Treatment Of Primary Brain Tumors Research Articles

Sleep disorders associated with cranial radiation - a systematic review.

Radiation is standard-of-care treatment for primary brain tumors but may have profound effects on sleep that have not yet been fully characterized. This systematic review aims to further our understanding of radiation therapy on risk of development of sleep disorders in patients with primary brain tumors (PBTs), as well as potential opportunities for prevention and treatment. A systematic search of PubMed, Embase, and Web of Science was performed (last Jan 2024) with predefined inclusion (PBT patients, radiation therapy, somnolence/circadian disruption) and exclusion (reviews/abstracts/cases/chapters, non-PBT cancer, lack of radiation) criteria, yielding 267 papers initially and 38 studies included. Data extraction and analysis (descriptive statistics, individual study summary) focused on incidence of sleep disturbances, radiation types/doses, and pharmacologic interventions. Risk of bias assessment was conducted with Effective Public Health Practice Project's Quality Assessment Tool for Quantitative Studies. The included 38 studies (n=2948 patients) demonstrated high incidence of sleep disturbances in patients with primary brain tumors throughout radiation therapy, but primarily from the end of radiation to 6 months after. Sleep symptoms were associated with radiation (dose-dependent), and pharmacotherapies were helpful in patients with formal sleep disorder diagnoses. Terminology and incidence reporting of sleep symptoms are inconsistent, and many studies had high risk of bias. This systematic review highlights the ongoing challenges with sleep symptoms/disorders related to cranial irradiation treatment in the primary brain tumor population. Further investigations on the interconnectedness of sleep disturbance constructs and possible pharmacotherapies to alleviate symptoms are warranted.

Blood-Brain Barrier Disruption for the Treatment of Primary Brain Tumors: Advances in the Past Half-Decade.

To review relevant advances in the past half-decade in the treatment of primary brain tumors via modification of blood-brain barrier (BBB) permeability. BBB disruption is becoming increasingly common in the treatment of primary brain tumors. Use of mannitol in BBB disruption for targeted delivery of chemotherapeutics via superselective intra-arterial cerebral infusion (SIACI) is the most utilized strategy to modify the BBB. Mannitol is used in conjunction with chemotherapeutics, oligonucleotides, and other active agents. Convection-enhanced delivery has become an attractive option for therapeutic delivery while bypassing the BBB. Other technologic innovations include laser interstitial thermal therapy (LITT) and focused ultrasound (FUS) which have emerged as prime modalities to directly target tumors and cause significant local BBB disruption. In the past 5years, interest has significantly increased in studying modalities to disrupt the BBB in primary brain tumors to enhance treatment responses and improve clinical outcomes.

Evaluation of the effectiveness of multicomponent treatment in the progression of primary low-grade brain gliomas. Own experience

BACKGROUND: Despite the improved results of treatment of brain tumors achieved over the past decade, most patients experience relapses of the disease 1–2 years after treatment. Numerous clinical studies have made it possible to obtain standard protocols for the treatment of primary brain tumors; however, protocols for the treatment of recurrent tumors have not been developed. The choice of treatment usually includes reoperation, systemic chemotherapy, and reirradiation alone or in combination. However, the treatment of recurrent glial tumors is challenging given the lack of effective treatment options and the lack of randomized controlled trials on which to base therapy.
 AIM: To determine the most important prognostic factors, as well as the most effective treatment option in patients with continued growth of primary low-grade gliomas of the brain.
 METHODS: This study included 40 patients with a confirmed diagnosis of progression of low-malignant glial brain tumors, who underwent inpatient treatment at the Chelyabinsk Regional Clinical Center of Oncology and Nuclear Medicine from 2007 to 2022. The ratio of men and women: 1:1.5. The mean age was 45.6±11.5 years. Patients with grade I astrocytomas predominated (n=23), oligodendroglioma was diagnosed in 8 patients.
 Reoperation was performed in 11 patients as the first stage of progression treatment. In 7 cases, monochemotherapy with temozolomide was performed. Repeated radiation therapy was performed in 29 patients, of which: 9 patients received a course of combined photon-neutron therapy; 9 patients — stereotactic radiation therapy (was performed on the CyberKnife device); 11 patients — external beam radiation therapy.
 RESULTS: The median overall survival (OS) for all patients with continued growth of low-grade cerebral gliomas after treatment was 120 months. 1-year OS — 97.3%; 3-year — 86.8%; 5-year — 78.2%. Median OS after relapse treatment was 36 months. The median OS was higher in the age group under 50 compared to the older age group: 120 and 95 months (p 0.05).
 The best results of treatment were noted in patients who underwent reoperation followed by a course of radiation therapy or chemotherapy with temozolomide for 48 months and 36 months respectively (p 0.05). When analyzing the results of treatment after a course of repeated radiation therapy in an independent variant, there were undoubted advantages in patients who underwent stereotactic radiation therapy and photon-neutron therapy for 60 months and 24 months respectively (p 0.05).
 CONCLUSIONS: The optimal approach to the treatment of patients with continued growth of primary low-grade glioma brain tumors is to perform a second operation, followed by radiation therapy or chemotherapy. The method of choice for a repeat course of radiotherapy may be photon-neutron therapy or stereotactic radiation therapy.

