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. 2021 Jul 12;10(7):48. doi: 10.1038/s41389-021-00339-6

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — A Schematics showing how DOT1L regulates the H3K79 dimethyl mark and how the pharmacological inhibition of DOT1L via EPZ-5676 leads to suppression of the mark. B EPZ-5676 inhibitor structure and formula. C EPZ-5676 inhibitor studies in clinical trials as reported on ClinicalTrials.gov. D The common names, synonyms, and disease associations of the ovarian cancer cell lines used in this study. E The indicated ovarian cancer cell lines were treated with various concentrations of the DOT1L inhibitor EPZ-5676 for 48 h. H3K79 dimethyl marks were then measured. Histone H3 and ACTINB proteins were measured as loading controls.