3 results match your criteria: "The George Washington University Cancer Center (GWCC)[Affiliation]"

Article Synopsis
  • Transposable elements (TEs) are usually silenced in healthy tissues by DNA methylation but become more active in various cancers, correlating with global hypomethylation in those cancer genomes.
  • The study examined TE expression and DNA methylation during the transformation of fibroblast cells, showing that TE expression significantly increased at each transformation stage, particularly after the final stage, mirroring observations in human tumors.
  • The research highlighted that hypomethylation of TEs started during the immortalization phase and continued into the transformation, with many upregulated TEs being linked to cancers in The Cancer Genome Atlas dataset.
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Epigenetically programmed resistance to chemo- and immuno-therapies.

Adv Cancer Res

March 2023

The George Washington University Cancer Center (GWCC), Washington, DC, United States; Department of Microbiology, Immunology & Tropical Medicine, The George Washington University, Washington, DC, United States. Electronic address:

Resistance to cancer treatments remains a major barrier in developing cancer cures. While promising combination chemotherapy treatments and novel immunotherapies have improved patient outcomes, resistance to these treatments remains poorly understood. New insights into the dysregulation of the epigenome show how it promotes tumor growth and resistance to therapy.

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Epithelial ovarian carcinomas are particularly deadly due to intratumoral heterogeneity, resistance to standard-of-care therapies, and poor response to alternative treatments such as immunotherapy. Targeting the ovarian carcinoma epigenome with DNA methyltransferase inhibitors (DNMTi) or histone deacetylase inhibitors (HDACi) increases immune signaling and recruits CD8 T cells and natural killer cells to fight ovarian carcinoma in murine models. This increased immune activity is caused by increased transcription of repetitive elements (RE) that form double-stranded RNA (dsRNA) and trigger an IFN response.

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