Glioblastomas (GBM), the most aggressive primary brain tumors, remain challenging to treat due to their rapid proliferation, invasiveness, and resistance to current therapies. Emerging evidence highlights pyroptosis and ferroptosis as critical regulators of tumor progression. This review elucidates the pivotal role of mitochondrial dysfunction in driving these programmed cell death pathways in GBM. Specifically, mitochondrial abnormalities induce overproduction of reactive oxygen species (ROS) and disrupt iron homeostasis, thereby triggering pyroptosis through inflammasome activation and ferroptosis via lipid peroxidation accumulation. Impaired mitochondrial dynamics, such as membrane potential collapse, pro-inflammatory cytokine release, and defective mitophagy, synergistically determine tumor cell fates. We propose novel therapeutic strategies targeting mitochondrial ROS-scavenging systems, iron-sulfur cluster biosynthesis, and mitophagy modulation to overcome resistance to treatment of GBM. These investigations not only advance the understanding of the pathobiology of GBM but also underscore mitochondria as multifaceted therapeutic hubs and offer translational potential for other diseases linked to mitochondrial dysregulation. By integrating cutting-edge research data, this review establishes a foundation for developing precision therapies centered on pyroptosis and ferroptosis modulation, bridging mechanistic discoveries with clinical innovation in neuro-oncology.

Almost all high-grade gliomas, particularly glioblastoma (GBM), are highly migratory and aggressive. Migrasomes are organelles produced by highly migratory cells capable of mediating intercellular communication. Thus, GBM cells may produce migrasomes during migration. However, it remains unclear whether migrasomes can influence GBM migration and invasion. In this study, we observed the presence and formation of migrasomes in GBM cells. We found that expression levels of key migrasome formation factor, tetraspanin 4 (TSPAN4), correlated positively with pathological grade and poor prognosis of GBM based on the databases and clinical samples analysis. Subsequently, we knocked down TSPAN4 and found that GBM cell migration and invasion were significantly inhibited due to the reduced formation of migrasomes. We further confirmed that migrasomes are enriched in extracellular matrix (ECM)-related proteins such as p21-activating kinase 4 (PAK4) and laminin alpha 4 (LAMA4). Our experimental results suggest that migrasomes promote GBM cells migration by releasing such proteins into the extracellular space. Overall, we identified migrasomes in GBM and the molecular mechanisms by which they regulate them, providing potential targets for treating GBM. Observation of migrasomes in glioblastoma (GBM) and analysis of migrasome-enriched proteins revealed that migrasomes promote GBM migration and invasion by releasing the extracellular matrix-associated proteins PAK4 and LAMA4.

High-grade infiltrating gliomas are highly aggressive and fatal brain tumors that present significant challenges for research and treatment due to their complex microenvironment and tissue structure. Recent discovery of tumor microtubes (TMs) has provided new insights into how high-grade gliomas develop in the brain and resist treatment. TMs are unique, ultra-long, and highly functional membrane protrusions that form multicellular networks and play crucial roles in glioma invasiveness, drug resistance, recurrence, and heterogeneity. This review focuses on the different roles that TMs play in glioma cell communication, material transport, and tumor cell behavior. Specifically, non-connecting TMs primarily promote glioma invasiveness, likely related to their role in enhancing cell motility. On the other hand, interconnecting TMs form functional and communication networks by connecting with surrounding astrocytes and neurons, thereby promoting glioma malignancy. We summarize the factors that influence the formation of TMs in gliomas and current strategies targeting TMs. As the understanding of TMs advances, we are closer to uncovering whether they might be the long-sought Achilles' heel of treatment-resistant gliomas. By delving deeper into TMs research, we hope to develop more effective therapeutic strategies for patients with malignant gliomas.

Exogenous or endogenous factors such as hypoxia, nutritional deficiencies, acidic microenvironments and their own high metabolic demands usually lead to tumor endoplasmic reticulum dysfunction and trigger endoplasmic reticulum stress (ERS). ERS sensors intercept such stress signals, which subsequently initiate the unfolded protein response (UPR), enabling tumor cells to adapt robustly in the hostile environment. Many studies have found that the ERS response affects a variety of tumor-infiltrating immune cells and suppresses their anti-tumor responses through different mechanisms. Given that glioblastoma (GBM) are immunosuppressive "cold tumors" with a poor prognosis. This paper not only discusses the promotion of GBM growth by ERS response, but also reviews the mechanisms by which ERS response promotes an immunosuppressive microenvironment.