PAK3 downregulation induces cognitive impairment following cranial irradiation.

Cranial irradiation is used for prophylactic brain radiotherapy as well as the treatment of primary brain tumors. Despite its high efficiency, it often induces unexpected side effects, including cognitive dysfunction. Herein, we observed that mice exposed to cranial irradiation exhibited cognitive dysfunction, including altered spontaneous behavior, decreased spatial memory, and reduced novel object recognition. Analysis of the actin cytoskeleton revealed that ionizing radiation (IR) disrupted the filamentous/globular actin (F/G-actin) ratio and downregulated the actin turnover signaling pathway p21-activated kinase 3 (PAK3)-LIM kinase 1 (LIMK1)-cofilin. Furthermore, we found that IR could upregulate microRNA-206-3 p (miR-206-3 p) targeting PAK3. As the inhibition of miR-206-3 p through antagonist (antagomiR), IR-induced disruption of PAK3 signaling is restored. In addition, intranasal administration of antagomiR-206-3 p recovered IR-induced cognitive impairment in mice. Our results suggest that cranial irradiation-induced cognitive impairment could be ameliorated by regulating PAK3 through antagomiR-206-3 p, thereby affording a promising strategy for protecting cognitive function during cranial irradiation, and promoting quality of life in patients with radiation therapy.

PAK3 downregulation induces cognitive impairment following cranial irradiation

Cranial irradiation is used for prophylactic brain radiotherapy as well as the treatment of primary brain tumors. Despite its high efficiency, it often induces unexpected side effects, including cognitive dysfunction. Herein, we observed that mice exposed to cranial irradiation exhibited cognitive dysfunction, including altered spontaneous behavior, decreased spatial memory, and reduced novel object recognition. Analysis of the actin cytoskeleton revealed that ionizing radiation (IR) disrupted the filamentous/globular actin (F/G-actin) ratio and downregulated the actin turnover signaling pathway p21-activated kinase 3 (PAK3)-LIM kinase 1 (LIMK1)-cofilin. Furthermore, we found that IR could upregulate microRNA-206–3 p (miR-206–3 p) targeting PAK3. As the inhibition of miR-206–3 p through antagonist (antagomiR), IR-induced disruption of PAK3 signaling is restored. In addition, intranasal administration of antagomiR-206–3 p recovered IR-induced cognitive impairment in mice. Our results suggest that cranial irradiation-induced cognitive impairment could be ameliorated by regulating PAK3 through antagomiR-206–3 p, thereby affording a promising strategy for protecting cognitive function during cranial irradiation, and promoting quality of life in patients with radiation therapy.

Treatment of glioblastoma using MRIdian® A3i BrainTx™: Imaging and treatment workflow demonstration.

For patients with newly diagnosed glioblastoma, the current standard-of-care includes maximal safe resection, followed by concurrent chemoradiotherapy and adjuvant temozolomide, with tumor treating fields. Traditionally, diagnostic imaging is performed pre- and post-resection, without additional dedicated longitudinal imaging to evaluate tumor volumes or other treatment-related changes. However, the recent introduction of MR-guided radiotherapy using the ViewRay MRIdian A3i system includes a dedicated BrainTx package to facilitate the treatment of intracranial tumors and provides daily MR images. We present the first reported case of a glioblastoma imaged and treated using this workflow. In this case, a 67-year-old woman underwent adjuvant chemoradiotherapy after gross total resection of a left frontal glioblastoma. The radiotherapy treatment plan consisted of a traditional two-phase design (46 Gy followed by a sequential boost to a total dose of 60 Gy at 2 Gy/fraction). The treatment planning process, institutional workflow, treatment imaging, treatment timelines, and target volume changes visualized during treatment are presented. This case example using our institutional A3i system workflow successfully allows for imaging and treatment of primary brain tumors and has the potential for margin reduction, detection of early disease progression, or to detect the need for dose adaptation due to interfraction tumor volume changes.

