Roles of mTOR-p70S6K signaling pathway and HO-1 inethylbenzene-induced hepatoxic effects in L02 cells.

Ethylbenzene (EB)-induced hepatotoxic effects has been indicated as oxidative damage and mitochondria-mediated apoptosis in vivo in our previous study, yet the mechanisms remain unclear. This study aimed to explore the role of the mTOR-p70S6K signaling pathway in EB-induced hepatoxic effects in vitro. Normal human hepatocytes (L02 cells) were exposed to different concentrations of ethylbenzene (0-10 mM) for 24 hours. In vitro, we found that EB treatment decreased the viability of L02 cells, via inducing oxidative stress, mitochondrial impairments, excessive apoptosis and autophagy. These were accompanied by the inactivation of the mTOR-p70S6K signaling cascade, as manifested by the decreased levels of related molecules Atg family proteins and Heme oxygenase-1 (HO-1). These findings were further confirmed by mTOR inhibitor treatment and immunofluorescence analysis. Jointly, our results indicate that EB induces hepatoxic effects by triggering mitochondrial impairments and excess apoptosis and autophagy in L02 cells via suppressing the mTOR-p70S6K signaling, and oxidative stress affects the passive up-regulation of HO-1.

Histopathologic observations in a coccidiosis model of Eimeria tenella.

BACKGROUND: Species of the genus Eimeria cause coccidiosis in chickens, resulting in a huge burden to the poultry industry worldwide. Eimeria tenella is one of the most prevalent chicken coccidia in China, and E. tenella infection causes hemorrhagic cecitis. METHODS: Using an established model of coccidiosis in chickens combined with necropsy, imaging of pathological tissue sections, and other techniques, we evaluated the gross and microscopic lesions of cecal tissue within 15 days after inoculation with sporulated oocysts and described the endogenetic developmental process and relationship between E. tenella infection and enteritis development in chickens. RESULTS: We observed three generations of merogony and gamogony in E. tenella. We observed gross lesions in the cecum from 84 hpi (hours post inoculation) and microscopic lesions from 60 hpi. The lesions in the cecum mainly exhibited hemorrhagic enteritis. Their severity increased with the onset of the second generation of merogony. The lesions began to alleviate by the end of the endogenous stages of E. tenella. CONCLUSION: We show, for the first time, the complete observation of a series of changes in enteritis caused by 5 × 103 E. tenella oocysts. This study provides reference materials for E. tenella research and pathological diagnosis.

A NH2-Cu-MOF for promising antibacterial application.

A copper-based metal-organic framework named NH2-Cu-MOF has been synthesized and utilized as an effective broad-spectrum antimicrobial material in this article. The obtained NH2-Cu-MOF exhibits satisfying antibacterial activity against both gram-positive bacteria (S. aureus and S. epidermidis) and gram-negative bacteria (E. coli and K. peneumoniae). Additionally, the biocompatibility of this NH2-Cu-MOF has been validated through animal studies, showing no significant adverse effects, thereby confirming its high biocompatibility. These findings prove that NH2-Cu-MOF has positive effects upon the treatment of bacteria-infected wounds, which holds great potential to be applied in biochemistry field.

Artificial river flow regulation triggered spatio-temporal changes in marine macrobenthos of the Yellow River Estuary.

The Water Sediment Discharge Regulation (WSR) in the Yellow River transports a vast quantity of freshwater and materials to the Bohai Sea within 20 days, significantly altering the ambient environment of the estuary. To elucidate the ecological impacts of this typically artificial flood event, we investigated the benthic habitats and macrobenthic biodiversity within the Affected Core Area (ACA) influenced by this discharge. Our results show that: (1) The discharge created an area with extreme environmental conditions, extending from the southern estuary to Laizhou Bay. This led to a rapid transformation of the habitat, as evidenced by a significant increase in turbidity, ammonium, and silicate levels. Among these factors, nitrogen nutrients and pH were the dominant drivers of environmental filtration, shaping the macrobenthos community structure; (2) The changing habitat triggered spatial shifts in macrobenthos abundance based on the distance from the estuary. Compared to the northern estuary, species composition and C-diversity in the southern area decreased significantly. These changes collectively established a short-term biodiversity front in the estuary region; (3) Community stability declined, as evidenced by a 24.20% reduction in niche width for generalist species and a 90.91% shift in specialist species. Furthermore, the connectivity between species decreased, and the average path length of the network increased, resulting in a more fragmented community structure. Notably, some ecological patches dominated by generalist species (e.g. Alpheus distinguendus) emerged. These findings enhance our understanding of marine ecological responses to artificial flood events within the context of global environmental changes.