Gliomas are primary tumors that originate in the central nervous system. The conventional treatment options for gliomas typically encompass surgical resection and temozolomide (TMZ) chemotherapy. However, despite aggressive interventions, the median survival for glioma patients is merely about 14.6 months. Consequently, there is an urgent necessity to explore innovative therapeutic strategies for treating glioma. The foundational study of regulated cell death (RCD) can be traced back to Karl Vogt’s seminal observations of cellular demise in toads, which were documented in 1842. In the past decade, the Nomenclature Committee on Cell Death (NCCD) has systematically classified and delineated various forms and mechanisms of cell death, synthesizing morphological, biochemical, and functional characteristics. Cell death primarily manifests in two forms: accidental cell death (ACD), which is caused by external factors such as physical, chemical, or mechanical disruptions; and RCD, a gene-directed intrinsic process that coordinates an orderly cellular demise in response to both physiological and pathological cues. Advancements in our understanding of RCD have shed light on the manipulation of cell death modulation - either through induction or suppression - as a potentially groundbreaking approach in oncology, holding significant promise. However, obstacles persist at the interface of research and clinical application, with significant impediments encountered in translating to therapeutic modalities. It is increasingly apparent that an integrative examination of the molecular underpinnings of cell death is imperative for advancing the field, particularly within the framework of inter-pathway functional synergy. In this review, we provide an overview of various forms of RCD, including autophagy-dependent cell death, anoikis, ferroptosis, cuproptosis, pyroptosis and immunogenic cell death. We summarize the latest advancements in understanding the molecular mechanisms that regulate RCD in glioma and explore the interconnections between different cell death processes. By comprehending these connections and developing targeted strategies, we have the potential to enhance glioma therapy through manipulation of RCD.

Background Epithelial-mesenchymal transition (EMT) plays a crucial role in the migration and invasion capabilities of glioblastoma (GBM) cells. Several studies have established tubulin as a significant regulator of the EMT process. Tubulin beta 2B class IIb (TUBB2B), a critical component of microtubules, has been linked to the prognosis of various tumors. However, the specific biological function and mechanism of TUBB2B in GBM remain unclear. Methods In vitro experiments demonstrated that TUBB2B knockdown inhibited the migration and invasion of GBM cells, while its overexpression enhanced these capabilities. Western blot, immunofluorescence (IF) and co-immunoprecipitation (Co-IP) assays revealed that TUBB2B interacts with Vimentin. Molecular docking and residue mutation scanning indicated that TUBB2B interacts with Vimentin at the R391/K392/A393/F394 sites. In vivo experiments using nude mice confirmed that TUBB2B knockdown inhibited GBM cell invasion and migration. Results TUBB2B was upregulated in GBM tissue samples compared with normal tissues. The sites of TUBB2B(R391/K392/A393/F394) physically interacts with Vimentin to induce EMT, which promotes migration and invasion. Conclusion TUBB2B may regulate EMT and promote the migration and invasion of GBM cells through its interaction with Vimentin, highlighting TUBB2B as a potential therapeutic target for GBM.

RATIONALE:Cerebral venous sinus thrombosis (CVST) represents 0.5% to 1% of all strokes. CVST can cause headaches, epilepsy, and subarachnoid hemorrhage (SAH). CVST is easily misdiagnosed because of the variety and non-specificity of symptoms. Herein, we report a case of infectious thrombosis of the superior sagittal sinus with SAH.PATIENT CONCERNS:A 34-year-old man presented to our hospital with a 4-hour history of sudden and persistent headache and dizziness with tonic convulsions of the limbs. Computed tomography revealed SAH with edema. Enhanced magnetic resonance imaging showed an irregular filling defect in the superior sagittal sinus.DIAGNOSES:The final diagnosis was hemorrhagic superior sagittal sinus thrombosis and secondary epilepsy.INTERVENTIONS:He was treated with antibiotic, antiepileptic, fluids to rehydrate, and intravenous dehydration.OUTCOMES:After treatment, the seizures did not recur and the symptoms were relieved. One month after the antibiotic treatment, the muscle strength of the patient's right extremity was restored to level 5, and there was no recurrence of his neurological symptoms.LESSONS:We describe a case of infectious thrombosis of the superior sagittal sinus manifested as SAH, which is easily misdiagnosed, especially when patients present with an infection. Clinicians must therefore take care during the diagnosis and selection of the treatment strategy.

