UV‐induced somatic mutations elicit a functional T cell response in the YUMMER 1.7 mouse melanoma model
Open accessAbstract
Summary: Human melanomas exhibit relatively high somatic mutation burden compared to other malignancies. These somatic mutations may produce neoantigens that are recognized by the immune system, leading to an antitumor response. By irradiating a parental mouse melanoma cell line carrying three driver mutations with UVB and expanding a single‐cell clone, we generated a mutagenized model that exhibits high somatic mutation burden. When inoculated at low cell numbers in immunocompetent C57 BL/6J mice, YUMMER 1.7 (Yale University Mouse Melanoma Exposed to Radiation) regresses after a brief period of growth. This regression phenotype is dependent on T cells as YUMMER 1.7 tumors grow significantly faster in immunodeficient Rag1−/− mice and C57 BL/6J mice depleted of CD 4 and CD 8 T cells. Interestingly, regression can be overcome by injecting higher cell numbers of YUMMER 1.7, which results in tumors that grow without effective rejection. Mice that have previously rejected YUMMER 1.7 tumors develop immunity against higher doses of YUMMER 1.7 tumor challenge. In addition, escaping YUMMER 1.7 tumors are sensitive to anti‐CTLA‐4 and anti‐PD‐1 therapy, establishing a new model for the evaluation of immune checkpoint inhibition and antitumor immune responses.
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The lack of difference in CD8+ T cell infiltration is likely because the BPC GEMM is a poorly immunogenic mouse model, which may preclude immune differences from developing by this time point.
“This is likely because the BPC GEMM is a poorly immunogenic mouse model (26), which may preclude immune differences from developing by this time point.”
From Apolipoprotein E2 Stimulates Protein Synthesis and Promotes Melanoma Progression and Metastasis (2023) · cites this paper as [26]
The Methods identify YUMM1.7 as derived from a melanoma with BrafV600E, Pten−/− and Cdkn2a−/− alterations. The Discussion says YUMM1.7 showed similar growth with or without a functional adaptive immune system, consistent with weak immunogenicity. The paper studies implanted cell-line tumors, however, rather than establishing the immunogenicity of the BPC genetically engineered mouse model itself. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe slower progression in APOE4 versus APOE2 mice was validated in the independent YUMM3.3 model and in the YUMMER1.7 melanoma model.
“We validated these findings in the independent YUMM3.3 model and in the YUMMER1.7 melanoma model, a more immunogenic derivative of the YUMM1.7 model17 (Fig. 1c–d).”
From Common germline variants of the human APOE gene modulate melanoma progression and survival (2020) · cites this paper as [17]
The subcutaneously engrafted BRAFV600E melanoma model is clinically relevant and resistant to immune checkpoint inhibitors.
“We used a subcutaneously engrafted BRAFV600E melanoma model, which is clinically relevant and ICI-resistant23,24.”
From Exercise-induced microbiota metabolite enhances CD8 T cell antitumor immunity promoting immunotherapy efficacy (2025) · cites this paper as [24]
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References 26 · Cited by 199
- Authors
- Wang, J., Perry, C. J., Meeth, K., Thakral, D., Damsky, W., Micevic, G., Kaech, S., Blenman, K., & Bosenberg, M.
- Affiliations
- Yale University (US)
- Corresponding author
- Bosenberg, Marcus
- ORCID
- Venue
- Pigment Cell & Melanoma Research
- Publisher
- Wiley
- Published
- 2017-06-08
- Volume
- 30
- Issue
- 4
- Pages
- 428-435
- ISSN
- 1755-1471 (ISSN-L)
- 1755-148X
- PMC
- PMC5820096
- OpenAlex
- W2604145804
- Cited by
- 199
- References
- 26
- Citations by year
- 2026: 16 · 2025: 29 · 2024: 26 · 2023: 33 · 2022: 23 · 2021: 28 · 2020: 19 · 2019: 16 · 2018: 8 · 2017: 1
- FWCI
- 5.30
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Pigment Cell & Melanoma Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (P01 CA128814, R01 CA196660)
- Melanoma Research Alliance
- Melanoma Research Foundation
- Hervey Foundation
- Topics
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- mouse melanoma, UVB irradiation, somatic mutations, neoantigens, tumor immunogenicity, CTLA-4 blockade, anti-PD-1 therapy, immune checkpoint blockade, tumor regression, CD4 and CD8 T cells, immunocompetent mice
- MeSH terms
- Exome Sequencing, Animals, Disease Models, Animal, Melanoma, Mice, Inbred C57BL, Mitosis, Mutation, T-Lymphocytes, Ultraviolet Rays, Apoptosis, Green Fluorescent Proteins
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