ArticleThe Journal of experimental medicine2001
Point mutation in essential genes with loss or mutation of the second allele: relevance to the retention of tumor-specific antigens.
Article in The Journal of experimental medicine, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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Who cites it
28 citing papers in PubMed, 47 citations in OpenAlex.
- CD4Science immunology · 2024Article
- One CD4+TCR and One CD8+TCR Targeting Autochthonous Neoantigens Are Essential and Sufficient for Tumor Eradication.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- The Transcriptional Landscape ofInternational journal of molecular sciences · 2022Article
- Nonreplicating Adenoviral Vectors: Improving Tropism and Delivery of Cancer Gene Therapy.Cancers · 2021Review
- Loss of CBX2 induces genome instability and senescence-associated chromosomal rearrangements.The Journal of cell biology · 2020Article
- Article
- The ribosome, (slow) beating heart of cancer (stem) cell.Oncogenesis · 2018Review
- 'Final common pathway' of human cancer immunotherapy: targeting random somatic mutations.Nature immunology · 2017Review
- Transfer of Allogeneic CD4+ T Cells Rescues CD8+ T Cells in Anti-PD-L1-Resistant Tumors Leading to Tumor Eradication.Cancer immunology research · 2017Article
- Eradication of Large Solid Tumors by Gene Therapy with a T-Cell Receptor Targeting a Single Cancer-Specific Point Mutation.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Targeting cancer-specific mutations by T cell receptor gene therapy.Current opinion in immunology · 2015Review
- A novel approach to biomarker discovery in head and neck cancer using an autoantibody signature.Oncogene · 2013Article
- Getting personal with neoantigen-based therapeutic cancer vaccines.Cancer immunology research · 2013Article
- Nucleolar trafficking of the mouse mammary tumor virus gag protein induced by interaction with ribosomal protein L9.Journal of virology · 2013Article
- Combined immunotherapy with Listeria monocytogenes-based PSA vaccine and radiation therapy leads to a therapeutic response in a murine model of prostate cancer.Cancer immunology, immunotherapy : CII · 2012Article
- Progression of cancer from indolent to aggressive despite antigen retention and increased expression of interferon-gamma inducible genes.Cancer immunity · 2011Article
- Negative regulation of HDM2 to attenuate p53 degradation by ribosomal protein L26.Nucleic acids research · 2010Article
- Ribosomal versus non-ribosomal cellular antigens: factors determining efficiency of indirect presentation to CD4+ T cells.Immunology · 2010Article
- RPL41, a small ribosomal peptide deregulated in tumors, is essential for mitosis and centrosome integrity.Neoplasia (New York, N.Y.) · 2010Article
- Functional characterization of ribosomal protein L15 from Saccharomyces cerevisiae.Current genetics · 2009Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Antigens that are tumor specific yet retained by tumor cells despite tumor progression offer stable and specific targets for immunologic and possibly other therapeutic interventions. Therefore, we have studied two CD4(+) T cell-recognized tumor-specific antigens that were retained during evolution of two ultraviolet-light-induced murine cancers to more aggressive growth. The antigens are ribosomal proteins altered by somatic tumor-specific point mutations, and the progressor (PRO) variants lack the corresponding normal alleles. In the first tumor, 6132A-PRO, the antigen is encoded by a point-mutated L9 ribosomal protein gene. The tumor lacks the normal L9 allele because of an interstitial deletion from chromosome 5. In the second tumor, 6139B-PRO, both alleles of the L26 gene have point mutations, and each encodes a different tumor-specific CD4(+) T cell-recognized antigen. Thus, for both L9 and L26 genes, we observe "two hit" kinetics commonly observed in genes suppressing tumor growth. Indeed, reintroduction of the lost wild-type L9 allele into the 6132A-PRO variant suppressed the growth of the tumor cells in vivo. Since both L9 and L26 encode proteins essential for ribosomal biogenesis, complete loss of the tumor-specific target antigens in the absence of a normal allele would abrogate tumor growth.
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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.