Pharmacokinetic and tissue distribution study of pectolinarigenin in rats using UPLC-MS/MS.

Pectolinarigenin (PEC), a natural flavonoid isolated from Cirsium japonicum, exhibits promising therapeutic potential for multiple cancers. In present study, a simple and sensitive UPLC-MS/MS method was established for the quantification of PEC in rat plasma and tissues. The assay procedure involved a one-step protein precipitation with tadalafil as the internal standard, and separation on a Welch Xtimate UHPLC C18 column by gradient elution of acetonitrile/aqueous formic acid (0.1 %, v/v) at a flow rate of 0.2 m L·min-1. The detection was conducted using multiple-reaction monitoring via an electrospray ionization source in positive ionization mode. The established method was proved to be highly sensitive with a good linearity (R2 > 0.99) in respective concentration range (0.1-100 ng·mL-1 in plasma and 1-10,000 ng·mL-1 in tissues) and acceptable extraction recovery (≥71.17 %), matrix effect and stability, which was applied to study the pharmacokinetics and tissue distribution of PEC after intravenous (100 µg·kg-1) and oral administration (10, 20 and 40 mg·kg-1). PEC was promptly absorbed (Tmax ≤ 0.222 h) and maintained at a low level with slow elimination (t1/2 z ≥ 14.47 h) in rats after oral administration, resulting in extremely low bioavailability (0.56-0.68 %). However, PEC is widely distributed in rat tissues with high exposure in GI tract, liver and kidney. The bioavailability and tissue affinity were firstly revealed, which would guide directions for further development of PEC as an anti-tumor drug candidate.

Development of a disulfidptosis-related prognostic model for endometrial cancer with potential therapeutic target.

Prognosis biomarkers for endometrial cancer (EC) are in need. Recent evidence demonstrated the critical role of disulfidptosis, a novel cell death modality, in cancer. However, limited studies have developed a disulfidptosis-related gene model for EC. Disulfidptosis prognosis score of EC (disulfidptosis-PSEC) were constructed using disulfidptosis-related differently expression genes with the RNA data of 544 EC patients from The Cancer Genome Atlas (TCGA) dataset. Model was evaluated using time-dependent receiver operating characteristic curve analysis for overall survival (OS) and disease-free survival (DFS), along with the hazard ratio (HR) between risk groups. Then, the cellular and molecular profile for different risk groups were performed, along with drug target inference. Disulfidptosis-PSEC demonstrated outstanding prognostic value for OS and DFS, with 5-year area under curve of 0.71 (95% CI, 0.58-0.75) and 0.69 (95% CI, 0.62-0.76), respectively. Low risk group demonstrated better survival with an HR of 0.38 (95% CI, 0.24-0.59) and 0.46 (95% CI, 0.32-0.66) for OS and DFS, respectively. The model was independent of TCGA subtype. Low risk group were featured with more immune cell infiltration and less gene mutation. Serval drug targets, and the therapeutic value of serotonin receptor among copy number (CN)-low subpopulation, were identified. Disulfidptosis-PSEC was a potential prognosis biomarker for EC with targetable biological process.

Loss of Annexin A1 in macrophages restrains efferocytosis and remodels immune microenvironment in pancreatic cancer by activating the cGAS/STING pathway.

