IDH1 mutations are closely related to the development and progression of various human cancers, such as glioblastoma, sarcoma, and acute myeloid leukemia.
Continuous administration of DS-1001b impaired tumor growth and decreased 2-HG levels in subcutaneous and intracranial xenograft models derived from a glioblastoma patient with IDH1 mutation.
In application to the glioblastoma dataset from The Cancer Genome Atlas, MHN proposed a novel interaction in line with consecutive biopsies: IDH1 mutations are early events that promote subsequent fixation of TP53 mutations.
The Consortium to Inform Molecular and Practical Approaches to CNS Tumor Taxonomy (cIMPACT-NOW) has recommended that isocitrate dehydrogenase 1 and 2 wildtype (IDH1/2wt) diffuse lower-grade gliomas (LGGs) WHO grade II or III that present with a) a telomerase reverse transcriptase promoter mutation (pTERTmt), and/or b) gain of chromosome 7 combined with loss of chromosome 10, and/or c) epidermal growth factor receptor (EGFR) amplification should be reclassified as diffuse astrocytic glioma, IDH1/2-wildtype, with molecular features of glioblastoma, WHO grade IV (IDH1/2wt astrocytomas WHO IV).
T1+Gad performed best for IDH typing of glioblastoma (sensitivity 91.9%, specificity 100%, AUC 0.945) and ADC for non-Gadolinium-enhancing gliomas (sensitivity 85.7%, specificity 78.4%, AUC 0.877).
We studied the association of immunohistochemical expression of hypoxia inducible factor-1 alpha (HIF-1α), telomerase reverse transcriptase (TERT), isocitrate dehydrogenase 1 (IDH1) and tumor protein p53 with overall survival (OS) in glioblastoma patients uniformly treated by standard of care, with adequate follow-up.
From Jan 2009 to Dec 2016, 161 patients with newly diagnosed IDH-wild type GB were treated with surgery and adjuvant concurrent chemoradiotherapy with the Stupp's regimen, and then genomic research proceeded with their surgical specimens.
Patients with IDH wild type anaplastic astrocytoma and glioblastoma had a significantly shorter median PFS (19.3 months vs. NR, p = 0.001) and median OS (43.5 months vs NR, p = 0.007) than those with IDH mutated grade III anaplastic astrocytoma and oligodendroglioma.
<b>Abbreviations</b>: AAAIR: Average Annual Age-Adjusted Incidence Rate; AI/AN: American Indian or Alaska Native; API: Asian or Pacific Islander; CBTRUS: Central Brain Tumor Registry of the United States; CUMC: Columbia University Medical Center; EOR: Extent of Resection; Exc: Excluded; GBM: Glioblastoma; GTR: Gross Total Resection; IDH-1: Isocitrate Dehydrogenase 1; MGMT: O6-Methylguanine DNA Methyltransferase; NCDB: National Cancer Database; OS: Overall Survival; O/U: Other/Unknown; PFS: Progression-Free Survival; SEER: Surveillance, Epidemiology, and End Results; S&W BTR: Scott & White Brain Tumor Registry; UCLA: University of California Los Angeles; UM: University of Miami.
Widely metastatic IDH1-mutant glioblastoma with oligodendroglial features and atypical molecular findings: a case report and review of current challenges in molecular diagnostics.
GTR and MGMT promoter methylation are independent prognosticators for improved overall and progression-free survival in a homogeneous cohort of newly diagnosed patients with IDH wild-type glioblastoma.
MATH values were increased in patients with glioma with the wild-type isocitrate dehydrogenase (NADP<sup>(+)</sup>) (IDH)1/2 (IDH-wt) gene (P=0.001) and glioblastoma (GBM; P=0.001).
The autoradiographic study shows the entirely higher radioactivity of the U251/IDH1R132H tumor tissue section than that of the U251/IDH1 Wild-type tumor.
Additionally, the concordance of low ALDOC and high non-mutated IDH1 expressions predicted a stronger poor prognosis in glioblastoma patients compared to each of above tests presented alone.
Enrichment analyses of intragenic DNA methylation profiles with epigenetic signatures prioritized the intragenic DNA methylation of ZMIZ1 as a possible glioblastoma prognostic marker that is independent of MGMT methylation in IDH1 wild-type patients.
TMZ-naïve hypermutated tumors were marked by absence of IDH1 somatic mutation and MGMT promoter (pMGMT) methylation, two genomic traits that were significantly associated with the TMZ-induced hypermutagenic event in glioblastoma, and harbored inherited alterations in the mismatch repair (MMR) machinery.
An analysis of 2589 patient samples showed that CLEC5A expression is higher in (1) glioblastoma than in lower-grade glioma and nontumor tissue, (2) in the mesenchymal subtype than in other subtypes, and (3) in IDH1-wild type glioblastoma than in IDH1-mutated glioblastoma.
Recent DNA methylation analyses revealed a small group of IDH mutant diffuse gliomas exhibiting decreased DNA hypermethylation resulting in substantial unfavorable prognosis comparable to glioblastoma.
In this study, we compared the two groups of survival outliers of glioblastoma with IDH wild-type, consisting of the glioblastoma patients who lived longer than 3 years (n = 17) and the patients who lived less than 1 year (n = 12) in terms of genome-wide DNA methylation profile.