OBJECTIVE: To establish a new method for fast exposure of the internal maxillary artery (IMA) during extracranial-intracranial bypass surgery.METHODS: To explore the positional relationship between the IMA and the maxillary nerve and pterygomaxillary fissure, 11 formalin-fixed cadaveric specimens were dissected. Three bone windows of the middle fossa were created for further analysis. Then the IMA length that could be pulled up above the middle fossa was measured after different degrees of removal of bony structure. The IMA branches under each bone window were also explored in detail.RESULTS: The top of the pterygomaxillary fissure was located 11.50 mm anterolateral to the foramen rotundum. The IMA could be identified just inferior to the infra-temporal segment maxillary nerve in all specimens. After drilling of the first bone window, the IMA length that could be pulled above the middle fossa bone was 6.85 mm. After drilling of the second bone window and further mobiliza-tion, the IMA length that could be harvested was signifi-cantly longer (9.04 mm vs. 6.85 mm; P < 0.001). Removal of the third bone window did not significantly improve the IMA length that could be harvested.CONCLUSIONS: The maxillary nerve could be used as a reliable landmark for the exposure of the IMA in the pter-ygopalatine fossa. With our technique, the IMA could be easily exposed and sufficiently dissected without zygo-matic osteotomy and extensive middle fossa floor removal.

Abstract Background Numerous close relationships between the gut microbiota and various cancers have been described, and several studies suggest that the gut microbiota can influence the central nervous system (CNS), but the relationship between the intestinal microbiome and brain tumors is unclear. Furthermore, the role of action of the gut microbiota on brain tumors has not been well understood, especially in the CNS, which has been considered an immune-privileged organ due to the presence of the blood-brain barrier. Results In the present work, we systematically compared the gut microbiome and metabolite alterations in patients with a brain tumor, including patients with meningioma (MEG), glioma and brain metastasis (BM), with those of healthy controls (HCs) using faecal metagenomics and metabolomics, and used this in relation to clinical indicators to explore their possible causative mechanisms in the disease. In the disease group, bacterial abundance was altered, showing a significant decrease in Gram-positive bacteria such as Lachnospiraceae and a substantial increase in Gram-negative bacteria such as Enterobacteriaceae, while lipopolysaccharide‒associated pathways were also enriched. Additionally, metabolites were changed: most amino acid and fatty acid metabolites increased, while bile acids (BAs) and carbohydrates decreased. However, the differences in bacteria and metabolites between the disease groups were less than those between the HCs. Furthermore, a variety of immune-related clinical indicators, bacteria, metabolites and pathways were significantly altered in the disease groups. Finally, markers based on bacterial flora and metabolites were effective in differentiating the disease groups from the HCs. Conclusions The multiomics data from this study revealed that dysbiosis and metabolic abnormalities were present in the gut of patients with brain tumors. At the same time, host immune abnormalities may be associated with dysbiosis and may lead to tumour development and progression through inflammatory, immune, and metabolic interactions; these altered microbiome-metabolome-host interactions may help explain the pathogenesis of brain tumors, and provide new ideas for the prevention and treatment of brain tumors. The microbiome and its derived metabolites are a promising noninvasive tool for the accurate detection and differentiation of patients with different brain tumors.

Abstract Purpose Glioma patients have varying degrees of psychiatric symptoms, which severely affect the quality of life of patients and their families. The present study investigated the correlation between preoperative psychiatric symptoms and local cerebral perfusion parameters of in glioma patients. Patients and methods The depression, anxiety, and cognitive impairment (CI) scores of 39 patients were assessed separately, and all of the patients underwent a preoperative perfusion computed tomography scan. Results This study found that: (1) The incidence of preoperative symptoms of depression, anxiety, and CI was 46.15%, 48.72%, and 25.64%, respectively. (2) Cerebral blood volume (CBV) (lesion‐sided [LS] occipital lobe white matter [WM] and parietal lobe WM and normal‐sided temporal lobe WM), permeability surface (PS) (LS temporal lobe gray matter [GM] and parietal lobe WM) in the depression group were significantly decreased (p < .05). (3) CBV (LS occipital lobe WM), cerebral blood flow (LS parietal lobe GM, centrum ovale and frontal lobe WM and normal‐sided frontal lobe WM, temporal lobe WM and parietal lobe WM), and mean transition time (MTT) (normal‐sided frontal lobe WM and temporal lobe WM) in the anxiety group were significantly increased (p < .05). (4) CBV (LS temporal lobe GM), MTT (LS anterior limb of internal capsule), and PS (LS thalamus) in the CI group were significantly increased (p < .05). Conclusion This study showed that glioma patients had different levels of psychological distress in glioma patients before surgery, which may be related to the changes in brain perfusion caused by the tumor.