OBJECTIVE: Pancreatic cancer is an incurable malignant disease with extremely poor prognosis and a complex tumor microenvironment. We sought to characterize the role of Annexin A1 (ANXA1) in pancreatic cancer, including its ability to promote efferocytosis and antitumor immune responses. METHODS: The tumor expression of ANXA1 and cleaved Caspase-3 (c-Casp3) and numbers of tumor-infiltrating CD68+ macrophages in 151 cases of pancreatic cancer were examined by immunohistochemistry and immunofluorescence. The role of ANXA1 in pancreatic cancer was investigated using myeloid-specific ANXA1-knockout mice. The changes in tumor-infiltrating immune cell populations induced by ANXA1 deficiency in macrophages were assessed by single-cell RNA sequencing and flow cytometry. RESULTS: ANXA1 expression in pancreatic cancer patient samples correlated with the number of CD68+ macrophages. The percentage of ANXA1+ tumor-infiltrating macrophages negatively correlated with c-Casp3 expression and was significantly associated with worse survival. In mice, myeloid-specific ANXA1 deficiency inhibited tumor growth and was accompanied by the accumulation of apoptotic cells in pancreatic tumor tissue caused by inhibition of macrophage efferocytosis, which was dependent on cGAS-STING pathway-induced type I interferon signaling. ANXA1 deficiency significantly remodeled the intratumoral lymphocyte and macrophage compartments in tumor-bearing mice by increasing the number of effector T cells and pro-inflammatory macrophages. Furthermore, combination therapy of ANXA1 knockdown with gemcitabine and anti-programmed cell death protein-1 antibody resulted in synergistic inhibition of pancreatic tumor growth. CONCLUSION: This research uncovers a novel role of macrophage ANXA1 in pancreatic cancer. ANXA1-mediated regulation of efferocytosis by tumor-associated macrophages promotes antitumor immune response via STING signaling, suggesting potential treatment strategies for pancreatic cancer.

Differences in BRAF V600E mutation between the epithelium and mesenchyme in classic ameloblastoma.

PURPOSE: Laser capture microdissection (LCM) was used to pinpoint the mutated tissue in ameloblastoma and investigate whether B-Raf proto-oncogene, serine/threonine kinase (BRAF) mutation is the main pathogenic gene in classic ameloblastoma. STUDY DESIGN: A total of 24 patients with ameloblastoma scheduled to undergo surgery between 2000 and 2024 were included in the study. LCM was used to isolate tumor cells. Oxford nanopore technology (ONT) was used to analyze the collected cells. GO and KEGG enrichment analyses were then performed on the 300 most highly expressed genes in the epithelial tissue and mesenchyme. RESULTS: Mandibular follicular ameloblastoma showed BRAF V600E mutations in all epithelial cells but not in the mesenchyme. The mutation rate was significantly higher in mandibular ameloblastomas compared to the maxilla (P < .05). RNA-seq showed that traditional follicular ameloblastoma epithelium was enriched in "growth factor receptor binding" and "angiogenesis regulation," while the mesenchyme was enriched in "ECM receptor interaction." KEGG enrichment analysis showed differential gene expression, mainly in MAPK and PI3K-AKT pathways. CONCLUSION: Classical follicular ameloblastoma shows the presence of BRAF V600E mutation in epithelial tissue, with a higher mutation rate in the mandible than in the maxilla. The signaling pathways of MAPK and PI3K may be significantly involved in epithelial signal transduction.

Lymphopenia in sepsis: a narrative review.

This narrative review provides an overview of the evolving significance of lymphopenia in sepsis, emphasizing its critical function in this complex and heterogeneous disease. We describe the causal relationship of lymphopenia with clinical outcomes, sustained immunosuppression, and its correlation with sepsis prediction markers and therapeutic targets. The primary mechanisms of septic lymphopenia are highlighted. In addition, the paper summarizes various attempts to treat lymphopenia and highlights the practical significance of promoting lymphocyte proliferation as the next research direction.

[Advances in the treatment of Clostridium difficile infection in children]. / 儿童艰难梭菌感染的治疗进展.

Clostridium difficile infection (CDI) is a major cause of hospital-acquired gastrointestinal infections in children. Current treatment for pediatric CDI primarily involves antibiotics; however, some children experience recurrence after antibiotic treatment, and those with initial recurrence remain at risk for further recurrences following subsequent antibiotic therapy. In such cases, careful consideration of treatment options is necessary. Fecal microbiota transplantation has been shown to be effective for recurrent CDI and has a high safety profile. This article reviews the latest research on the pathogenesis, risk factors, diagnosis, and treatment of pediatric CDI domestically and internationally, with a particular focus on fecal microbiota transplantation therapy.

Decadal variation and temporal stability of the macrobenthic community in the Bohai Sea, China.

