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• W2909470894 abstract "Whereas human subtelomeres are heterochromatic, telomeres exhibit euchromatic marks in most commonly studied human cell lines. The epigenetic marks present in human telomeric regions influence oncogenic processes. Drugs that decrease their genome-wide levels are currently being used or tested in specific cancer therapies. Although epigenetic drugs can challenge cancer by targeting the expression and/or activity of key cellular proteins, they should also compromise oncogenic processes by impairing telomeres function. Clinical trials combining epigenetic drugs among them and with other oncogenic drugs are currently being performed to improve cancer therapies. Studies of telomeric chromatin structure and telomeres dysfunction should help to define the rationale for the combination of such drugs. The integrity of the chromatin associated with telomeric regions, which include telomeres and subtelomeres, is essential for telomeres function and cell viability. Whereas human subtelomeres are heterochromatic, telomeres are labeled with euchromatic marks like H4K20me1 and H3K27ac in most commonly studied human cell lines. The epigenetic marks of human telomeric regions influence oncogenic processes. Indeed, different drugs that decrease their genome-wide levels are currently being used or tested in specific cancer therapies. These drugs can challenge cancer by altering the function of key cellular proteins. However, they should also compromise oncogenic processes by modifying the epigenetic landscape of telomeric regions. We believe that studies of telomeric chromatin structure and telomeres dysfunction should help to design epigenetic therapies for cancer treatment. The integrity of the chromatin associated with telomeric regions, which include telomeres and subtelomeres, is essential for telomeres function and cell viability. Whereas human subtelomeres are heterochromatic, telomeres are labeled with euchromatic marks like H4K20me1 and H3K27ac in most commonly studied human cell lines. The epigenetic marks of human telomeric regions influence oncogenic processes. Indeed, different drugs that decrease their genome-wide levels are currently being used or tested in specific cancer therapies. These drugs can challenge cancer by altering the function of key cellular proteins. However, they should also compromise oncogenic processes by modifying the epigenetic landscape of telomeric regions. We believe that studies of telomeric chromatin structure and telomeres dysfunction should help to design epigenetic therapies for cancer treatment. alternative lengthening of telomeres; a recombinational mechanism that allows telomere maintenance and cancer progression in the absence of telomerase. a protein complex that controls sister chromatid cohesion and other cellular processes including the regulation of transcription and chromatin architecture. a CCCTC-binding factor involved in different cellular processes including the regulation of recombination, transcription, and chromatin architecture. drugs that modify the epigenetic status of cells at genome-wide level. Although only DNA methylation and histone deacetylase inhibitors (HDACi) have been approved to treat cancer, many others are under clinical trials. immune checkpoint blockade; inhibition of T cell regulators that prevents the immune system from attacking cells indiscriminately. Different ICB drugs such as pembrolizumab, nivolumab, atezolizumab, and ipilimumab have already been approved for the treatment of cancer. The 2018 Nobel Prize in Physiology and Medicine has acknowledged ICB therapy. a prominent tumor suppressor protein involved in DNA damage sensing, cell cycle arrest, and DNA repair as well as in the entry into senescence or apoptotic pathways, thus preventing malignant transformation. a three-stranded nucleic acid structure in which RNA invades double-stranded DNA, generating a DNA–RNA hybrid and the associated single-stranded DNA. R-loops can cause DNA damage and genome instability. a protein complex that binds to telomeres, protects them, and facilitates their replication. It is composed of six proteins in humans (TRF1, TRF2, Rap1, TPP1, TIN2, and POT1). telomere dysfunction-induced foci; telomeres associated with DNA damage response proteins as visualized by microscopy. They reflect DNA damage at telomeric regions. telomere position effect; silencing of transcription by subtelomeric heterochromatin. telomere sister chromatid exchange; exchange of telomeric sequences between two sister chromatids primarily by homologous recombination as a result of DNA damage at telomeric regions." @default.
• W2909470894 created "2019-01-25" @default.
• W2909470894 creator A5023728777 @default.
• W2909470894 creator A5027262389 @default.
• W2909470894 date "2019-04-01" @default.
• W2909470894 modified "2023-09-30" @default.
• W2909470894 title "Targeting Cancer through the Epigenetic Features of Telomeric Regions" @default.
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• W2909470894 doi "https://doi.org/10.1016/j.tcb.2018.12.006" @default.
• W2909470894 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30660503" @default.
• W2909470894 hasPublicationYear "2019" @default.
• W2909470894 type Work @default.

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