Brain Tumor In Adults Research Articles

Biomolecular Predictors of Recurrence Patterns and Survival in IDH-Wild-Type Glioblastoma: A Retrospective Analysis of Patients Treated with Radiotherapy and Temozolomide

Background and Aim: Glioblastoma (GBM) is the most aggressive primary brain tumor in adults, with poor prognosis despite maximal surgical resection, radiotherapy (RT), and temozolomide (TMZ) per the Stupp protocol. IDH-wild-type GBM, the predominant molecular subtype, frequently harbors EGFR amplification and is resistant to therapy, while MGMT promoter methylation predicts improved TMZ response. This study aimed to assess the prognostic impact of EGFR and MGMT status on survival and recurrence patterns in IDH-wild-type GBM. Materials and Methods: We retrospectively analyzed 218 patients with IDH-wild-type GBM treated at the Azienda Ospedaliero-Universitaria Senese (2016–2024). All patients underwent maximal safe surgical resection whenever feasible. The cohort includes patients who received gross total resection (GTR), subtotal resection (STR), or biopsy only, depending on tumor location and clinical condition, followed by intensity-modulated RT (59.4–60 Gy) with concurrent and adjuvant TMZ. EGFR amplification was assessed via FISH/NGS and immunohistochemistry; MGMT promoter methylation was determined using methylation-specific PCR. Progression-free survival (PFS), overall survival (OS), and recurrence patterns (in-field, marginal, out-field) were evaluated using Kaplan–Meier, Cox regression, and logistic regression analyses. Results: Among patients (64.7% male; mean age 61.8), 58.7% had EGFR amplification and 49.1% showed MGMT methylation. Median OS and PFS were 14 and 8 months, respectively. EGFR non-amplified/MGMT methylated tumors had the best outcomes (OS: 22.0 months, PFS: 10.5 months), while EGFR-amplified/MGMT unmethylated tumors fared worst (OS: 10.0 months, PFS: 5.0 months; p < 0.001). MGMT methylation was an independent positive prognostic factor (HR: 0.48, p < 0.001), while EGFR amplification predicted worse survival (HR: 1.57, p = 0.02) and higher marginal recurrence (OR: 2.42, p = 0.01). Conclusions: EGFR amplification and MGMT methylation significantly influence survival and recurrence dynamics in IDH-wild-type GBM. Incorporating these biomarkers into treatment planning may enable tailored therapeutic strategies, potentially improving outcomes in this challenging disease. Prospective studies are needed to validate biomolecularly guided management approaches.

Comprehensive transcriptomic profiling of fusions and abnormal variant transcripts in pilocytic astrocytoma using NanoString nCounter technology.

Comprehensive transcriptomic profiling of fusions and abnormal variant transcripts in pilocytic astrocytoma using NanoString nCounter technology.

In vitro investigation of epigenetic regulators related to chemo-resistance and stemness of CD133+VE cells sorted from U87MG cell line.

In vitro investigation of epigenetic regulators related to chemo-resistance and stemness of CD133+VE cells sorted from U87MG cell line.

Mechanotransduction as a therapeutic target for brain tumours.

Mechanotransduction as a therapeutic target for brain tumours.

Epidemiology of adult brain tumors in the Philippine General Hospital from 2018 to 2022: Initial steps to a national brain tumor registry in a lower-middle income country.

Epidemiology of adult brain tumors in the Philippine General Hospital from 2018 to 2022: Initial steps to a national brain tumor registry in a lower-middle income country.

Effects of Proton Therapy on Cardiac Fibrosis, Calcium Homeostasis, and AQP4 Expression in Hypergravity-Exposed Rats

Proton therapy is increasingly used to treat pediatric and adult brain tumors, but there is still uncertainty surrounding the biological effects of protons on the heart. Also, the molecular and functional responses to proton irradiation are still unknown. This study investigates the effect of protons on cardiac disease by comparing their effects on the hearts of rats exposed to hypergravity. A total of 20 Sprague Dawley rats were tested, including a group that was irradiated with 0.1 Gy of protons to the heart, a group exposed to hypergravity, a group exposed to both protons and hypergravity, and a control group. Changes in AQP4, calcium homeostasis, and fibrosis-related markers were investigated using Western blotting, immunohistochemistry, etc. The proton-irradiated group showed no changes compared to the control group. In rats exposed to hypergravity, the cardiac fibrosis markers TGF-ꞵ1, MMP9, and MMP2 were increased. On the other hand, the group exposed to hypergravity followed by proton irradiation tended to display a significant decrease in these markers. Along with reduced fibrosis-related markers, the consistent tendency was also confirmed in the cardiac calcium homeostasis-related proteins and AQP4 through Western blotting. In summary, our findings indicate that rats subjected to hypergravity experienced both cardiac hypertrophy and fibrosis, while proton therapy appeared to mitigate the effects of cardiac disease. These results suggest that proton therapy prevents heart disease triggered by hypergravity, providing insights for protecting astronauts’ cardiovascular health.