P11.63.B Thrombocytopenia limits the feasibility of salvage lomustine chemotherapy in recurrent glioblastoma: a secondary analysis of EORTC 26101

Abstract Background Chemotherapies used for the treatment of primary brain tumors frequently induce hematological toxicity. Thrombocytopenia represents the main cause of stopping chemotherapy for toxicity. Here we explored the incidence, and the consequences for treatment exposure and survival, of thrombocytopenia induced by lomustine chemotherapy at first recurrence of glioblastoma. Methods We performed a retrospective analysis of thrombocytopenia at first recurrence of glioblastoma, its consequences for treatment delivery, and associations with outcome in the phase II and III parts of EORTC 26101, a randomized trial designed to define the role of lomustine versus bevacizumab versus their combination in glioblastoma patients at first relapse. Results 225 patients were treated with lomustine alone (median 1 cycle) (group 1) and 283 patients were treated with lomustine plus bevacizumab (median 3 lomustine cycles) (group 2). Among cycle delays and dose reductions of lomustine for toxicity, thrombocytopenia was the leading cause. Among 129 patients of group 1 and 187 patients of group 2 experiencing at least one episode of thrombocytopenia, 36 patients in group 1 and 93 in group 2 had their treatment modified because of thrombocytopenia. Lomustine was discontinued for thrombocytopenia in 16 patients (7.1%) in group 1 and in 38 patients (13.4%) in group 2. Patients with O6-methylguanine DNA methyltransferase (MGMT) promoter-methylated glioblastoma treated with lomustine alone experienced more interference with study treatment than patients with tumors without MGMT promoter methylation. On adjusted analysis accounting for major prognostic factors, treatment modification by thrombocytopenia was a positive prognostic factor for overall survival, and this effect was entirely driven by patients with tumors without MGMT promoter methylation only. Conversely, thrombocytopenia was associated with inferior progression-free survival in patients with MGMT promoter-methylated tumors, suggesting a link to insufficient lomustine exposure. Conclusion Drug-induced thrombocytopenia is a major limitation to adequate exposure to lomustine salvage chemotherapy in patients with recurrent glioblastoma. Its association with survival suggests that mitigating thrombocytopenia to allow enhanced drug exposure in patients with MGMT promoter methylated tumors might improve outcome.

GD2-targeting CAR-T cells enhanced by transgenic IL-15 expression are an effective and clinically feasible therapy for glioblastoma

BackgroundAggressive primary brain tumors such as glioblastoma are uniquely challenging to treat. The intracranial location poses barriers to therapy, and the potential for severe toxicity. Effective treatments for primary brain...

P36-9 Dosimetric comparison of coplanar, non-coplanar and multi-planar VMAT for radiotherapy patients with primary brain tumor

Radiotherapy plays an important role in the treatment of primary brain tumors. In clinical practice, coplanar (cVMAT), non-coplanar (ncVMAT) and multi-planar VMAT (mpVMAT) are commonly adopted. The aim of the study is to investigate the overall plan quality and radiation dose to organs at risk, so as to determine which plan is more preferential for patients with primary brain tumor.

Advances in Chimeric Antigen Receptor (CAR) T-Cell Therapies for the Treatment of Primary Brain Tumors.

Immunotherapy has revolutionized the care of cancer patients. A diverse set of strategies to overcome cancer immunosuppression and enhance the tumor-directed immune response are in clinical use, but have not achieved transformative benefits for brain tumor patients. Adoptive cell therapies, which employ a patient’s own immune cells to generate directed anti-tumor activity, are emerging technologies that hold promise to improve the treatment of primary brain tumors in children and adults. Here, we review recent advances in chimeric antigen receptor (CAR) T-cell therapies for the treatment of aggressive primary brain tumors, including glioblastoma and diffuse midline glioma, H3 K27M-mutant. We highlight current approaches, discuss encouraging investigational data, and describe key challenges in the development and implementation of these types of therapies in the neuro-oncology setting.

Chemoattraction of Neoplastic Glial Cells with CXCL10, CCL2 and CCL11 as a Paradigm for a Promising Therapeutic Approach for Primary Brain Tumors.

