ArticleThe Journal of experimental medicine1998
The sequence alteration associated with a mutational hotspot in p53 protects cells from lysis by cytotoxic T lymphocytes specific for a flanking peptide epitope.
Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 118 citations in OpenAlex.
- Generating p53-specific cytotoxic T lymphocytes by recombinant adenoviral vector-based vaccination in mice, but not man.Gene therapy · 2002Trial
- Neo-Splicetopes in Tumor Therapy: A Lost Case?Frontiers in immunology · 2022Review
- The p53 Saga: Early Steps in the Development of Tumor Immunotherapy.Journal of immunology (Baltimore, Md. : 1950) · 2020Review
- A Potent Tumor-Reactive p53-Specific Single-Chain TCR without On- or Off-Target Autoimmunity In Vivo.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
- Article
- Preventing tumor escape by targeting a post-proteasomal trimming independent epitope.The Journal of experimental medicine · 2016Article
- The T210M Substitution in the HLA-a*02:01 gp100 Epitope Strongly Affects Overall Proteasomal Cleavage Site Usage and Antigen Processing.The Journal of biological chemistry · 2015Article
- INGN-225: a dendritic cell-based p53 vaccine (Ad.p53-DC) in small cell lung cancer: observed association between immune response and enhanced chemotherapy effect.Expert opinion on biological therapy · 2010Review
- Mutation or loss of Wilms' tumor gene 1 (WT1) are not major reasons for immune escape in patients with AML receiving WT1 peptide vaccination.Journal of translational medicine · 2010Article
- Relationship of p53 overexpression on cancers and recognition by anti-p53 T cell receptor-transduced T cells.Human gene therapy · 2008Article
- Development of multi-epitope vaccines targeting wild-type sequence p53 peptides.Expert review of vaccines · 2008Review
- Article
- Recognition of fresh human tumor by human peripheral blood lymphocytes transduced with a bicistronic retroviral vector encoding a murine anti-p53 TCR.Journal of immunology (Baltimore, Md. : 1950) · 2005Article
- Escape mutations alter proteasome processing of major histocompatibility complex class I-restricted epitopes in persistent hepatitis C virus infection.Journal of virology · 2005Article
- Long-term multiepitopic cytotoxic-T-lymphocyte responses induced in chimpanzees by combinations of Plasmodium falciparum liver-stage peptides and lipopeptides.Infection and immunity · 2004Article
- Hepatitis C virus mutation affects proteasomal epitope processing.The Journal of clinical investigation · 2004Article
- The role of p53 in the immunobiology of cutaneous squamous cell carcinoma.Clinical and experimental immunology · 2003Review
- Complementary role of CD4+ T cells and secondary lymphoid tissues for cross-presentation of tumor antigen to CD8+ T cells.The Journal of experimental medicine · 2003Article
- Evidence of a role for CD200 in regulation of immune rejection of leukaemic tumour cells in C57BL/6 mice.Clinical and experimental immunology · 2001Article
- Generation of cytotoxic T cell responses to an HLA-A24 restricted epitope peptide derived from wild-type p53.British journal of cancer · 2001Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
A high proportion of tumors arise due to mutation of the p53 tumor suppressor protein. A p53 hotspot mutation at amino acid position 273 from R to H, flanking a peptide epitope that spans residues 264-272, renders cells resistant to killing by human histocompatibility leukocyte antigen (HLA)-A*0201-restricted cytotoxic T lymphocytes (CTLs) specific for this epitope. Acquisition of the R to H mutation at residue 273 of the human p53 protein promotes tumor growth in vivo by selective escape from recognition by p53.264-272 peptide-specific CTLs. Synthetic 27-mer p53 polypeptides covering the antigenic nonamer region 264-272 of p53 were used as proteasome substrates to investigate whether the R to H mutation at the P1' position of the COOH terminus of the epitope affects proteasome-mediated processing of the protein. Analysis of the generated products by tandem mass spectrometry and the kinetics of polypeptide processing in conjunction with CTL assays demonstrate that the R to H mutation alters proteasomal processing of the p53 protein by inhibiting proteolytic cleavage between residues 272 and 273. This prevents the release of the natural CTL epitope that spans flanking residues 264-272 as well as a putative precursor peptide. These results demonstrate that mutation of p53 not only leads to malignant transformation but may also, in some instances, affect immune surveillance and should be considered in the design of cancer vaccines.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.