Exploiting Synthetic Lethality of PRMT5 for Precision Treatment of MTAP-Deficient Glioblastoma

Glioblastoma (GBM) is the most aggressive primary brain tumor in adults, characterized by a dismal prognosis and limited therapeutic options. Its highly invasive nature and pronounced intratumoral heterogeneity underscores the urgent need for innovative and targeted therapeutic strategies. One promising approach is synthetic lethality, which exploits cancer-specific genetic vulnerabilities to selectively eliminate tumor cells. A well-characterized example involves the deletion of methylthioadenosine phosphorylase (MTAP), commonly observed in GBM and other malignancies. This review focuses on synthetic lethality targeting protein arginine methyltransferase 5 (PRMT5) in MTAP-deleted GBM. Loss of MTAP leads to the accumulation of methylthioadenosine (MTA), a metabolite that partially inhibits PRMT5, thereby creating a selective vulnerability to PRMT5 inhibition which is used to inhibit the residual function of PRMT5. We critically evaluate preclinical and clinical data on both first- and second-generation PRMT5 inhibitors, with particular emphasis on MTA-cooperative compounds that selectively exploit MTAP deficiency. Despite promising anti-tumor activity in vitro, the clinical efficacy of PRMT5 inhibitors is often limited by the tumor microenvironment, particularly the impact of non-malignant cells that attenuate drug activity. Finally, we explore rational combination strategies that integrate PRMT5 inhibition with existing therapies to enhance clinical outcomes in GBM.

Targeting FOXP3 in glioblastoma: Blockade of tumor intrinsic effects boosts response to chemo-radiotherapy.

Targeting FOXP3 in glioblastoma: Blockade of tumor intrinsic effects boosts response to chemo-radiotherapy.

Hybrid Therapy for Newly Diagnosed and Recurrent Glioblastoma: Staged Procedure Integrating Open Surgical Resection With Laser Interstitial Thermal Therapy.

Glioblastoma (GBM) is the most common and aggressive primary malignant brain tumor in adults with a median overall survival of 15.6 months. Despite advancements, 5-year survival rates have not significantly improved. Laser interstitial thermal therapy (LITT) has been used to treat both newly diagnosed (nGBM) and recurrent GBM (rGBM) with demonstrable safety and efficacy. Traditionally, LITT has been limited to smaller lesions given physical and thermal constraints. We present 2 case examples of a novel, hybrid treatment approach to GBM, using both surgery and laser ablation as part of a staged procedure. Two geriatric (older than 65 years) patients with nGBM or rGBM were treated with surgical resection followed by LITT the subsequent day. Both patients underwent preoperative MRI showing multifocal disease with a dominant component, causing mass effect in the second case, and an unresectable component. The first case underwent surgical resection of a large, multicentric rGBM in the parieto-occipital region, followed by LITT of an unresectable lesion in the inferior temporal gyrus. The second patient underwent surgical resection of the dominant temporal lobe component and LITT of the insular component. Neither patient had intraoperative or ablation complications. Both patients had stable postoperative neurological examinations and were discharged on the day after ablation, with no new deficits at follow-up. The prognosis for GBM remains dismal despite attempts at advancements in patient management. Surgical resection is a critical component of the GBM treatment paradigm, although, alone, is not sufficient for maximal therapeutics in many patients. LITT is a minimally invasive means of cytoreduction that has shown promise for improving GBM outcomes. We demonstrate a novel, hybrid approach to GBM using hybrid surgical resection and LITT in a staged procedure to overcome traditional constraints of both open resection or LITT alone.

RGN6024 is a brain-penetrant, small molecule tubulin destabilizer for the treatment of glioblastoma.