Chemoattraction is a normal and essential process, but it can also be involved in tumorigenesis. This phenomenon plays a key role in glioblastoma (GBM). The GBM tumor cells are extremely difficult to eradicate, due to their strong capacity to migrate into the brain parenchyma. Consequently, a complete resection of the tumor is rarely a possibility, and recurrence is inevitable. To overcome this problem, we proposed to exploit this behavior by using three chemoattractants: CXCL10, CCL2 and CCL11, released by a biodegradable hydrogel (GlioGel) to produce a migration of tumor cells toward a therapeutic trap. To investigate this hypothesis, the agarose drop assay was used to test the chemoattraction capacity of these three chemokines on murine F98 and human U87MG cell lines. We then studied the potency of this approach in vivo in the well-established syngeneic F98-Fischer glioma-bearing rat model using GlioGel containing different mixtures of the chemoattractants. In vitro assays resulted in an invasive cell rate 2-fold higher when chemokines were present in the environment. In vivo experiments demonstrated the capacity of these specific chemoattractants to strongly attract neoplastic glioblastoma cells. The use of this strong locomotion ability to our end is a promising avenue in the establishment of a new therapeutic approach in the treatment of primary brain tumors.

CLRM-04. PHASE I/II SAFETY AND EFFICACY STUDY OF BET BROMODOMAIN INHIBITOR OTX-015 WITH OLAPARIB AND LOMUSTINE IN PATIENTS WITH RECURRENT GLIOBLASTOMA

Standard of care for patients with glioblastoma (GBM) includes resection with concurrent temozolomide (TMZ) and radiotherapy, with inevitable disease recurrence. Upon recurrence, tumors are often resistant to first-line therapies and/or have infiltrated eloquent or deep brain regions, precluding repeat resection. There is currently no standard of care for recurrent GBM and patients succumb to their disease burden within 12- 15 months of their initial diagnosis of recurrence, exposing an unmet need to find novel therapies to treat recurrent disease. Bromodomain and extraterminal (BET) proteins are chromatin readers that affect transcription of genes. The oral BET inhibitor (BETi) OTX-015 has shown promise in a dose-escalation, phase I study in patients with acute leukemia and other BET inhibitors are currently in phase I studies for the treatment of primary brain tumors. We have recently shown that BET inhibition increases DNA damage and mitotic catastrophe in oncogenic cells by increasing transcription-replication conflicts and downregulating expression of key DNA damage checkpoint proteins, and have also shown its efficacy in decreasing tumor burden and improving survival when combined with TMZ in intracranial mouse models of glioma. We have also demonstrated that BETi's synergize with Olaparib by downregulating expression of the BRCA-driven DNA damage repair pathway and further leverages additive effects when triply combined with other DNA damaging agents such as Lomustine to decrease tumor burden and improve survival in patient-derived mouse models of GBM and medulloblastoma. We therefore hypothesize that the synergistic and additive effects of this triple combination seen in our preclinical studies will achieve therapeutic benefits in patients with recurrent GBM.

Peptide Receptor Radionuclide Therapy and Primary Brain Tumors: An Overview.

Primary brain tumors (PBTs) are some of the most difficult types of cancer to treat, and despite advancements in surgery, chemotherapy and radiotherapy, new strategies for the treatment of PBTs are needed, especially for those with poor prognosis such as inoperable/difficult-to-reach lesions or relapsing disease. In regard to the last point, malignant primary brain tumors remain some of the most lethal types of cancer. Nuclear medicine may provide exciting new weapons and significant contributions in the treatment of PBTs. In this review, we performed literature research in order to highlight the possible role of peptide receptor radionuclide therapy (PRRT) in the treatment of PBTs with radiolabeled molecules that bind with high-affinity transmembrane receptors such as somatostatin receptors (SSTRs), neurokinin type-1 receptor and prostate-specific membrane antigen (PSMA). These receptors are overexpressed in some cancer types such as gliomas, meningiomas, pituitary tumors and medulloblastomas. A comprehensive overview of possible applications in this field will be shown, providing knowledge about benefits, feasibility, developments and limitations of PRRT in this type of tumor, also revealing new advantages in the management of the disease.

