Chromatin state profiling reveals PRC2 inhibition as a therapeutic target in NRAS–mutant melanoma

Recently, we have generated 284 epigenomic maps in melanoma. Using chromatin state profiling we identify an association of NRAS-mutants with bivalent Histone H3 lysine 27 trimethylation (H3K27me3) and broad H3K4me3 domains. Reprogramming of bivalent H3K27me3 occurs on critical invasive-regulators an...

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Autor principal: Terranova, Christopher J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2021
Materias:
Commentary
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8632323/
https://www.ncbi.nlm.nih.gov/pubmed/34859147
http://dx.doi.org/10.1080/23723556.2021.1986350
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author Terranova, Christopher J.
author_facet Terranova, Christopher J.
author_sort Terranova, Christopher J.
collection PubMed
description Recently, we have generated 284 epigenomic maps in melanoma. Using chromatin state profiling we identify an association of NRAS-mutants with bivalent Histone H3 lysine 27 trimethylation (H3K27me3) and broad H3K4me3 domains. Reprogramming of bivalent H3K27me3 occurs on critical invasive-regulators and its resolution using Enhancer of Zeste Homolog 2 (EZH2) inhibition reduces invasive capacity and tumor burden in NRAS-mutant patient samples.
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spelling pubmed-86323232021-12-01 Chromatin state profiling reveals PRC2 inhibition as a therapeutic target in NRAS–mutant melanoma Terranova, Christopher J. Mol Cell Oncol Commentary Recently, we have generated 284 epigenomic maps in melanoma. Using chromatin state profiling we identify an association of NRAS-mutants with bivalent Histone H3 lysine 27 trimethylation (H3K27me3) and broad H3K4me3 domains. Reprogramming of bivalent H3K27me3 occurs on critical invasive-regulators and its resolution using Enhancer of Zeste Homolog 2 (EZH2) inhibition reduces invasive capacity and tumor burden in NRAS-mutant patient samples. Taylor & Francis 2021-10-27 /pmc/articles/PMC8632323/ /pubmed/34859147 http://dx.doi.org/10.1080/23723556.2021.1986350 Text en © 2021 The Author(s). Published with license by Taylor & Francis Group, LLC. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) ), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.
spellingShingle Commentary
Terranova, Christopher J.
Chromatin state profiling reveals PRC2 inhibition as a therapeutic target in NRAS–mutant melanoma
title Chromatin state profiling reveals PRC2 inhibition as a therapeutic target in NRAS–mutant melanoma
title_full Chromatin state profiling reveals PRC2 inhibition as a therapeutic target in NRAS–mutant melanoma
title_fullStr Chromatin state profiling reveals PRC2 inhibition as a therapeutic target in NRAS–mutant melanoma
title_full_unstemmed Chromatin state profiling reveals PRC2 inhibition as a therapeutic target in NRAS–mutant melanoma
title_short Chromatin state profiling reveals PRC2 inhibition as a therapeutic target in NRAS–mutant melanoma
title_sort chromatin state profiling reveals prc2 inhibition as a therapeutic target in nras–mutant melanoma
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8632323/
https://www.ncbi.nlm.nih.gov/pubmed/34859147
http://dx.doi.org/10.1080/23723556.2021.1986350
work_keys_str_mv AT terranovachristopherj chromatinstateprofilingrevealsprc2inhibitionasatherapeutictargetinnrasmutantmelanoma

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