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• W2808902544 endingPage "597" @default.
• W2808902544 startingPage "583" @default.
• W2808902544 abstract "Low response rates to immunotherapy in multiple tumor types highlight the need for improved treatment. Functional inactivation of tumor suppressors and loss of DNA methylation cause misregulation of repetitive genomic elements early in oncogenesis. Tumors employ multiple tolerance strategies to evade negative selection due to decreased fitness and increased immunogenicity. DNA demethylating agents induce viral mimicry beyond a threshold of tolerance and increase cancer immunotherapy response. Tumor-specific compensatory silencing of repeat elements may present a therapeutic opportunity to maximize cancer treatment responses. Tumor-specific compensatory antiviral signaling mechanisms may also present therapeutic opportunities. Nearly half of the human genome is comprised of repetitive elements that are tightly regulated to protect the host genome from deleterious consequences associated with their inappropriate activation. Cancer cells often misexpress these elements, in part, due to decreases in DNA methylation. Recent discoveries suggest that tumor suppressor proteins contribute to repression of repetitive elements, and their functional inactivation promotes repeat element misexpression during carcinogenesis. Recent findings also suggest that increased expression of repetitive elements beyond a threshold of tolerance can augment cancer therapy responses. Such advances, reviewed here, paint a picture in which deregulated expression of repetitive genome elements not only contributes to the development of cancer but may also provide a tumor-specific Achilles heel for cancer treatment. Nearly half of the human genome is comprised of repetitive elements that are tightly regulated to protect the host genome from deleterious consequences associated with their inappropriate activation. Cancer cells often misexpress these elements, in part, due to decreases in DNA methylation. Recent discoveries suggest that tumor suppressor proteins contribute to repression of repetitive elements, and their functional inactivation promotes repeat element misexpression during carcinogenesis. Recent findings also suggest that increased expression of repetitive elements beyond a threshold of tolerance can augment cancer therapy responses. Such advances, reviewed here, paint a picture in which deregulated expression of repetitive genome elements not only contributes to the development of cancer but may also provide a tumor-specific Achilles heel for cancer treatment." @default.
• W2808902544 created "2018-06-29" @default.
• W2808902544 creator A5048967374 @default.
• W2808902544 creator A5049518193 @default.
• W2808902544 creator A5069130022 @default.
• W2808902544 date "2018-08-01" @default.
• W2808902544 modified "2023-10-18" @default.
• W2808902544 title "Deregulation of Retroelements as an Emerging Therapeutic Opportunity in Cancer" @default.
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