Experimental assessment of inter-centre variation in stopping-power and range prediction in particle therapy

PurposeExperimental assessment of inter-centre variation and absolute accuracy of stopping-power-ratio (SPR) prediction within 17 particle therapy centres of the European Particle Therapy Network. Material and methodsA head and body phantom with seventeen tissue-equivalent materials were scanned consecutively at the participating centres using their individual clinical CT scan protocol and translated into SPR with their in-house CT-number-to-SPR conversion. Inter-centre variation and absolute accuracy in SPR prediction were quantified for three tissue groups: lung, soft tissues and bones. The integral effect on range prediction for typical clinical beams traversing different tissues was determined for representative beam paths for the treatment of primary brain tumours as well as lung and prostate cancer. ResultsAn inter-centre variation in SPR prediction (2σ) of 8.7%, 6.3% and 1.5% relative to water was determined for bone, lung and soft-tissue surrogates in the head setup, respectively. Slightly smaller variations were observed in the body phantom (6.2%, 3.1%, 1.3%). This translated into inter-centre variation of integral range prediction (2σ) of 2.9%, 2.6% and 1.3% for typical beam paths of prostate-, lung- and primary brain-tumour treatments, respectively. The absolute error in range exceeded 2% in every fourth participating centre. The consideration of beam hardening and the execution of an independent HLUT validation had a positive effect, on average. ConclusionThe large inter-centre variations in SPR and range prediction justify the currently clinically used margins accounting for range uncertainty, which are of the same magnitude as the inter-centre variation. This study underlines the necessity of higher standardisation in CT-number-to-SPR conversion.

The Synergistic Effect of Co-delivery of Anticancer Drugs Into Astrocytes Isolated From Human Glioblastoma Multiforme

Background: Chemotherapy drugs are not effective in the treatment of primary brain tumors due to the low efficacy of these drugs and drug transfer from the blood-brain barrier (BBB) toward the tumor site. Our purpose in this study was to assess the co-delivery of anticancer drugs to increase drug permeability from BBB.Methods: In this study, two chemotherapy drugs, namely methotrexate (MTX) and paclitaxel (PTX), were inserted into polyvinyl alcohol and poloxamer188-conjugated nanoparticles (NPs). Astrocytes were treated with different concentrations of 0-50 μg/ml from MTX, PTX, the MTX-PTX mixture, PTX-loaded NPs, MTX-loaded NPs, and PTX-MTX co-loaded NPs for 48 hours. The tumoricidal effect was assessed using the survival rate, Hoechst staining, and western blotting.Results: The results indicated significant reduction of the survival rate in astrocytes treated with PTX-MTX co-loaded NPs. In addition, apoptosis hallmarks consisting of fragmented DNA, overexpression of Bax, and expression reduction of Bcl-2 were in the cultured astrocytes.Conclusions: Our study proposes that the PTX-MTX co-delivery to NPs could be used as a possible approach for anti-cancer drug delivery to glioblastoma multiforme.

Overview of Current Drug Delivery Methods Across the Blood–Brain Barrier for the Treatment of Primary Brain Tumors

Existing drug delivery methods have not led to a significant increase in survival for patients with malignant primary brain tumors. While the combination of conventional therapies consisting of surgery, radiotherapy, and chemotherapy has improved survival for some types of brain tumors (e.g., WNT medulloblastoma), other types of brain tumors (e.g., glioblastoma and diffuse midline glioma) still have a poor prognosis. The reason for the differences in response can be largely attributed to the blood–brain barrier (BBB), a specialized structure at the microvasculature level that regulates the transport of molecules across the blood vessels into the brain parenchyma. This structure hampers the delivery of most chemotherapeutic agents for the treatment of primary brain tumors. Several drug delivery methods such as nanoparticles, convection enhanced delivery, focused ultrasound, intranasal delivery, and intra-arterial delivery have been developed to overcome the BBB in primary brain tumors. However, prognosis of most primary brain tumors still remains poor. The heterogeneity of the BBB in primary brain tumors and the distinct vasculature of tumors make it difficult to design a drug delivery method that targets the entire tumor. Drug delivery methods that combine strategies such as focused ultrasound and nanoparticles might be a more successful approach. However, more research is needed to optimize and develop new drug delivery techniques to improve survival of patients with primary brain tumors.

Stem-Cell Therapy as a Potential Strategy for Radiation-Induced Brain Injury.

Radiation therapy is a standard and effective non-surgical treatment for primary brain tumors and metastases. However, this strategy inevitably results in damage of normal brain tissue, causing severe complications, especially the late-delayed cognitive impairment. Due to the multifactorial and complex pathological effects of radiation, there is a lack of effective preventative and restorative treatments for the irradiated brain. Stem-cell therapy has held considerable promise for decades in the treatment of central nervous system (CNS) disorders because of its unique capacity for tissue repair and functional integrity. Currently, there is growing interest in using stem cells as a novel option to attenuate the adverse effects of irradiation. In the present review, we discuss recent studies evaluating stem-cell therapies for the irradiated brain and their therapeutic effects on ameliorating radiation-related brain injury as well as their potential challenges in clinical applications. We discuss these works in context of the pathogenesis of radiation-induced injury to CNS tissue in an attempt to elucidate the potential mechanisms of engrafted stem cells to reverse radiation-induced degenerative processes.