Glioblastoma (GB) is the most common and aggressive malignant brain tumor in adults, with a median survival of ~15 months. Given the poor survival with the currently approved treatments, new therapies are urgently needed. Microtubule-targeting agents (MTAs) represent one of the most successful first-line therapies for cancers, however, the inability of approved MTAs to cross the blood-brain barrier (BBB) limits their use for central nervous system (CNS) cancers. The development of novel MTAs with good BBB penetrance, decreased toxicity, and an ability to overcome drug-induced resistance is an attractive prospect. Herein, we describe the characterization of RGN6024, a brain-penetrant small molecule tubulin destabilizer that binds the colchicine binding site of tubulin. RGN6024 has excellent in vitro potency against GB cell lines in viability assays with IC50 values in the low to mid nanomolar range. RGN6024 is less susceptible to common drug resistance mechanisms: its activity is unaffected by βIII-tubulin overexpression and it demonstrates good blood brain penetration in in vivo mouse and rat models. With oral dosing, RGN6024 shows excellent BBB penetration in both mice (Cmax = 3530 ng/g) and rats (Cmax = 1667 ng/g). Drug efficacy was confirmed in two xenograft models. In a TMZ-resistant LN-18 glioblastoma xenograft model, RGN6024 showed a reduction in tumor growth when dosed orally at 7.5 or 15 mg/kg. Additionally, RGN6024 suppressed the growth of BT142 glioblastoma cells in an orthotopic murine model and significantly prolonged survival. Taken together, these data provide support for the development of RGN6024 for the treatment of GB.

Targeting Topoisomerase I and DNA with LCS1269 Drives Glioblastoma Cell Death Despite ATM/Chk1/BRCA1/RAD51 Signaling Pathway Activation

Glioblastoma (GBM) is the most aggressive primary brain tumor in adults. The success of modern multimodal standards approved in anti-glioblastoma therapy remains limited. Consequently, new therapeutics are urgently needed. In this study, utilizing ex vivo, in silico, and in vitro approaches, we investigated the LCS1269 effects on two potential targets, DNA and Top I. We also elucidated the influence of LCS1269 on signaling pathways and GBM cell viability. Based on our docking data and competition studies results, we demonstrated that LCS1269 may bind to DNA, demonstrating selectivity toward AT-rich regions. We also showed that LCS1269 could dock both Top I/DNA binary complex and Top I active sites. LCS1269 caused Top I dysfunction and downregulated the expression of Top I. Moreover, the LCS1269 treatment of GBM cells facilitated DNA damage and the activation of the ATM/Chk1/BRCA1/Rad51 pathway. Meanwhile, DNA damage response induction and ATM/Chk1/BRCA1/Rad51 pathway activation were insufficient to prevent GBM cell death triggered by LCS1269 treatment. Our work shows that DNA and Top I are promising molecular targets of LCS1269, thus providing insight on several novel mechanisms of its anti-tumor activity. Nonetheless, we did not perform a biophysical validation of the LCS1269–DNA interaction, which is a limitation of our study.

GRPR-targeted gold nanoparticles as selective radiotherapy enhancers in glioblastoma

Objective.Glioblastoma multiforme (GBM) is the most diagnosed primary brain tumor in adults and remains associated with a poor prognosis due to its aggressive nature. As tumor recurrence is often observed after standard radiation treatment, the use of gold nanoparticles (AuNPs) to improve radiotherapy effectiveness has been proposed as an advanced treatment strategy for this condition. Toward this goal, we investigated the radiosensitizing potential of gastrin releasing peptide receptor (GRPR)-targeted gold nanoparticles (AuNP-BBN) carrying a bombesin peptide (BBN) in glioblastoma cells, when combined withγand x-ray radiation and in comparison with their non-targeted counterpart (AuNP-DOTA).Approach.Radiation response of U373 and U87 glioblastoma cells was studied upon exposure to Co-60γradiation or 160 kVp x-rays and U373 cells were subjected to combined treatment with the AuNPs using the same radiation qualities. The radiobiological effects were assessed via cell viability, clonogenic survival and DNA damage assays, including the determination of the sensitization enhancement ratio (SER). To rationalize the experimental results, Monte Carlo (MC) simulations were performed based on realistic microscopy-based glioblastoma cell models.Main results.U373 and U87 cells proved to be more sensitive to x-rays than toγradiation. Incubation with AuNP-BBN caused a dose enhancement effect when combined with kilovoltage x-rays but not with Co-60γradiation, resulting in reduced U373 cell viability, impaired proliferation and DNA damage. This outcome was not observed in cells treated with the non-targeted AuNP-DOTA, showing that the incorporation of the BBN was crucial for the radiosensitization of GRPR-positive GBM cells. MC simulated radiobiological outcomes were consistent with experimental findings.Significance.GRPR-targeted AuNP-BBN are promising nanotools for developing novel treatment strategies for GBM, acting as local and cell-specific radiotherapy enhancers. Their radiosensitizing effects were accurately predicted using an alternative MC simulation method based on realistic microscopy-based cell phantoms.