Over the past few decades, clinicians and experts applied kinds of therapies for patients with malignant gliomas such as chemotherapy, radiation or surgical extraction. However, they used to ignore the real seriousness of neuropsychiatric symptoms after glioma, including cognitive dysfunction, anxiety, and depression, which severely impeded patients' recovery and prognosis. Interestingly, one of our previous clinical studies have found some behavioral symptoms in glioma patients were associated with systemic inflammation. Notopterol is one of the principal extracts of the traditional Chinese medicinal herb Notopterygium incisum having anti-tumour and anti-inflammatory activity. However, whether notopterol is beneficial to the treatment of glioma has not been reported. In this study, we found that notopterol inhibited growth and increased apoptosis of glioma via inhibiting STAT3 activity. In addition, notopterol treatment improved cognitive impairment and depression-like behavior in GL261 cell-based glioma mice via preventing the loss of dendritic spines and the reduction of synapse related proteins (PSD95 and Synapsin-1) in hippocampal neurons. Notopterol significantly reduced the levels of cytokines (iNOS, TNF-α, IL-6, and IL-β) and the activity of STAT3/NF-kB signalling pathway in peritumoural brain tissues and GL261 conditioned medium (GCM) treated microglial cell line (BV2 cells). These results demonstrated that notopterol not only exerted anti-glioma effects via inhibiting STAT3 activity, but improved neuropsychiatric symptoms via inhibiting tumour associated inflammation through modulation of the STAT3/NF-kB pathway in glioma-bearing mice.

Glioma is a frequently occurring type of cancer that affects the central nervous system.Despite the availability of standardized treatment options including surgical resection, concurrent radiotherapy, and adjuvant temozolomide (TMZ) therapy, the prognosis for glioma patients is often unfavorable.Exosomes act as vehicles for intercellular communication, contributing to tissue repair, immune modulation, and the transfer of metabolic cargo to recipient cells.However, the transmission of abnormal substances can also contribute to pathologic states such as cancer, metabolic diseases, and neurodegenerative disorders.The field of exosome research in oncology has seen significant advancements, with exosomes identified as dynamic modulators of tumor cell proliferation, migration, and invasion, as well as angiogenesis and drug resistance.Exosomes have negligible cytotoxicity, low immunogenicity, and small size, rendering them an ideal therapeutic candidate for glioma.This comprehensive review discusses the dual effects of exosomes in glioma, with an emphasis on their role in facilitating drug resistance.Furthermore, the clinical applications and current limitations of exosomes in glioma therapy are also discussed in detail.

Cranial tuberculosis is a relatively infrequent inflammatory reaction caused by tuberculous bacilli invading the skull. Most cases of cranial tuberculosis are secondary to tuberculosis foci in other parts of the body; primary cranial tuberculosis is extremely rare. Herein, we report a case of primary cranial tuberculosis. A 50-year-old man presented to our hospital with a mass in the right frontotemporal region. Chest computed tomography and abdominal ultrasonography findings were normal. Magnetic resonance imaging of the brain revealed a mass in the right frontotemporal skull and scalp with cystic changes, adjacent bone destruction, and meningeal invasion. The patient underwent surgery and was diagnosed with primary cranial tuberculosis; he was treated with antitubercular therapy postoperatively. No recurrent masses or abscesses were observed during the follow-up.

Objective: The main responsibility of caring for patients with glioma is assumed by family caregivers who experience a considerable burden during the care process. This study aimed to investigate the level of caregiver burden and explore its associated factors among family caregivers of patients with glioma. Methods: We conducted a cross-sectional study among 131 family caregivers of glioma patients from October 2017 to November 2019. We used the following measurement tools: a demographic questionnaire, the Zarit Burden interview (ZBI), the Hamilton anxiety and depression scale, and the family APGAR index. We used multiple linear regression analysis to determine the factors related to caregiver burden. Results: The ZBI score for the family caregivers of glioma patients was 31.29 (SD = 13.54), and most caregivers (71.7%) reported moderate and severe caregiver burdens. Caregivers' daily sleep time and anxiety symptoms and patients' depressive symptoms independently predicted caregiver burden. Conclusions: Family caregivers of glioma patients experienced a moderate burden. Personalised psychological intervention and sleep health guidance for patients and caregivers should be considered to reduce family caregiver burden and enhance the quality of life and mental health of both patients and their caregivers.