Biodiversity in the Bohai Sea is threatened by climate change and human activities. An analysis based on decadal macrobenthic community data was conducted to assess the ecological health. These findings revealed the temporal and spatial variations in species composition and biodiversity, which were primarily influenced by depth, temperature and dissolved oxygen content. The community structure in 2014 exhibited a 70 % dissimilarity compared to other years, and biodiversity was lower in 2014. The dominant species showed a trend towards miniaturization. Abundance-biomass comparison curves indicated that community disturbance improved by implementing various policies. Overall, communities in the Bohai Sea remained stable, except in the Bohai Strait (BH), where synchronous fluctuations with an increasing trend were observed. Enhancing biodiversity and addressing the risks associated with losing single species are essential for maintaining community stability. The community also displayed synchronous tendencies in Laizhou Bay, emphasizing the need for continued long-term monitoring.

EAT-Lancet Diet Pattern, Genetic Predisposition, Inflammatory Biomarkers, and Risk of Lung Cancer Incidence and Mortality.

SCOPE: The association between a planetary and sustainable EAT-Lancet diet and lung cancer remains inconclusive, with limited exploration of the role of genetic susceptibility and inflammation. METHODS AND RESULTS: The study includes 175 214 cancer-free participants in the UK Biobank. Fourteen food components are collected from a 24-h dietary recall questionnaire. A polygenic risk score is constructed through capturing the overall risk variants for lung cancer. Sixteen inflammatory biomarkers are assayed in blood samples. Participants with the highest EAT-Lancet diet scores (≥12) have a lower risk of lung cancer incidence (hazard ratio [HR] = 0.64, 95% confidence interval [CI]: 0.51-0.80) and mortality (HR = 0.65, 95% CI: 0.48-0.88), compared to those with the lowest EAT-Lancet diet scores (≤8). Interestingly, there is a significantly protective trend against both lung adenocarcinoma and lung squamous cell carcinoma with higher EAT-Lancet diet scores. Despite no significant interactions, a risk reduction trend for lung cancer is observed with increasing EAT-Lancet diet scores and decreasing genetic risk. Ten inflammatory biomarkers partially mediate the association between the EAT-Lancet diet and lung cancer risk. CONCLUSION: The study depicts a lower risk of lung cancer conferred by the EAT-Lancet diet associated with lower inflammation levels among individuals with diverse genetic predispositions.

An Exploration of Shared Risk Factors for Coronary Artery Disease and Cancer from 109 Traits: The Evidence from Two-Sample Mendelian Randomization Studies.

Background: Although observational studies have reported several common biomarkers related to coronary artery disease (CAD) and cancer, there is a shortage of traditional epidemiological data to establish causative linkages. Thus, we conducted a comprehensive two-sample Mendelian randomization (MR) analysis to systematically investigate the causal associations of 109 traits with both CAD and cancer to identify their shared risk and protective factors. Methods: The genetic association datasets pertaining to exposure and outcomes were reviewed using the most recent and public genome-wide association studies (GWAS). Inverse variance weighting (IVW), weighted median (WM), and MR-Egger strategies were implemented for the MR analyses. The heterogeneity and pleiotropy were measured utilizing leave-one-out sensitivity testing, MR-PRESSO outlier detection, and Cochran's Q test. Results: The IVW analyses revealed that genetic-predicted mean sphered cell volume (MSCV) is a protective factor for CAD, and weight is a risk factor. MSCV and weight also show similar effects on cancer. Furthermore, our study also identified a set of risk and protective factors unique to CAD and cancer, such as telomere length. Conclusions: Our Mendelian randomization study sheds light on shared and unique risk and protective factors for CAD and cancer, offering valuable insights that could guide future research and the development of personalized strategies for preventing and treating these two significant health issues.

Mechanism investigation of highly selective inhibitors toward phosphodiesterase 5 and 6 via the in vitro calculation and simulation.

Introduction: In clinical practice, phosphodiesterase 5 (PDE5) inhibitors are commonly used to treat erectile dysfunction and pulmonary arterial hypertension. However, due to the high structural similarity between PDE5 and Phosphodiesterase 6 (PDE6), there is a risk that existing drugs will cause off-target effects on PDE6 resulting in visual disorders such as low visual acuity and color blindness. Previous research on the selectivity of PDE5 inhibitors focused on marketed drugs such as sildenafil and tadalafil. Methods: In this study, a highly selective PDE5 inhibitor, ligand3, was used as the subject, and molecular docking, molecular dynamics simulations, MM-GBSA, alanine scanning, and independent gradient model analysis were employed to investigate the biological mechanism underlying the selectivity of PDE5 inhibitors. Results and Discussion: The present work revealed that the binding mode of ligand3 to the PDE5A and PDE6C targets was distinctly different. Ligand3 exhibited stronger coulombic forces when binding to PDE5A, while showing stronger van der waals forces when binding to PDE6C. Ligand3 binds more deeply at the active site of PDE5A than at PDE6C, allowing its side chains to effectively bind to the critical TYR612, whereas in the case of the shallow binding to PDE6C, ligand3 lacks a similar effect. Mechanism investigations of highly selective inhibitors through computational simulation might provide an insight into potent treatment of drugs.