A Critical Review of CAR-T Therapies for Glioblastoma: What's Wrong with the Current Attempts?

Today, CAR-T therapy has been widely acknowledged as a "gold standard" treatment for certain hematologic diseases. There is a relatively small but enhancing body of clinical trials studying the effectiveness of CAR-T in treating glioblastoma, known as the most common and aggressive brain tumor in adults. Despite the promising findings, currently available data is still erratic. We aimed to overview the recent clinical attempts to apply CAR-T therapy as the treatment strategy for glioblastoma and highlight non-obvious problems occurring: flaws in the study design with suspicious inclusion criteria, absence of narrow nosologic focus, poor validation or even nonvalid imaging technologies and inconveniencing efficacy evaluation. We also discussed further upcoming advanced approaches for CAR-T cell manufacturing. We are convinced that our review could help to define the right place for CAR-T therapy in glioblastoma treatment strategy and would pave the way for future successful clinical trials.

Preoperative Nomogram-Based Assessment to Identify GBM Patients Who Do not Derive Survival Benefit From GTR Compared to STR.

Preoperative Nomogram-Based Assessment to Identify GBM Patients Who Do not Derive Survival Benefit From GTR Compared to STR.

Integration of omics data in the diagnosis and therapy of glioblastoma.

Since the 2016 update of the WHO Classification of Tumors of the Central Nervous System, omics data have been officially integrated into the diagnostic process for glioblastoma, the most prevalent and aggressive primary malignant brain tumor in adults. This review will examine the current and future integration of omics data in both the diagnosis and therapy of glioblastomas. The current clinical use of omics data primarily focuses on genomics for determining the IDH- and H3-wildtype status of the tumor, and on epigenomics, such as assessing MGMT promoter methylation status as a prognostic and predictive biomarker. However, it can be anticipated that the usage and importance of omics data will likely increase in the future. This work highlights how omics technologies have significantly enhanced our understanding of glioblastoma, particularly of its extensive heterogeneity. This enhanced understanding has not only improved diagnostic accuracy but has also facilitated the identification of new predictive and/or prognostic biomarkers. It is likely that the ongoing integration of omics data will transform many aspects of the diagnostic process, including sample acquisition. Additionally, omics data will be integrated into future glioblastoma treatment procedures, with possible applications ranging from identifying potential therapeutic targets to selecting individual treatment plans. The implications of the ongoing integration of omics data for clinical routine, future classification systems, and trial design are also discussed in this review, outlining the pivotal role omics data play in shaping future glioblastoma diagnosis and treatment.

Caffeinated and Decaffeinated Yerba Mate (Ilex paraguariensis) Infusion Extracts Alter CD73 and Reduce the Migration and Adhesion of Glioblastoma Cells.

Gliomas are the most common malignant brain tumors in adults, characterized by a high proliferation and invasiveness. Treatment remains challenging due to their immunomodulatory properties, which promote immune evasion and tumor progression. Given the substantial consumption of yerba mate in the southern hemisphere, this study evaluated the effects of caffeinated and decaffeinated yerba mate infusion extracts (ECaf and EDCaf, respectively) on glioblastoma cell lines (U87 and U251). Both extracts reduced cell viability in a dose-dependent manner, with U87 being more sensitive. ECaf and EDCaf inhibited cell migration and adhesion, particularly in U87 cells. Real-time PCR showed a reduction in CD73 and MMP2 expression in U87, whereas U251 exhibited a slight increase in MMP2 expression. CD73 enzymatic activity was reduced in U87 cells by both extracts but remained unaffected in U251 cells. Overall, the results suggest that caffeine absence does not alter the bioactivity of yerba mate extracts, highlighting their potential to modulate glioblastoma cell behavior.

PIK3R2 immunostaining status predicts prognosis in patients with newly diagnosed glioblastoma treated with an autologous tumor vaccine.

