Fig. 7: RAD18 suppresses hypermutation in recurrent GBM patients. | Nature Communications

Fig. 7: RAD18 suppresses hypermutation in recurrent GBM patients.

From: Trans-lesion synthesis and mismatch repair pathway crosstalk defines chemoresistance and hypermutation mechanisms in glioblastoma

Fig. 7

a Scatterplot showing the contribution of Signature 11 mutations to individual tumors from a cohort of TMZ-treated recurrent GBM (rGBM) patients. Tumor samples were stratified by MGMT status and RAD18 expression. RAD18 relative expression was corrected for proliferation and was designated high (upper tertile), medium, or low (lower tertile). Based on accepted convention, tumors harboring >500 signature 11 counts (indicated by the black dashed line) were considered “hypermutation”. b Model describing roles of RAD18, MMR, and MGMT in Hypermutation. (b) was created with BioRender.com.

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