Using the example of a recurrent tumor with a 10-year follow-up, the authors show that mutation of the IDH1/2 genes in astrocytomas is not always an early event in the pathogenesis of glioma, that in rare cases a 1p19q codeletion can be found in astrocytomas, and that IDH-mutant tumors can occur in childhood.

DnA methylation has recently been accepted as the most reliable and effective method of diagnosing central nervous system (CNS) tumors. Healthy organs and tumors of different localizations have their own unique methylation structure. Determination of total tumor DNA methylome is the detection of all methylated nucleotides in a tumor. The "gold standard" for analyzing the methylation state of individual cytosines is bisulfite conversion, in which unmethylated cytosines are converted to uracils and read as thymines, while methylated cytosines are protected from conversion.

Glioma metastasis outside the central nervous system is a quite rare phenomenon. The disease in a young woman manifested itself as back pain and loss of vision in the left eye. Magnetic resonance imaging (MRI) revealed a tumor of the optic nerve; positron emission tomography showed multiple secondary bone changes. At the same time, MRI detected no signs of neoplasm in the midline brain structures (the brain stem and subcortical nuclei) and spinal cord. Two biopsies (superior iliac spine trephine biopsy and optic nerve tumor biopsy) were performed. There were similar histological tumors; the optic nerve tumor was found to have K27M mutation in the H3F3A gene, whereas the metastatic tumor lacked this mutation (possibly due to the quality and quantity of DNA isolated from the tumor cells). The interesting features of this case are the simultaneous detection of primary and metastatic tumors before receiving any treatment and the absence of the K27M mutation in the H3F3A gene in the metastasis.

Intratumoral molecular genetic heterogeneity is not a less significant challenge in modern oncology than the intertumoral. The presence of cell populations within the same tumor, differing in their molecular properties, translated into phenotypic features of the cells, is one of the reasons for the inefficiency of many developments in the field of tumor therapy and the basis for the progression of malignant neoplasms. The issue under consideration is very relevant for glioblastoma (GBM) – being one of the deadliest human tumors; it practically does not lend itself to even promising experimental treatment methods. Therefore, this paper reviews intratumoral heterogeneity. The review in this aspect examines new experimental data, including those obtained using single-cell technologies, in particular, the key cell populations that make up the pool of tumor cells in glioblastoma, and their molecular metamodules, the presumptive role of some cell populations and their subpopulations in providing tumor malignancy properties. A promising groundwork for fundamentally new approaches to creating personalized diagnostic and therapeutic methods is indicated. Keywords: glioblastoma, intratumoral heterogeneity, glioblastoma genetics, single-cell sequencing

The heterogeneity of tumors properties is a serious diagnostic and therapeutic problem. It is manifested by the variability of genetic, proteomic and epigenetic parameters both between different samples of the same histological variant of the tumor, and between different sites within the same neoplasm with the presence of heterogeneous cell populations in this particular patient. Glioblastoma (GB) is one of the most frequent fatal tumors of the central nervous system in humans. The understanding the intertumor heterogeneity is the key to the development of both new diagnostic approaches and innovative personalized methods of patients’ management. In the framework of this review, the main data on intertumor heterogeneity of GB are sum-marized. The basic genetic, epigenetic and proteomic aspects of the modern understanding of GB molecular profile and intertumor heterogeneity are considered. Keywords: glioblastoma, intertumor heterogeneity, glioblastoma genetics, mutations