Supplementary Figures S1-S14 from Minor Changes in Expression of the Mismatch Repair Protein MSH2 Exert a Major Impact on Glioblastoma Response to Temozolomide

Supplementary Figures S1-S14. p53 levels in p53 knockdown GBM cells (S1); TMZR3 cells obtained from a p53 deficient background display increased ploidy (S2); H2AX activation in temozolomide treated parental and TMZR3 GBM cells (S3); In-cell Host cell reactivation (HCR) assays used to assess the MGMT and MMR repair capacity of GBM cells (S4); MSH6 and MSH2 levels in MSH6 and MSH2 knockdown GBM cells (S5); Cell cycle profiles and quantitation of cell cycle changes in TMZ-treated MSH6 knockdown cells two cell cycle times post-TMZ treatment (S6); Cell cycle profiles and quantitation of cell cycle changes in TMZ-treated MSH2 knockdown cells two cell cycle times post-TMZ treatment (S7); Minor decreases in MSH2 levels correlate with acquired TMZ resistance in LN229 and A172 GBM cells (S8); Effects of MSH6 or MSH2 knockdown on the protein level of its dimerization partner (S9); Msh2 knockdown in GL261 glioblastoma cells (S10); Moderate decreases in Msh2 confer a growth advantage to GL261 GBM cells after TMZ, but not BCNU, exposure in vitro (S11); Distribution of patient survival in TMZ treated TCGA GBM patients and effects of MSH2 transcript levels on the survival of TMZ treated patients in the 95th percentile for patient survival after TMZ therapy (S12); Overall survival of GBM patients stratified by MSH3, MLH1 and PMS2 tumor transcript levels (S13); PMS2 transcript levels correlate with increased chromosome 7 copy number (S14).