Glioblastoma (GBM) is the most common and aggressive primary brain tumor in adults, characterized by high invasiveness and a poor prognosis, with limited treatment options. Our previous study on fractionated radiotherapy, temozolomide, and an autologous formalin-fixed tumor vaccine (AFTV) for newly diagnosed grade 4 astrocytic tumors demonstrated that complete tumor resection and p53 negativity on immunohistochemistry were associated with favorable outcomes. PIK3R2, a key component of the PI3K-Akt signaling pathway, may modulate the host immune response to tumor antigens and influence the efficacy of immunotherapy. In this study, we further investigated whether PIK3R2, a candidate gene identified through gene panel sequencing as potentially associated with prognosis following AFTV treatment, influences patient outcomes after AFTV therapy. We analyzed 58 patients with newly diagnosed IDH wildtype GBM or IDH mutant grade 4 astrocytoma (Astro). Among them, 29 received standard treatment combined with AFTV (AFTV group), while 29 underwent standard treatment alone (control group). Immunostaining for PIK3R2 and p53 was performed, and patient characteristics, including age, sex, Karnofsky Performance Status at the time of surgery, and overall survival (OS), were evaluated. PIK3R2 expression levels were classified using a 34% cutoff value. In the AFTV group, survival analysis based on PIK3R2 status (positive/negative) revealed an increased survival in the PIK3R2-negative group when comparing AFTV and control groups (p = 0.075 in GBM/Astro cases and p = 0.030 in GBM cases). When stratifying patients into four subgroups based on p53 and PIK3R2 status (p53-negative/PIK3R2-negative, p53-positive/PIK3R2-positive, p53-negative/PIK3R2-positive, and p53-positive/PIK3R2-negative), a significant improvement in OS was observed in the p53-negative/PIK3R2-negative group both in GBM/Astro cases and GBM cases. PD-1 demonstrated the strongest correlation with PIK3R2 in the regression analysis. Negative immunostaining for PIK3R2 as well as negative p53 revealed an increased survival in patients receiving AFTV therapy for GBM. In patients receiving AFTV, these immunostaining results may serve as a predictor of treatment efficacy and overall survival.

Platinum(IV) anticancer therapies and cathepsin B: innovative strategies for overcoming resistance in glioblastoma cells

Glioblastoma (GBM) is the most frequent and aggressive brain tumor in adults. Due to its heterogeneity, the abundance of altered signaling pathways within the same tumoral mass, its low immunogenicity, and the presence of the blood–brain barrier, standard therapies based on surgical resection, radiotherapy, and chemotherapy result in ineffective tumor removal. For these reasons, the development of new drugs is mandatory to ameliorate patients’ life expectancy and quality of life. Cathepsins are lysosomal proteases involved in several physiological and pathological processes, and they play key roles in modulating cell death and pharmacological resistance. In particular, cathepsin B is a crucial regulatory protein in different types of cell death, and its overexpression contributes to GBM angiogenesis and tumor progression. Octahedral platinum(IV) (Pt(IV))-based prodrugs have already demonstrated improved anticancer efficacy compared to routinely used cisplatin. This work aims to investigate the effects of two such prodrugs—Pt(IV)Ac-POA ((OC-6-44)-acetatodiamminedichlorido(2-(2-propynyl)octanoato)platinum(IV)) and DB178 ((OC-6-44)-acetatodiamminedichlorido(4,5-dihydroxy-9,10-dioxo-9,10-dihydroanthracene-2-carboxylato)platinum(IV))—on two different glioblastoma cell lines, U251 and T98G, with particular attention to their effects on cathepsin B. The immunocytochemical and biochemical results obtained on the two cell lines highlight the maintenance of basal levels of cathepsin B while efficiently activating programmed cell death mechanisms, as investigated by optical and electronic microscopy. These findings may serve as a valid starting point for further approaches that incorporate cathepsins’ inhibitors to improve therapeutic efficacy and possibly reveal novel pharmacological targets.

Impact of sociodemographic factors and Medicaid expansion on postoperative outcomes for glioblastoma, 2004-2021.

