Alireza Heidari
Diffuse gliomas are the most mundane adult primary encephalon tumors, the majority of which are glioblastomas. Albeit cancer of the encephalon is relatively infrequent, representing only remotely more than 1% of all incipient cancer cases, it is a disproportionately mundane cause of cancer-cognate death and morbidity. The prognosis for patients with glioma is concretely poor due to its infiltrative nature and constrained sensitivity to radiation therapy and chemotherapy. This development was triggered by the apperception of a vigorous and propitious prognostic and predictive effect of the codeletion of chromosomal arms 1p and 19q on overall outcome and sensitivity to chemotherapy, respectively. Next, the major predictive value of methylation of the methylguanine methyltransferase (MGMT) promoter gene for outcome after adjuvant chemotherapy in patients with glioblastoma was reported. The more recent revelation of isocitrate dehydrogenase (IDH) mutations in the immensely colossal majority of grade II and III diffuse
gliomas represented another major step forward in the molecular characterization of gliomas. It was shown that IDH-mutated tumors have a much more auspicious prognosis than do tumors of kindred lineage and grade that express IDH gene wild type (IDHwt) and may even sanction identification of chemotherapy-sensitive subgroups of patients. Authors of more recent research have further refined this concept and have suggested that diffuse gliomas can be characterized as one of three different subtypes, depending on the presence of a handful of molecular markers copy number alterations of chromosomal arms 1p and 19q (in coalescence); chromosomal arm 10q and chromosome 7; and mutational status of the IDH, telomerase reverse transcriptase (TERT), tumor protein p53 (TP53), and α thalassemia/perspicacious incapacitation syndrome X–linked (ATRX) genes. Note that the TERT and ATRX mutations are mutually exclusive and have diagnostic value: TERT mutations are diagnostic of oligodendroglioma (with 1p19q codeletion) or glioblastoma (without 1p19q codeletion), while TP53 mutations in the presence of IDH mutation are indicative of astrocytoma. This molecular relegation additionally contains more prognostic information than do classic histopathologic evaluation results. According to which lowgrade tumors have a better prognosis than do highgrade tumors. Regardless of tumor grade, however, IDHwttumors, even those that are tenacious to be of low grade at histopathologic evaluation, are, biologically, all of the glioblastoma type (class 3) and have very impecunious prognosis. The WHO tumor grade may retain its prognostic information, albeit perhaps less so in IDH-mutated tumors. Results of studies have shown that, at the molecular level, commixed oligoastrocytomas do not subsist, because the presence or absence of 1p19q codeletion, respectively, relegates the tumor either as an oligodendroglioma or an astrocytoma.