“…RESULTS: FTL expression was enriched in high grade glioma (HGG) and its expression significantly associated with IDH1/2 wildtype and unfavorable prognosis of glioma patients. …”
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“…Activating EGFR mutations are common in IDH1 wild-type gliomas. However, the cooperative partners of EGFR driving gliomagenesis remain poorly understood. …”
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“…Clinically, PP occurred more frequently during active antineoplastic treatment, necessitated more steroid‐based interventions, and was associated with glioblastoma (81 vs. 40%), fewer IDH1 mutations, and shorter median overall survival. …”
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“…The molecular markers included GFAP, EMA, MGMT, P53, NeuN, Oligo2, EGFR, VEGF, IDH1, Ki-67, PR, CD3, H3K27M, TS, and 1p/19q status. …”
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“…RESULTS: Strong correlations were noted between mutations in oncogenes and tumor suppressor genes and non-T cell-inflamed tumors with examples including IDH1 and GNAQ as well as less well-known genes including KDM6A, CD11c, and genes with unknown functions. …”
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“…Additionally, deletion of CDKN2A/B, increased IDH1 expression, and decreased ARID1A expression were observed. …”
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“…Individual cases also showed copy number variants of EGFR and nucleotide variants and indels in pTERT, TP53, PIK3R1, AKT2, TSC2, FBXW7, JAK2, MEN1, VHL, IDH1, PTCH1, GNA11, GNAQ, SMARCA4 and CDH1. In addition to thyroidectomy and radioactive iodine, 10 patients received multi-kinase and/or selective kinase inhibitor therapy, with 6 durable, objective responses and 4 with progressive disease. …”
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“…The spatial analysis confirmed a positive spatial autocorrelation global between IDH mortality rates (Moran’s I: 0.633, p < 0.01). …”
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“…In multivariate analysis, the hazard ratio of FCER1G expression (Low versus High) was 0.66 and 95 % CI is 0.54 to 0.79 (P < 0.001), whereas age (HR = 1.26, 95 % CI  1.04–1.52), grade (HR = 2.75, 95 % CI 2.06–3.68), tumor recurrence (HR = 2.17, 95 % CI  1.81–2.62), IDH mutant (HR = 2.46, 95 % CI 1.97–3.01) and chemotherapeutic status (HR = 1.4, 95 % CI  1.20–1.80) are also included. …”
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“…BACKGROUND: Gliosarcoma is a rare variant of IDH- wild type glioblastoma with both glial and mesenchymal differentiation. …”
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“…CA12 expression in glioblastoma significantly correlates with clinically established, molecular markers of IDH1(WT) DNA, WHO grade IV or absence of 1p/19q chromosome arm co-deletion. …”
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“…At least one high-molecular risk mutations were presented in 45.1% (n=51) of patients, with ASXL1 in 38.9% (n=44), SRSF2 in 7.1% (n=8), IDH1/2 in 4.4% (n=5), and EZH2 in 3.5% (n=4) of patients. …”
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“…RESULTS: We identified several currently established diagnostic and prognostic biomarkers of glioma, including TP53 (33%), EGFR (26%), TERT (24%), PTEN (21%), PIK3CA (14%), ATRX (14%), BRAF (13%), and IDH1/2 (6%). Among all genetic aberrations with more than 5% occurrence rate, six mutations and three copy number gains were greatly associated with poor overall survival (univariate, P < 0.1). …”
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“…The novel prognostic nomogram was constructed based on the exo-lncRNA signature, patient age, pharmacotherapy, radiotherapy, IDH mutation status, and MGMT promoter status, with a concordance index of 0.878. …”
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“…In this respect, a lower incidence of intradialytic hypotension (IDH), and hence less tissue injury, may play a role. …”
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“…This study aimed to investigate whether perioperative markers could distinguish and predict PsP from TeP in de novo isocitrate dehydrogenase (IDH) wild-type GBM patients. Methods: New or progressive gadolinium-enhancing lesions that emerged within 12 weeks after CCRT were defined as early progression. …”
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“…We established a hypothetical model to describe the biochemical and molecular network with these specified miRNA/mRNA axes, finding: 1) HHcy causes metabolic reprogramming by increasing glucose uptake and oxidation, by glycogen debranching and NAD(+)/CoA synthesis, and by stimulating mitochondrial reactive oxygen species production via NNT/IDH2 suppression-induced NAD(+)/NADP-NADPH/NADP(+) metabolism disruption; 2) HHcy activates inflammatory responses by activating inflammasome-pyroptosis mainly through ↓miR193b→↑CASP-9 signaling and by inducing IL-1β and adhesion molecules through the ↓miR29c→↑NEDD9 and the ↓miR1256→↑ICAM-1 axes, as well as GPCR and interferon α/β signaling; 3) HHcy promotes cell degradation by the activation of lysosome autophagy and ubiquitin proteasome systems; 4) HHcy causes cell cycle arrest at G1/S and S/G2 transitions, suppresses spindle checkpoint complex and cytokinetic abscission, and suppresses proliferation through ↓miRNA335/↑VASH1 and other axes. …”
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“…Targetable mutations were observed in ERBB2, IDH1, MET, and MAP2K1 (one occurrence each). Mutational landscape of ConjMel characterizes distinct molecular subtypes with oncogenic drivers common with mucosal and skin melanomas. …”
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“…Based on TCGA and CGGA databases, we identified that m6A regulators clusterA could significantly predict better prognosis (p = 0.00016) which enriched in mTOR signaling pathway, basal transcription factors, accompanied by elevated immune cells infiltration, and decreased IDH and TP53 mutations. We also investigated the distribution of differential genes in m6A regulators clusters which was closely associated with tumor immune microenvironment through three independent cohort comparisons. …”
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