1614 Background: Glioblastoma (GBM), the most aggressive primary brain tumor in adults, has a median survival of ~15 months despite treatment and exhibits significant disparities in care access. Sociodemographic factors and policy interventions, such as Medicaid expansion under the ACA, show potential to mitigate inequities in other cancers. However, their impact on GBM outcomes remains underexplored. Methods: Using the National Cancer Database, we conducted a retrospective study of 85,631 GBM patients treated with surgery between 2004 and 2021. Multivariate regression models and Kaplan-Meier survival analyses evaluated associations between sociodemographic factors (e.g., race, income, education, rurality, insurance status) and outcomes, including postoperative hospital stay, 30-day readmission, 90-day mortality, and overall survival. All models adjusted for key clinical (e.g., tumor size, comorbidities, receipt of chemotherapy/radiation therapy) and patient (e.g., age, sex) covariates. A difference-in-differences analysis assessed the effects of Medicaid expansion on these outcomes. Results: Regarding postoperative length of hospital stay, disparities were observed by race (Black vs. White β = 1.45 days [1.22–1.68]; Asian American and Pacific Islander [AAPI] vs. White β = 0.86 days [0.50–1.22]), rurality (urban vs. metro β = -0.31 days [-0.47 to -0.15]), insurance status (private vs. uninsured β = -1.10 days [-1.41 to -0.80]), and education (highest vs. lowest quartile β = -0.28 days [-0.48 to -0.09]). Unplanned 30-day hospital readmission rates demonstrated disparities by race (Black vs. White OR = 1.19 [1.04–1.35]), income (highest vs. lowest quartile OR = 0.84 [0.75–0.96]), and education (highest vs. lowest quartile OR = 1.19 [1.05–1.34]). Moreover, 90-day mortality indicated disparities by race (Black vs. White OR = 0.85 [0.77–0.95]; AAPI vs. White OR = 0.64 [0.53–0.77]), income (highest vs. lowest quartile OR = 0.81 [0.74–0.89]), education (highest vs. lowest quartile OR = 1.13 [1.03–1.23]), and insurance status (private vs. uninsured OR = 0.71 [0.62–0.82]). Finally, overall survival demonstrated disparities by race (Black vs. White HR = 0.88 [0.85–0.91]; AAPI vs. White HR = 0.77 [0.73–0.82]), income (highest vs. lowest quartile HR = 0.83 [0.81–0.86]), education (highest vs. lowest quartile HR = 1.12 [1.09–1.15]), rurality (rural vs. metro HR = 1.06 [1.00–1.12]), and insurance status (Medicaid vs. no insurance HR = 1.09 [1.04–1.15]). Medicaid expansion did not significantly impact any outcomes, including overall survival (DID HR = 0.95 [0.84–1.07]). Conclusions: Significant sociodemographic disparities persist in GBM postoperative outcomes, with no improvement from Medicaid expansion. Targeted socioeconomic interventions are needed to address inequities in access to specialized neuro-oncological care and improve outcomes for underserved populations.

Protective effects of gallic acid against cadmium-induced neuroinflammation in glioblastoma cells.

e14018 Background: Environmental exposure to cadmium (Cd), a toxic heavy metal, was associated with an increased incidence risk of glioblastoma multiforme (GBM), the most common, malignant primary brain tumor in adults. One possible mechanism by which Cd exerts its carcinogenic effect is related to inflammation. Our previous studies have demonstrated that Cd induces cytokine response at low concentrations (1-10 µM) and early-time points both in primary human astrocytes and human U-87 MG astrocytes. Gallic acid (GA) is a natural phenolic compound with several therapeutic effects, including anti-inflammatory, antioxidant, and anti-tumor. GA has shown a neuroprotective effect under Cd induction in Wistar rats. However, the underlying mechanism has not been extensively reported. This study aims to investigate the protective effects and potential mechanism of GA against inflammation induced by Cd exposure in human U-87 MG astrocytes. Methods: The effect of GA on Cd-induced expression and release of cytokine was investigated in human astrocytoma U-87 MG astrocytes by real-time PCR and ELISA, respectively as well as molecular mechanisms involved in the anti-inflammatory effect of this drug was investigated by Western Blotting. Results: The results showed that pretreatment of GA suppressed an increased level of interleukin (IL)-6, IL-8, chemokine (C-C motif) ligand (CCL)2, and CCL3 secretion by human U-87 MG astrocytes. In addition, pretreatment of GA inhibited Cd-activated phosphorylation of ERK1/2 MAPK and phosphorylation of signal transducer and activator of transcription 3 (STAT3). Conclusions: These findings suggest that GA may help prevent inflammation-induced GBM.