Epigenetic mechanisms of tumor resistance to immunotherapy
Open accessAbstract
The recent impact of cancer immunotherapies has firmly established the ability and importance of the immune system to fight malignancies. However, the intimate interaction between the highly dynamic tumor and immune cells leads to a selection process driven by genetic and epigenetic processes. As the molecular pathways of cancer resistance mechanisms to immunotherapy become increasingly known, novel therapeutic targets are being tested in combination with immune-stimulating approaches. We here review recent insights into the molecular mechanisms of tumor resistance with particular emphasis on epigenetic processes and place these in the context of previous models.
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53BP1 is recruited to the site of DNA double strand breaks (DSBs) and binds to specific post-translationally modified histone residues, including H4K20me2, and H3K79me via its tandem Tudor domain.
“p53-binding protein 1 (53BP1) is recruited to the site of DNA double strand breaks (DSBs) and binds to specific post-translationally modified histone residues, including H4K20me2, and H3K79me via its tandem Tudor domain 31,201 .”
From The roles of DNA, RNA and histone methylation in ageing and cancer (2019) · cites this paper as [201]
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References 145 · Cited by 36
- Authors
- Arenas-Ramirez, N., Sahin, D., & Boyman, O.
- Affiliations
- University Hospital Zurich (CH)
- University of Zurich (CH)
- Corresponding author
- Arenas-Ramirez, Natalia
- Boyman, Onur
- Venue
- Cellular and Molecular Life Sciences
- Published
- 2018-08-23
- Volume
- 75
- Issue
- 22
- Pages
- 4163-4176
- ISSN
- 1420-682X (ISSN-L)
- 1420-9071
- PMC
- PMC11105392
- OpenAlex
- W2888721867
- Cited by
- 36
- References
- 145
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 1 · 2023: 4 · 2022: 4 · 2021: 8 · 2020: 4 · 2019: 7 · 2018: 2
- FWCI
- 0.55
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cellular and Molecular Life Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
- Funders
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (310030-172978)
- Swiss Cancer Research grant (KFS-4136-02-2017)
- Hochspezialisierte Medizin Schwerpunkt Immunologie
- Sassella Foundation
- Topics
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- cancer immunotherapy resistance, epigenetic mechanisms, cancer immunotherapy, tumor immune microenvironment, immune evasion, epigenetic regulation, combination therapy
- MeSH terms
- Enhancer of Zeste Homolog 2 Protein, Antigens, Neoplasm, DNA (Cytosine-5-)-Methyltransferases, Histone Deacetylases, Humans, Immunotherapy, Neoplasms, T-Lymphocytes, Drug Resistance, Neoplasm, Epigenesis, Genetic
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