Using the NTP method, we classified our GBM patient samples by four subtypes. When we compared xenograft subtypes and those of their parental patient samples, the matching rate was 60%. Although the matching rate was relatively high in the proneural and classical subtype, neural and mesenchymal Nitroprusside disodium dihydrate subtype GBMs showed low matching percent in the corresponding orthotopic xenograft tumors. We expect the reason is tumor microenvironments since the neural and mesenchymal subtype has been reported that they harbor similar gene expressional characteristics with normal neural tissue and stromal tissue, respectively. In the mRNA microarray experiments using surgical samples of patients and orthotopic xenograft tumors, neural and stromal cells need to be included to make influences on the results. Moreover, because the gene expression of tumor cells could be altered in the different tumor environment, the tumor subtype could also be changed. We identified molecular subtype specific drugs using a web database. Using the subtype specific drugs, we performed in vitro limiting dilution assay on patient-derived GBM cells that were primarily cultured from orthotopic GBM xenograft ����AVATAR���� animal models. The subtype specific drug showed significant Scopine HCl inhibitory effects on the in vitro clonogenicity of patient-derived GBM cells. In the case of treating TCGA-subtype specific drugs combined with TMZ on MGMT-unmethylated patient-derived GBM cells provided a synergistic effect inhibiting the clonogenicity. These results display that combining the TCGA molecular subtypes and the other prognostic markers such as MGMT methylation status could be more powerful tool for discriminating GBM patients who could be candidates for personalized therapy. Although EGFR mutations are most frequent in the classical subtype of GBM, gefitinib, an EGFR targeting agent, was unexpectedly selected for the proneural subtype by the web database analyzes in this study. Since EGFR gene alterations including mutations and amplifications are the most prevalent genetic events in GBM and found in.50% of GBM patients, proneural subtype GBMs also harbor EGFR mutations.