ArticlePloS one2011
An MSI tumor specific frameshift mutation in a coding microsatellite of MSH3 encodes for HLA-A0201-restricted CD8+ cytotoxic T cell epitopes.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Mechanism of neoantigen generation and advances in neoantigen-based immunotherapies in colorectal cancer.Medical oncology (Northwood, London, England) · 2026Review
- Vaccines for cancer prevention: exploring opportunities and navigating challenges.Nature reviews. Drug discovery · 2025Review
- Neoantigen: A Promising Target for the Immunotherapy of Colorectal Cancer.Disease markers · 2022Review
- Lynch Syndrome and MSI-H Cancers: From Mechanisms to "Off-The-Shelf" Cancer Vaccines.Frontiers in immunology · 2021Review
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- Colorectal cancer vaccines: Tumor-associated antigensWorld journal of gastroenterology · 2018Review
- Presentation of Cryptic Peptides by MHC Class I Is Enhanced by Inflammatory Stimuli.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Opportunities for immunotherapy in microsatellite instable colorectal cancer.Cancer immunology, immunotherapy : CII · 2016Review
- Leveraging premalignant biology for immune-based cancer prevention.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Deficient Mismatch Repair and the Role of Immunotherapy in Metastatic Colorectal Cancer.Current treatment options in oncology · 2016Review
- Viral infection causes a shift in the self peptide repertoire presented by human MHC class I molecules.Proteomics. Clinical applications · 2015Article
- Reactivity against microsatellite instability-induced frameshift mutations in patients with inflammatory bowel disease.World journal of gastroenterology · 2015Article
- Cryptic MHC class I-binding peptides are revealed by aminoglycoside-induced stop codon read-through into the 3' UTR.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Colorectal cancer and immunity: what we know and perspectives.World journal of gastroenterology · 2014Review
- Bilirubin and related tetrapyrroles inhibit food-borne mutagenesis: a mechanism for antigenotoxic action against a model epoxide.Journal of natural products · 2013Article
- Microsatellite instability in hematological malignancies: Hypermutation vs. immune control-who is challenging who?Oncoimmunology · 2013Article
- Towards a vaccine to prevent cancer in Lynch syndrome patients.Familial cancer · 2013Review
- Human endogenous retroviruses and cancer: causality and therapeutic possibilities.World journal of gastroenterology · 2012Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMicrosatellite instability (MSI) resulting from inactivation of the DNA mismatch repair system (MMR) characterizes a highly immunological subtype of colorectal carcinomas. Those tumors express multiple frameshift-mutated proteins which present a unique pool of tumor-specific antigens. The DNA MMR protein MSH3 is frequently mutated in MSI(+) colorectal tumors, thus making it an attractive candidate for T cell-based immunotherapies. METHODOLOGY/PRINCIPAL
findingsFSP-specific CD8(+) T cells were generated from a healthy donor using reverse immunology. Those T cells specifically recognized T2 cells sensitized with the respective peptides. Specific recognition and killing of MSI(+) colorectal carcinoma cells harbouring the mutated reading frame was observed. The results obtained with T cell bulk cultures could be reproduced with T cell clones obtained from the same cultures. Blocking experiments (using antibodies and cold target inhibition) confirmed peptide as well as HLA-A0201-specificity.
conclusionsWe identified two novel HLA-A0201-restricted cytotoxic T cell epitopes derived from a (-1) frameshift mutation of a coding A(8) tract within the MSH3 gene. These were (386)-FLLALWECSL (FSP18) and (387)-LLALWECSL (FSP19) as well as (403)-IVSRTLLLV (FSP23) and (402)-LIVSRTLLLV (FSP31), respectively. These results suggest that MSH3(-1) represents another promising MSI(+)-induced target antigen. By identifying two distinct epitopes within MSH3(-1), the sustained immunogenicity of the frameshift mutated sequence was confirmed. Our data therefore encourage further exploitation of MSH3 as a piece for peptide-based vaccines either for therapeutic or--even more important--preventive purposes.
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