Fig 1.
Oncoplots of the top 20 somatic mutations in GBM across four independent datasets including CGGA, TCGA, CPTAC, and MAYO-PDX.
Each oncoplot comprises two bar plots, with the top bar plot showing the frequency of different variant classifications across the samples, and the right bar plot indicating the frequencies of various variant classifications in each gene.
Table 1.
Demographic information of four independent GBM datasets.
Fig 2.
Common somatic mutations were observed in four independent GBM datasets including CGGA, TCGA, CPTAC, and MAYO-PDX.
a) A Venn-diagram depicting the overlap and unique somatic mutations detected in the four GBM datasets. b) TMB box plots for the 10 commonly mutated genes in GBM datasets, compared to each gene’s wild-type samples. c) Somatic interactions are shown as co-occurrence or mutually exclusive events among the 10 commonly mutated genes in GBM.
Fig 3.
OS Analysis of OBSCN and AHNAK2 mutations in integrated GBM datasets and their association with clinical factors.
a) The Kaplan-Meier curve for OS analysis in OBSCN mutant and wild-type (Wt) GBM patients. b) The Kaplan-Meier curve for OS analysis in AHNAK2 mutant and wild-type (WT) GBM patients c) Univariate Cox regression analysis for OBSCN and/or AHNAK2 mutations versus wild-type GBM patients. d) The Kaplan-Meier curve for GBM patients with OBSCN and AHNAK2 double mutations (Double-Mut) compared to Single-Mut and Double-WT phenotypes. e) TMB levels in Double-WT, Single-Mut and Double-Mut phenotypes based on OBSCN and AHNAK2 statuses. f) The number of GBM patients with AHNAK2 mutation or wild-type status concerning age, gender, and IDH1 mutational status. g) The number of GBM patients with OBSCN mutation or wild-type status concerning age, gender, and IDH1 status. h) The number of GBM patients with OBSCN and AHNAK2 Double-Mut, Single-Mut, and wild-type phenotypes concerning age, gender, and IDH1 status.
Fig 4.
Prediction of drug sensitivity using gene expression data with the pRophetic R package.
(a) Eight potential targeted and chemotherapeutic drugs significantly sensitize OBSCN mutants compared to OBSCN wild-type GBM patients. (b) The associated gene targets for drugs suggested for OBSCN mutations. (c) The effects of OSI.906 and BMS.754807, which are inhibitors of IGF-1R, on GBM patients with OBSCN and AHNAK2 Double-Mut, Single-Mut, and wild-type phenotypes.
Fig 5.
Protein-level analysis of mutations of OBSCN and AHNAK2 genes in GBM patients.
a) A lollipop plot illustrating various OBSCN mutations (missense or nonsense) in different domains of the OBSCN protein. b) A lollipop plot depicting various AHNAK2 mutations (missense, nonsense, or frameshift deletions) throughout the AHNAK2 protein. c) The Kaplan-Meier curve for OS analysis between GBM patients with mutations in different domains of the OBSCN protein. d) The Kaplan-Meier curve for OS analysis in GBM patients with mutations in the immunoglobulin domain of the OBSCN protein compared to patients with mutations in other immunoglobulin-related domains. e) The Kaplan-Meier curve for OS analysis in GBM patients with mutations in different segments of the AHNAK2 protein.