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Cited by 42Immunotherapy and Immune ResponsesHistone Deacetylase Inhibitors ResearchCancer Immunotherapy and Biomarkers

An epigenetically altered tumor cell vaccine

Open access
Khan, A.NazmulH., Magner, WilliamJ., Tomasi, ThomasB.·2004·Cancer Immunology, Immunotherapy
DOI 10.1007/s00262-004-0513-0PMC PMC11032794
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Abstract

Functional inactivation of genes critical to immunity may occur by mutation and/or by repression, the latter being potentially reversible with agents that modify chromatin. This study was constructed to determine whether reversal of gene silencing, by altering the acetylation status of chromatin, might lead to an effective tumor vaccine. We show that the expression of selected genes important to tumor immunity, including MHC class II, CD40, and B7-1/2 are altered by treating tumor cells in vitro with a histone deacetylase inhibitor, trichostatin A (TSA). Tumor cells treated in vitro with TSA showed delayed onset and rate of tumor growth in 70% of the J558 plasmacytoma and 100% of the B16 melanoma injected animals. Long-term tumor specific immunity was elicited to rechallenge with wild-type cells in approximately 30% in both tumor models. Splenic T cells from immune mice lysed untreated tumor cells, and SCID mice did not manifest immunity, suggesting that T cells may be involved in immunity. We hypothesize that repression of immune genes is involved in the evasion of immunity by tumors and suggest that epigenetically altered cancer cells should be further explored as a strategy for the induction of tumor immunity.

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  • HDAC inhibitors changed immunogenicity and enhanced antitumor immunity via decreasing MDSC ratio and upregulating MHC-I/II, CD40, CD80, and CD86 expression.

    “Beyond direct cytotoxicity, histone deacetylases (HDAC) inhibitors changed immunogenicity and enhanced antitumor immunity, via decreasing MDSC ratio and upregulating MHC-I/II, CD40, CD80, and CD86 expression [326–328].”

    From Combination strategies with PD-1/PD-L1 blockade: current advances and future directions (2022) · cites this paper as [328]

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Research works printed but not linked: 7

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Authors
Khan, A. N., Magner, W., & Tomasi, T.
Affiliations
Roswell Park Comprehensive Cancer Center (US)
Venue
Cancer Immunology, Immunotherapy
Publisher
Springer Science and Business Media LLC
Published
2004-02-28
Volume
53
Issue
8
Pages
748-54
ISSN
  • 0340-7004 (ISSN-L)
  • 1432-0851
DOI
10.1007/s00262-004-0513-0
PMC
PMC11032794
OpenAlex
W2008755866
Cited by
42
References
25
Citations by year
2026: 1 · 2022: 1 · 2021: 1 · 2019: 2 · 2018: 3 · 2017: 3 · 2016: 3 · 2015: 1 · 2013: 3 · 2012: 1
FWCI
1.56
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • Cancer Immunology Immunotherapy (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Cancer Institute (P30CA016056)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD017013)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Histone Deacetylase Inhibitors Research
  • Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
Keywords
tumor cell vaccine, epigenetic silencing, histone deacetylase inhibitors, trichostatin A, chromatin acetylation, tumor immune evasion, MHC class II, CD40, B16 melanoma, tumor-specific immunity, T cell immunity, SCID mice
MeSH terms
Animals, Histocompatibility Antigens Class II, Cell Division, Enzyme Inhibitors, Genes, MHC Class II, Genes, MHC Class I, Humans, Hydroxamic Acids, Mammary Neoplasms, Experimental, Melanoma, Experimental, Membrane Glycoproteins, Mice, Inbred BALB C, Mice, Inbred C57BL, Plasmacytoma, Spleen, T-Lymphocytes, Cytotoxic, Tumor Cells, Cultured, Antigens, CD, Survival Rate, Mice, SCID, B7-1 Antigen, CD40 Antigens, Cancer Vaccines, Mice, B7-2 Antigen, Histone Deacetylase Inhibitors

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