FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2904230974> ?p ?o ?g. }

• W2904230974 endingPage "158" @default.
• W2904230974 startingPage "145" @default.
• W2904230974 abstract "In cancer, mutations in noncoding distal regulatory elements and aberrant chromatin remodeling can alter the chromatin interaction landscape, resulting in the dysregulation of gene expression. Chromatin interactions and regulatory elements can potentially serve as diagnostic and predictive biomarkers for epigenetically driven cancers. Chromatin interaction analysis can guide the selection of regulatory elements for genetic and epigenetic editing, as well as identify potential off-target effects. General inhibitors of transcription preferentially target cancer addiction to oncogenes driven by super-enhancers, but their effects on chromatin interactions in off-target normal cells remain to be elucidated. The mechanisms of chromatin interaction formation need to be better understood to translate epigenetic therapies to the clinic safely and effectively. Chromatin interactions regulate gene expression by bringing distal regulatory elements, such as super-enhancers, to promoters in close spatial proximity. It has been recognized that in cancer, chromatin interactions can be dysregulated, leading to aberrant oncogene expression. Chromatin interactions may potentially serve as biomarkers, or be modulated via CRISPR therapy and small molecule inhibitors against transcription. However, these methods face challenges that must be resolved and raise questions for further research. Understanding chromatin interactions is essential for safety aspects of anticancer therapies, such as the mechanism of action of epigenetic regulators and transcription factors in cancer, and potential off-target effects arising from targeting super-enhancers and promoters. In this review article, we discuss how chromatin interactions and regulatory elements may become dysregulated in cancer, potential methods to target them for clinical therapy, and outline outstanding questions that require addressing before epigenetic therapies can translate to the clinic safely and effectively. Chromatin interactions regulate gene expression by bringing distal regulatory elements, such as super-enhancers, to promoters in close spatial proximity. It has been recognized that in cancer, chromatin interactions can be dysregulated, leading to aberrant oncogene expression. Chromatin interactions may potentially serve as biomarkers, or be modulated via CRISPR therapy and small molecule inhibitors against transcription. However, these methods face challenges that must be resolved and raise questions for further research. Understanding chromatin interactions is essential for safety aspects of anticancer therapies, such as the mechanism of action of epigenetic regulators and transcription factors in cancer, and potential off-target effects arising from targeting super-enhancers and promoters. In this review article, we discuss how chromatin interactions and regulatory elements may become dysregulated in cancer, potential methods to target them for clinical therapy, and outline outstanding questions that require addressing before epigenetic therapies can translate to the clinic safely and effectively. the physical interaction between two or more genetic loci in the genome. clustered regularly interspaced short palindromic repeats. CRISPR-associated proteins (CRISPR-Cas) can bind to DNA sequences determined by single-guide RNAs (sgRNAs) through complementary base pairing. distal regulatory region that interacts with gene promoters via long-range chromatin interactions to recruit transcription factors and chromatin remodelers to activate transcription. a category of potentially heritable features that regulates gene expression without involving changes to the DNA sequences. These features include chromatin interactions, histone modifications (such as acetylation and methylation of lysine residues), DNA methylation, nucleosome positioning, and RNA signaling. studies that identify genetic variants, such as SNPs, that occur at higher frequencies in a particular disease compared to the normal population. genomic regions binding proteins that function as barriers to constrain enhancer–promoter interactions. RNA transcripts longer than 200 bases that do not have protein coding function. the localized concentration and interaction between certain cellular components form droplets of higher density that separate from the liquid environment surrounding it, akin to how oil separates from water. proximal regulatory regions upstream of gene transcription start sites that contain binding sites for RNA polymerases and other transcription factors. a distal regulatory region, bound by repressive transcription factors, that represses gene transcription via long-range chromatin interactions to promoters. compartmentalized DNA regions formed via insulator chromatin interactions. TADs show higher intra-region gene interactions and reduced chromatin interactions between two different regions." @default.
• W2904230974 created "2018-12-22" @default.
• W2904230974 creator A5025798085 @default.
• W2904230974 creator A5060729309 @default.
• W2904230974 creator A5087492673 @default.
• W2904230974 date "2019-02-01" @default.
• W2904230974 modified "2023-10-16" @default.
• W2904230974 title "Chromatin Interactions and Regulatory Elements in Cancer: From Bench to Bedside" @default.
