ArticleOncotarget2017
HLA class I loss in metachronous metastases prevents continuous T cell recognition of mutated neoantigens in a human melanoma model.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Cold and hot tumors: immunological determinants, cancer-immunity cycle dysregulation, and nanotechnology-driven therapeutic approaches.Molecular biomedicine · 2026Review
- Peptide Loading Complex in Cancer: From Peptide Translocation, Editing, and Loading into MHC-I to a Potential Therapeutic Target.Current medical science · 2026Review
- Review
- Impaired T cell and neoantigen retention in time-serial analysis of metastatic non-small cell lung cancer in patients unresponsive to TIL cell therapy.Nature cancer · 2025Article
- Programmed Cell Death Ligand 1 (PD-L1) and Major Histocompatibility Complex Class I (MHC Class I) Expression Patterns and Their Pathologic Associations in Triple-Negative Breast Cancer.Breast cancer (Dove Medical Press) · 2025Article
- Primary and acquired resistance to first-line therapy for clear cell renal cell carcinoma.Cancer drug resistance (Alhambra, Calif.) · 2023Review
- Targeting the melanoma-associated antigen CSPG4 with HLA-C*07:01-restricted T-cell receptors.Frontiers in immunology · 2023Article
- Cancer Immunoediting in the Era of Immuno-oncology.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Targeting WEE1/AKT Restores p53-Dependent Natural Killer-Cell Activation to Induce Immune Checkpoint Blockade Responses in "Cold" Melanoma.Cancer immunology research · 2022Article
- Engineering neoantigen vaccines to improve cancer personalized immunotherapy.International journal of biological sciences · 2022Review
- Interaction Between Modern Radiotherapy and Immunotherapy for Metastatic Prostate Cancer.Frontiers in oncology · 2021Review
- Cancer Immune Evasion Through Loss of MHC Class I Antigen Presentation.Frontiers in immunology · 2021Review
- Combination Strategies for Immune-Checkpoint Blockade and Response Prediction by Artificial Intelligence.International journal of molecular sciences · 2020Review
- Parameters for Optoperforation-Induced Killing of Cancer Cells Using Gold Nanoparticles Functionalized With the C-terminal Fragment ofInternational journal of molecular sciences · 2019Article
- Oncolytic adenovirus drives specific immune response generated by a poly-epitope pDNA vaccine encoding melanoma neoantigens into the tumor site.Journal for immunotherapy of cancer · 2019Article
- Next-generation sequencing technologies accelerate advances in T-cell therapy for cancer.Briefings in functional genomics · 2019Review
- Genomic loss of HLA alleles may affect the clinical outcome in low-risk myelodysplastic syndrome patients.Oncotarget · 2018Article
- Identifying neoantigens for use in immunotherapy.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Neoantigen Targeting-Dawn of a New Era in Cancer Immunotherapy?Frontiers in immunology · 2017Review
- Evolution of melanoma cross-resistance to CD8OncoimmunologyArticle
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T lymphocytes against tumor-specific mutated neoantigens can induce tumor regression. Also, the size of the immunogenic cancer mutanome is supposed to correlate with the clinical efficacy of checkpoint inhibition. Herein, we studied the susceptibility of tumor cell lines from lymph node metastases occurring in a melanoma patient over several years towards blood-derived, neoantigen-specific CD8+ T cells. In contrast to a cell line established during early stage III disease, all cell lines generated at later time points from stage IV metastases exhibited partial or complete loss of HLA class I expression. Whole exome and transcriptome sequencing of the four tumor lines and a germline control were applied to identify expressed somatic single nucleotide substitutions (SNS), insertions and deletions (indels). Candidate peptides encoded by these variants and predicted to bind to the patient's HLA class I alleles were synthesized and tested for recognition by autologous mixed lymphocyte-tumor cell cultures (MLTCs). Peptides from four mutated proteins, HERPUD1G161S, INSIG1S238F, MMS22LS437F and PRDM10S1050F, were recognized by MLTC responders and MLTC-derived T cell clones restricted by HLA-A*24:02 or HLA-B*15:01. Intracellular peptide processing was verified with transfectants. All four neoantigens could only be targeted on the cell line generated during early stage III disease. HLA loss variants of any kind were uniformly resistant. These findings corroborate that, although neoantigens represent attractive therapeutic targets, they also contribute to the process of cancer immunoediting as a serious limitation to specific T cell immunotherapy.
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