ArticleClinical cancer research : an official journal of the American Association for Cancer Research2014
Genetic evolution of T-cell resistance in the course of melanoma progression.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.
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Who cites it
102 citing papers in PubMed, 166 citations in OpenAlex.
- Mutational and putative neoantigen load predict clinical benefit of adoptive T cell therapy in melanoma.Nature communications · 2017Trial
- Immune landscape of melanoma: Tumor microenvironment, resistance mechanisms, and predictive biomarkers.World journal of clinical oncology · 2026Review
- Mechanisms and therapeutic strategies for immunotherapy resistance in gastric cancer.Cancer cell international · 2025Review
- Primary and Acquired Resistance to Immunotherapy with Checkpoint Inhibitors in NSCLC: From Bedside to Bench and Back.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2025Review
- Pharmacological strategies to overcome immune checkpoint inhibitor resistance in non-small cell lung cancer.Frontiers in oncology · 2025Review
- Loss of p14 diminishes immunogenicity in melanoma via non-canonical Wnt signaling by reducing the peptide surface density.Molecular oncology · 2024Article
- Tumour mutational burden: clinical utility, challenges and emerging improvements.Nature reviews. Clinical oncology · 2024Review
- IFNγ mediates the resistance of tumor cells to distinct NK cell subsets.Journal for immunotherapy of cancer · 2024Article
- DUX4 is a common driver of immune evasion and immunotherapy failure in metastatic cancers.eLife · 2024Article
- Review
- DUX4 is a common driver of immune evasion and immunotherapy failure in metastatic cancers.bioRxiv : the preprint server for biology · 2023Article
- Exploring the Complex and Multifaceted Interplay between Melanoma Cells and the Tumor Microenvironment.International journal of molecular sciences · 2023Review
- Correlation of the tumor escape phenotype with loss of PRELP expression in melanoma.Journal of translational medicine · 2023Article
- Acquired resistance to anti-PD1 therapy in patients with NSCLC associates with immunosuppressive T cell phenotype.Nature communications · 2023Article
- New developments in the mechanism and application of immune checkpoint inhibitors in cancer therapy (Review).International journal of oncology · 2023Review
- Smart drug delivery systems to overcome drug resistance in cancer immunotherapy.Cancer biology & medicine · 2023Review
- Prevalence and Associations of Beta2-Microglobulin Mutations in MSI-H/dMMR Cancers.The oncologist · 2023Article
- Single-cell characterization of anti-LAG-3 and anti-PD-1 combination treatment in patients with melanoma.The Journal of clinical investigation · 2023Article
- Wnt/β-Catenin Signaling and Resistance to Immune Checkpoint Inhibitors: From Non-Small-Cell Lung Cancer to Other Cancers.Biomedicines · 2023Review
- Shaping the Future of Immunotherapy Targets and Biomarkers in Melanoma and Non-Melanoma Cutaneous Cancers.International journal of molecular sciences · 2023Review
42 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 2 countries.
Funding
Abstract
purposeCD8(+) T lymphocytes can kill autologous melanoma cells, but their activity is impaired when poorly immunogenic tumor phenotypes evolve in the course of disease progression. Here, we analyzed three consecutive melanoma lesions obtained within one year of developing stage IV disease for their recognition by autologous T cells. EXPERIMENTAL
designOne skin (Ma-Mel-48a) and two lymph node (Ma-Mel-48b, Ma-Mel-48c) metastases were analyzed for T-cell infiltration. Melanoma cell lines established from the respective lesions were characterized, determining the T-cell-stimulatory capacity, expression of surface molecules involved in T-cell activation, and specific genetic alterations affecting the tumor-T-cell interaction.
resultsMetastases Ma-Mel-48a and Ma-Mel-48b, in contrast with Ma-Mel-48c, were infiltrated by T cells. The T-cell-stimulatory capacity was found to be strong for Ma-Mel-48a, lower for Ma-Mel-48b, and completely abrogated for Ma-Mel-48c cells. The latter proved to be HLA class I-negative due to an inactivating mutation in one allele of the beta-2-microglobulin (B2M) gene and concomitant loss of the other allele by a deletion on chromosome 15q. The same deletion was already present in Ma-Mel-48a and Ma-Mel-48b cells, pointing to an early acquired genetic event predisposing to development of β2m deficiency. Notably, the same chronology of genetic alterations was also observed in a second β2m-deficient melanoma model.
conclusionOur study reveals a progressive loss in melanoma immunogenicity during the course of metastatic disease. The genetic evolvement of T-cell resistance suggests screening tumors for genetic alterations affecting immunogenicity could be clinically relevant in terms of predicting patient responses to T-cell-based immunotherapy.
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Registered trials
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.