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

Figure 6.

Figure 6

MYBL2 High lung adenocarcinoma exhibit significant replication stress, concerted upregulation of MMEJ and HJ-rejection genes, and genomic evidence of error-prone repair. (A) MYBL2 High tumors overexpressed genes involved in replication stress response, ATR/CHK1 checkpoint signaling, and microhomology-mediated end joining (MMEJ) repair. (B) Reverse phase protein array (RPPA) data revealed elevated CHK1 (T-test, two-sided) and phospho-CHK1 (pS345, T-test, two-sided) protein in MYBL2 High tumors (N = 82), compared to MYBL2 Low (N = 91). (C) TCGA MYBL2 High tumors selectively overexpressed genes driving MMEJ and HJ-rejection pathways. (D) COSMIC mutational signature data revealed transcription-coupled nucleotide excision repair (TC-NER, T-test, two-sided) and microhomology mediated end-joining (MMEJ, T-test, two-sided) accounted for significantly greater proportions of mutations in MYBL2 High LUAD (N = 107) (26, 43). Mismatch repair deficiency (MMR Deficiency, T-test, two-sided) accounts for significantly more mutations in MYBL2 Low tumors (N = 140) (43). Lines denote mean mutation contribution per tumor.