Background: Dysregulation of RecQ protein-like 1 (RECQL1), a member of the RecQ DNA helicase, has been determined to participate in malignant process of numerous tumors such as immunosuppression and proliferation and may serve as a biomarker for certain malignancies. Nevertheless, whether there is a similar association between RECQL1 and low-grade glioma (LGG) is uncertain. We therefore turned our attention to exploring the association of RECQL1 with tumor immune infiltration and prognostic significance in LGG. Methods: The differential expression analysis of the RecQ DNA helicases was conducted through the GLIOVIS database and GSE4290 dataset, and verified by the Gene Expression Profiling Interactive Analysis 2 database. Kaplan-Meier plots, Univariate and multivariate Cox regression analysis were employed to assess the prognostic value of RECQL1 expression level and other six variables in LGG patients, and subsequently an efficient nomogram model was generated for clinical prediction. Tumor Immune Estimation Resource database and the single sample Gene Set Enrichment Analysis were used to assess the correlation between RECQL1 and immune infiltration of LGG. The biological processes that may be related to RECQL1 in LGG were learned through functional enrichment analysis by Gene Set Enrichment Analysis software. Results: Among the five RecQ DNA helicases detected, only RECQL1 was over-expression in LGG with the most convincing evidence (log2FoldChange >1.5, q value <0.01). High RECQL1 expression demonstrated worse overall survival and progression-free survival of LGG patients (P<0.05). Dysregulation of RECQL1 was an independent prognostic indicator for outcomes of LGG (HR >1.4, P<0.05). RECQL1 may participates in the carcinogenic pathways of LGG such as adherens junction and JAK-STAT signaling pathways. The transcription expression level of RECQL1, was obviously associated with tumor immune infiltrating cells and their marker genes. Conclusions: High RECQL1 expression detected in LGG not only implies adverse clinical outcome of patients, but also correlates with tumor immune infiltration and certain oncogenic pathways. Our study proposes potential novel biomarker and therapeutic target for the treatment of LGG patients.

Drug resistance and toxicity are major challenges observed during cancer treatment. In recent years, gut microbiota has been found to be strongly associated with the efficacy, toxicity, and side effects of chemotherapy, radiotherapy, and immunotherapy. Both preclinical studies and clinical trials have demonstrated the potential of microbiota modulation for cancer treatment. The human gut microbiota has exciting prospects for developing biomarkers to predict the outcome of cancer treatment. Moreover, multiple approaches can alter the gut microbiota composition, including faecal microbiota transplantation (FMT), probiotics, antibiotics (ATB), and diet. We describe the mechanisms by which the gut microbiota influences the efficacy and toxicity of cancer therapy, disease-related biomarkers, and methods to target the gut microbiota to improve outcomes. The purpose of this review is to provide new ideas for optimising cancer therapy by providing up-to-date information on the relationship between gut microbiota and cancer therapy, and hopes to find new targets for cancer treatment from human microbiota.

