260, 10.1002/jso.2930480409 · DOI
- El-Deiry, 2014, Targeting tumor suppressor p53 for cancer therapy: strategies, challenges and opportunities, Current drug targets, 15, 80, 10.2174/1389450114666140106101412 · DOI · Paper page
- Jung, 2010, p53 inhibits tumor cell invasionthe degradation of snail protein in hepatocellular carcinoma, FEBS letters, 584, 2231, 10.1016/j.febslet.2010.04.006 · DOI
- Elledge, 2009, Principles of cancer therapy: oncogene and non-oncogene addiction, Cell, 136, 823, 10.1016/j.cell.2009.02.024 · DOI · Paper page
- Batra, 2011, Activated KrasG(1)(2)D is associated with invasion and metastasis of pancreatic cancer cells through inhibition of E-cadherin, Br J Cancer, 104, 1038, 10.1038/bjc.2011.31 · DOI
- Liu, 2003, Silencing of H-ras gene expression by retrovirus-mediated siRNA decreases transformation efficiency and tumorgrowth in a model of human ovarian cancer, Oncogene, 22, 5694, 10.1038/sj.onc.1206858 · DOI
- Xiefu, 2014, Knockdown of EGFR inhibits growth and invasion of gastric cancer cells, Cancer Gene Ther, 21, 491, 10.1038/cgt.2014.55 · DOI
- Strebhardt, 2004, Silencing of the HER2/neu gene by siRNA inhibits proliferation and induces apoptosis in HER2/neu-overexpressing breast cancer cells, Neoplasia, 6, 786, 10.1593/neo.04313 · DOI
- Kiessling, 2004, Small interfering RNA (siRNA) inhibits the expression of the Her2/neu gene, upregulates HLA class I and induces apoptosis of Her2/neu positive tumor cell lines, Int J Cancer, 108, 71, 10.1002/ijc.11497 · DOI
- Rotter, 2007, Transcription regulation by mutant p53, Oncogene, 26, 2202, 10.1038/sj.onc.1210294 · DOI · Paper page
- Lozano, 2012, p53-mediated senescence impairs the apoptotic response to chemotherapy and clinical outcome in breast cancer, Cancer Cell, 21, 793, 10.1016/j.ccr.2012.04.027 · DOI · Paper page
- Poon, 2004, How many mutant p53 molecules are needed to inactivate a tetramer?, Mol Cell Biol, 24, 3536, 10.1128/MCB.24.8.3536-3551.2004 · DOI · Paper page
- Carpizo, 2014, Small molecule compounds targeting the p53 pathway: are we finally making progress?, Apoptosis, 19, 1055, 10.1007/s10495-014-0990-3 · DOI · Paper page
- Wiman, 2014, Mutant p53 reactivation by small molecules makes its way to the clinic, FEBS letters, 588, 2622, 10.1016/j.febslet.2014.04.017 · DOI · Paper page
- Fang, 2014, Development of synthetic lethality anticancer therapeutics, J Med Chem, 57, 7859, 10.1021/jm500415t · DOI
- Saini, 2012, RNA interference therapeutics for cancer: challenges and opportunities (review), Mol Med Rep, 6, 9
- Fogal, 2012, Targeted tumor-penetrating siRNA nanocomplexes for credentialing the ovarian cancer oncogene ID4, Sci Transl Med, 4, 147ra112
- He, 2014, Enhanced gene delivery efficiency of cationic liposomes coated with PEGylated hyaluronic acid for anti P-glycoprotein siRNA: A potential candidate for overcoming multi-drug resistance, International journal of pharmaceutics, 477, 590, 10.1016/j.ijpharm.2014.11.012 · DOI
- Harashima, 2014, “Programmed packaging” for gene delivery, J Control Release, 193, 316, 10.1016/j.jconrel.2014.04.023 · DOI
- Wang, 2008, Targeting the MDM2-p53 interaction for cancer therapy, Clin Cancer Res, 14, 5318, 10.1158/1078-0432.CCR-07-5136 · DOI · Paper page
- Rusin, 2013, Nutlin-3a, an MDM2 antagonist and p53 activator, helps to preserve the replicative potential of cancer cells treated with a genotoxic dose of resveratrol, Molecular biology reports, 40, 5013, 10.1007/s11033-013-2602-7 · DOI
- Iwakuma, 2010, CD117 and Stro-1 Identify Osteosarcoma Tumor-Initiating Cells Associated with Metastasis and Drug Resistance, Cancer Res, 70, 4602, 10.1158/0008-5472.CAN-09-3463 · DOI · Paper page
- Lee, 2009, Combined integrin phosphoproteomic analyses and small interfering RNA--based functional screening identify key regulators for cancer cell adhesion and migration, Cancer Res, 69, 3713, 10.1158/0008-5472.CAN-08-2515 · DOI
- Wagner, 2004, Cell cycle arrest and cell death are controlled by p53-dependent and p53-independent mechanisms in Tsg101-deficient cells, J Biol Chem, 279, 35984, 10.1074/jbc.M400408200 · 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
Therapeutic targeting of p53: all mutants are equal, but some mutants are more equal than others
Sabapathy, K., & Lane, D. P. (2018) · Nature Reviews Clinical Oncology · doi:10.1038/nrclinonc.2017.151 · Cited by 517
Drugs Targeting p53 Mutations with FDA Approval and in Clinical Trials
Nishikawa, S., & Iwakuma, T. (2023) · Cancers · doi:10.3390/cancers15020429 · Cited by 115
Self-citation
Metadata
- Authors
- Iyer, S. V., Parrales, A., Begani, P., Narkar, A., Adhikari, A. S., Martinez, L. A., & Iwakuma, T.
- Affiliations
- Department of Cancer Biology, The University of Kansas Cancer Center, University of Kansas Medical Center, Kansas City, KS, USA
- Center for Advanced Preclinical Research, Center for Cancer Research, National Cancer Institute, Frederick, MD, USA
- Department of Pathology, Stony Brook School of Medicine, Stony Brook, NY, USA
- Venue
- Oncotarget
- Publisher
- Impact Journals, LLC
- Published
- 2015-12-16
- Volume
- 7
- Issue
- 5
- Pages
- 5401-5415
- ISSN
- 1949-2553
- Cited by
- 28
- References
- 8
- 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
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Allele-specific silencing of mutant p53 attenuates dominant-negative and gain-of-function activities. https://app.cochat.ai/papers/10.18632/oncotarget.6634
- The paper
- Iyer, S. V., Parrales, A., Begani, P., Narkar, A., Adhikari, A. S., Martinez, L. A., & Iwakuma, T. (2016). Allele-specific silencing of mutant p53 attenuates dominant-negative and gain-of-function activities. Oncotarget. https://doi.org/10.18632/oncotarget.6634
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.