• W2904230974 cites W1565385417 @default.
• W2904230974 cites W1859117663 @default.
• W2904230974 cites W1889137377 @default.
• W2904230974 cites W1963175326 @default.
• W2904230974 cites W1969830384 @default.
• W2904230974 cites W1971578941 @default.
• W2904230974 cites W1973062929 @default.
• W2904230974 cites W1978902427 @default.
• W2904230974 cites W1981030303 @default.
• W2904230974 cites W1982875955 @default.
• W2904230974 cites W1985621639 @default.
• W2904230974 cites W2001528153 @default.
• W2904230974 cites W2004966039 @default.
• W2904230974 cites W2009576540 @default.
• W2904230974 cites W2012935431 @default.
• W2904230974 cites W2014787267 @default.
• W2904230974 cites W2016866626 @default.
• W2904230974 cites W2028163659 @default.
• W2904230974 cites W2054609414 @default.
• W2904230974 cites W2060484997 @default.
• W2904230974 cites W2070021921 @default.
• W2904230974 cites W2072684537 @default.
• W2904230974 cites W2073026107 @default.
• W2904230974 cites W2074678156 @default.
• W2904230974 cites W2090037139 @default.
• W2904230974 cites W2090632681 @default.
• W2904230974 cites W2091688007 @default.
• W2904230974 cites W2094160175 @default.
• W2904230974 cites W2101749257 @default.
• W2904230974 cites W2128313472 @default.
• W2904230974 cites W2129237258 @default.
• W2904230974 cites W2140471643 @default.
• W2904230974 cites W2147960762 @default.
• W2904230974 cites W2149765709 @default.
• W2904230974 cites W2152314234 @default.
• W2904230974 cites W2153947250 @default.
• W2904230974 cites W2156988725 @default.
• W2904230974 cites W2158799906 @default.
• W2904230974 cites W2160051211 @default.
• W2904230974 cites W2170846478 @default.
• W2904230974 cites W2171613528 @default.
• W2904230974 cites W2189671405 @default.
• W2904230974 cites W2222531233 @default.
• W2904230974 cites W2224911713 @default.
• W2904230974 cites W2268032794 @default.
• W2904230974 cites W2282923723 @default.
• W2904230974 cites W2294327742 @default.
• W2904230974 cites W2295037017 @default.
• W2904230974 cites W2316895501 @default.
• W2904230974 cites W2324665822 @default.
• W2904230974 cites W2383217883 @default.
• W2904230974 cites W2401568148 @default.
• W2904230974 cites W2416127993 @default.
• W2904230974 cites W2419237034 @default.
• W2904230974 cites W2499687690 @default.
• W2904230974 cites W2521981506 @default.
• W2904230974 cites W2523690171 @default.
• W2904230974 cites W2524890297 @default.
• W2904230974 cites W2546024031 @default.
• W2904230974 cites W2550936880 @default.
• W2904230974 cites W2553838260 @default.
• W2904230974 cites W2556513628 @default.
• W2904230974 cites W2586373162 @default.
• W2904230974 cites W2588654455 @default.
• W2904230974 cites W2593758470 @default.
• W2904230974 cites W2598091501 @default.
• W2904230974 cites W2603000633 @default.
• W2904230974 cites W2607363971 @default.
• W2904230974 cites W2612037027 @default.
• W2904230974 cites W2616964127 @default.
• W2904230974 cites W2618657542 @default.
• W2904230974 cites W2736857446 @default.
• W2904230974 cites W2738259427 @default.
• W2904230974 cites W2739908631 @default.
• W2904230974 cites W2756900458 @default.
• W2904230974 cites W2757422579 @default.
• W2904230974 cites W2761794675 @default.
• W2904230974 cites W2762272043 @default.
• W2904230974 cites W2769418303 @default.
• W2904230974 cites W2774733631 @default.
• W2904230974 cites W2776559018 @default.
• W2904230974 cites W2780843582 @default.
• W2904230974 cites W2786141666 @default.
• W2904230974 cites W2787863806 @default.
• W2904230974 cites W2797313452 @default.
• W2904230974 cites W2797600975 @default.
• W2904230974 cites W2804270751 @default.
• W2904230974 cites W2808076791 @default.
• W2904230974 cites W2809057270 @default.
• W2904230974 cites W2809265915 @default.

• next