Objective: To explore the relationship between preoperative psychological personality traits of glioma patients and preoperative psychological distress of their primary caregivers.Methods: A retrospective analysis was conducted on 85 glioma patients (tumor group) who were admitted to our hospital from February 2016 to December 2018 and 85 primary caregivers. Forty-one healthy volunteers were used as controls.Results: The scores of 9 scales of the Minnesota Multiphasic Personality Inventory (MMPI) increased significantly in the tumor group compared to the healthy controls (P < 0.05), including L (lie): [(56.0 +/- 11.5 vs. 50.0 +/- 10.0)], F (fake): [(53.0 +/- 10.6 vs. 41.7 +/- 8.8)], Hs (hypochondriasis): [(55.6 +/- 11.2 vs. 44.2 +/- 8.3)], D (depressive personality): [(49.2 +/- 9.6 vs. 42.2 +/- 10.3)], Mf (masculinity-femininity): [(49.9 +/- 9.4 vs. 42.8 +/- 14.0)], Pt (psychasthenia): [(51.5 +/- 10.0 vs. 40.9 +/- 11.5)], Sc (schizophrenia): [(51.2 +/- 10.6 vs. 40.2 +/- 10.6)], Ma (hypomania): [(51.8 +/- 9.1 vs. 47.7 +/- 9.4)] and Si (social introversion): [(46.6 +/- 8.7 vs. 36.7 +/- 13.0)]. However, the K (defensive responses) scale score in the tumor group decreased significantly (52.1 +/- 13.9 vs. 58.8 +/- 12.1, P = 0.009). The F (fake): [(rs=0.253, P=0.019 / rs=0.215, P=0.048)], Hs (hypochondriasis): [(rs=0.310, P=0.004 / rs=0.345, P=0.001)], Pt (psychasthenia): [(rs=0.299, P=0.006 / rs=0.258, P=0.017)], and Sc (schizophrenia): [(rs=0.325,P=0.002/rs=0.322, P=0.003)] of preoperative glioma patients were positively correlated with their preoperative psychological distress (depression/anxiety); the D (depressive personality): [(rs=0.229, P=0.035)] of preoperative glioma patients was positively correlated with the preoperative depression symptoms of their primary caregivers, and the Hy (hysteria): [(rs=0.233, P=0.002)] and Pd (psychopathic deviate): [(rs=0.215, P=0.006)] of preoperative glioma patients were positively correlated with the preoperative anxiety symptoms of their primary caregivers.Conclusions: The preoperative psychological personality traits of glioma patients were positively correlated with preoperative symptoms of depression and anxiety in primary caregivers.

Bone marrow-derived mesenchymal stem cells (BM-MSCs) display high tumor tropism and cause indirect effects through the cytokines they secrete. However, the effects of BM-MSCs on the biological behaviors of glioblastoma multiforme remain unclear. In this study, the conditioned medium from BM-MSCs significantly inhibited the proliferation of C6 cells (P < 0.05) but promoted their migration and invasion (P < 0.05). Two-dimensional fluorescence difference gel electrophoresis (2D-DIGE) proteomic analysis revealed 17 proteins differentially expressed in C6 cells exposed to the BM-MSC-conditioned medium including five upregulated proteins and 12 downregulated proteins. Among these, six differentially expressed proteins (Calr, Set, Oat, Npm1, Ddah1, and Tardbp) were closely related to cell proliferation and differentiation, and nine proteins (Pdia6, Sphk1, Anxa4, Vim, Tuba1c, Actr1b, Actn4, Rap2c, and Tpm2) were associated with motility and the cytoskeleton, which may modulate the invasion and migration of tumor cells. Above all, by identifying the differentially expressed proteins using proteomics and bioinformatics analysis, BM-MSCs could be genetically modified to specifically express tumor-suppressive factors when BM-MSCs are to be used as tumor-selective targeting carriers in the future.

BACKGROUND Glioblastoma has a high degree of malignancy and poor prognosis. It is common to have in situ recurrence and intracranial metastasis, while extracranial metastasis is rare, and extracranial multiorgan metastasis is extremely rare. We report a case of glioblastoma with extracranial multiorgan metastasis, which will strengthen clinicians’ attention to the extracranial metastasis of glioblastoma and its treatment. CASE SUMMARY A male patient visited our hospital for treatment of dizziness and headache. Magnetic resonance imaging of the brain revealed a space-occupying lesion in the right temporoparietal occipital region. Chest computed tomography and abdominal ultrasound were normal, and no space-occupying lesions were observed in other organs of the body. The patient underwent surgery and diagnosed with glioblastoma. Postoperative concurrent radiotherapy and chemotherapy were completed. During the follow-up, the tumor was found to have metastasized to the scalp and neck, and a second tumor resection was performed. Postoperative follow-up revealed extracranial metastases to multiple extracranial organs including skull, scalp, ribs, spine, liver and lung. His family members refused further treatment, and requested only symptomatic treatment such as pain relief, and the patient died of systemic multiple organ failure. Survival time from diagnosis to death was 13 mo and from extracranial metastasis to death was 6 mo. CONCLUSION Glioblastoma extracranial metastasis is extremely rare, clinicians should always pay attention to its existence. The mechanism of glioblastoma extracranial metastasis is still unclear, and genetic and molecular studies are required.