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. 2021 Jan 8;10:585551. doi: 10.3389/fonc.2020.585551

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Copyright © 2021 Morris, Wages, Grant, Stukenberg, Gentzler, Hall, Akerley, Varghese, Arnold, Williams, Coppola, Jones, Auble and Mayo

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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MYBL2 High tumors display an elevated DNA damage response and contain defective single-strand break repair pathways. (A) Gene set enrichment analysis (GSEA) revealed that MYBL2 High tumors significantly overexpressed genes involved in the biologic processes shown. (B) MYBL2 High lung adenocarcinoma displayed transcriptional alterations in DNA damage response (DDR) pathways. HR, Homologous recombination; FA, Fanconi anemia; NHEJ, non-homologous end joining; BER, base excision repair; NER, nucleotide excision repair; MMR, mismatch repair; DR, direct repair; TLS, translesion synthesis. (C) Oncoprint profiling of key mismatch repair (MMR) and nucleotide excision repair (NER) genes for MYBL2 High and MYBL2 Low tumors (27).