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• W2891802945 abstract "Methylation of cytosine residues exerts a critical role in silencing gene transcription. Importantly, DNA methylation patterns are often altered in cancer, with many tumors showing site-specific gain of methylation marks in a background of global hypomethylation (1).In PNAS, Stone et al. (2) show in an ovarian cancer model that treatment with the demethylating agent 5-azacytidine resulted in reexpression of human endogenous retroviruses (HERVs), activation of type I IFN signaling, and increased CD8+ T cells in the tumor microenvironment. These data provide important insights into the role of DNA methylation in suppressing immunogenic pathways and provide additional support for the notion that hypomethylation can resculpt the host antitumor response through derepression of HERV and activation of type I IFN signaling (3, 4).We hypothesized that such elevated HERV expression and type I IFN signaling are also present in tumors that are characterized by constitutive DNA hypomethylation. Seminoma, a type of testicular germ cell tumor (TGCT), provides an opportunity to test this hypothesis. The majority of seminomas are … [↵][1]1To whom correspondence may be addressed. Email: mhaffne4{at}jhmi.edu or syegnasu{at}jhmi.edu. [1]: #xref-corresp-1-1" @default.
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• W2891802945 date "2018-09-04" @default.
• W2891802945 modified "2023-09-23" @default.
• W2891802945 title "Hypomethylation, endogenous retrovirus expression, and interferon signaling in testicular germ cell tumors" @default.
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• W2891802945 doi "https://doi.org/10.1073/pnas.1803292115" @default.
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