Labeling Monoclonal Antibody with α-emitting 211At at High Activity Levels via a Tin Precursor.

Background: In a previous clinical study, the authors evaluated the potential of antitenascin C monoclonal antibody (mAb) 81C6 labeled with 211At via the prosthetic agent N-succinimidyl 3-[211At]astatobenzoate (SAB) for the treatment of primary brain tumors. Although encouraging results were obtained, labeling chemistry failed while attempting to escalate the dose to 370 MBq. The goal of the current study was to develop a revised procedure less susceptible to radiolysis-mediated effects on 211At labeling that would be suitable for use at higher activity levels of this α-emitter. Materials and Methods: Addition of N-chlorosuccinimide to the methanol used to remove the 211At from the cryotrap after bismuth target distillation was done to thwart radiolytic decomposition of reactive 211At and the tin precursor. A series of 11 reactions were performed to produce SAB at initial 211At activity levels of 0.31-2.74 GBq from 50 μg of N-succinimidyl 3-trimethylstannylbenzoate (Me-STB), which was then reacted with murine 81C6 mAb without purification of the SAB intermediate. Radiochemical purity, immunoreactive fraction, sterility, and apyrogenicity of the 211At-labeled 81C6 preparations were evaluated. Results: Murine 81C6 mAb was successfully labeled with 211At using these revised procedures with improved radiochemical yields and decreased overall synthesis time compared with the original clinical labeling procedure. Conclusions: With 2.74 GBq of 211At, it was possible to produce 1.0 GBq of 211At-labeled 81C6 with an immunoreactive fraction of 92%. These revised procedures permit production of 211At-labeled mAbs suitable for use at clinically relevant activity levels.

Ultrasound-induced blood-brain barrier disruption for the treatment of gliomas and other primary CNS tumors.

The treatment of primary brain tumors, especially malignant gliomas, remains challenging. The failure of most treatments for this disease is partially explained by the blood-brain barrier (BBB), which prevents circulating molecules from entering the brain parenchyma. Ultrasound-induced BBB disruption (US-BBBD) has recently emerged as a promising strategy to improve the delivery of therapeutic agents to brain tumors. A large body of preclinical studies has demonstrated that the association of low-intensity pulsed ultrasound with intravenous microbubbles can transiently open the BBB in a localized manner. The safety of this technique has been assessed in numerous preclinical studies in both small and large animal models. A large panel of therapeutic agents have been delivered to the brain in preclinical models, demonstrating both tumor control and increased survival. This technique has recently entered clinical trials with encouraging preliminary data. In this review, we describe the mechanisms and histological effects of US-BBBD and summarize the preclinical studies published to date. We furthermore provide an overview of the current clinical development and future potential of this promising technology.

Topical issues of the clinic of primary brain tumors

The article is devoted to the issue of clinical and neurological features of primary brain tumors (PBT). PBT account for 2% of the total number of human tumors. PBT represent an urgent social problem, causing disability and mortality. The incidence rate of primary tumors of the brain and other parts of the central nervous system in the United States from 2011 to 2015 amounted to 23.03 cases per 100,000 population. The most common histological types of PBT: meningioma (36.4%), pituitary tumors (15.5%) and glioblastoma (15.1%). The clinical picture of PBT is represented by cerebral and focal symptoms. Neurological deficit is determined by the location and volume of the neoplasm. The initial manifestations of tumor growth may be symptoms of irritation of the squeezed area of the brain tissue, which will be replaced later by symptoms of prolapse. Cerebral symptoms in most cases are associated with increased intracranial pressure and the development of cerebral edema. The subsequent development of the tumor process leads to the dislocation of brain structures and the formation of wedge syndromes. The most common clinical symptoms are: cognitive deficit (36%), convulsive syndrome (35%), headache (31%), ataxia (24%) and motor deficiency (22%). The article summarizes the data of world and domestic clinical studies aimed at determining the prevailing symptoms of primary brain tumors for the purpose of early diagnosis, timely medical care and assessment of the effectiveness of the treatment. Knowing the specifics of the clinical picture will significantly increase oncological alertness, which will lead to early diagnosis and timely treatment of PBT, which play a key role in improving the quality of life and increasing its duration.