Negatively Charged Carbon Dots Employed Symplastic and Apoplastic Pathways to Enable Better Plant Delivery than Positively Charged Carbon Dots.

Efficient delivery of nanoparticles (NPs) to plants is important for agricultural application. However, to date, we still lack knowledge about how NPs' charge matters for its translocation pathway, i.e., symplastic and apoplastic pathways, in plants. In this study, we synthesized and used negatively charged citrate sourced carbon dots (C-CDs, -37.97 ± 1.89 mV), Cy5 coated C-CDs (Cy5-C-CDs, -41.90 ± 2.55 mV), positively charged PEI coated carbon dots (P-CDs, +43.03 ± 1.71 mV), and Cy5 coated P-CDs (Cy5-P-CDs, +48.80 ± 1.21 mV) to investigate the role of surface charges and coatings on the employed translocation pathways (symplastic and apoplastic pathways) of charged NPs in plants. Our results showed that, different from the higher fluorescence intensity of P-CDs and Cy5-P-CDs in extracellular than intracellular space, the fluorescence intensity of C-CDs and Cy5-C-CDs was similar between intracellular and extracellular space in cucumber and cotton roots. It suggests that the negatively charged CDs were translocated via both symplastic and apoplastic pathways, but the positively charged CDs were mainly translocated via the apoplastic pathway. Furthermore, our results showed that root applied negatively charged C-CDs demonstrated higher leaf fluorescence than did positively charged P-CDs in both cucumber (8.09 ± 0.99 vs 3.75 ± 0.23) and cotton (7.27 ± 1.06 vs 3.23 ± 0.22), indicating that negatively charged CDs have a higher translocation efficiency from root to leaf than do positively charged CDs. It should be noted that CDs do not affect root cell activities, ROS level, and photosynthetic performance in cucumber and cotton, showing its good biocompatibility. Overall, this study not only figured out that root applied negatively charged CDs employed both symplastic and apoplastic pathways to do the transportation in roots compared with mainly the employment of apoplastic pathway for positively charge CDs, but also found that negatively charge CDs could be more efficiently translocated from root to leaf than positively charged CDs, indicating that imparting negative charge to NPs, at least CDs, matters for its efficient delivery in crops.

Demographic and socioeconomic disparity in knowledge, attitude, and practice towards tuberculosis in Northwest, China: evidence from multilevel model study.

BACKGROUND: Tuberculosis (TB) remains a serious global public health problem in China. The right knowledge, attitude, and practice (KAP) towards TB are indispensable to appropriate healthcare-seeking behaviors and treatment services timely. However, there are few studies that addressed the KAP towards TB in high-risk and under-developing regions in China. This study aims to evaluate the KAP towards TB in Ningxia Northwest, China, and identify factors that influence it. The findings can guide future health education and promotion interventions. METHODS: A stratified multistage random sampling method was used to conduct a face-to-face questionnaire survey with 33 items for selected residents. The composite score of Knowledge, Attitudes, and Practices (KAP) was divided into two groups, which are poor (scores below the average) and good (scores above the average). A two-level logistic model with a random intercept equation accounted for the similarity of residents within communities to examine the association between individual-level KAP and demographic and socioeconomic factors. RESULTS: A total of 2,341 residents were recruited, the mean age was 50, and 41.2% were female. The percentages of residents who were total awareness of TB knowledge and had positive attitudes and behavior toward TB were 51.9%, 75.3%, and 76.2%, respectively. The two-level logistic model demonstrated that residents with a high annual family income, urban living, primary school education or higher, occupation of teacher or doctor, a very good self-perceived status, medical insurance, knowing DOTS, and family members or friends with TB history had better knowledge of TB (P < 0.05). Residents living in urban areas, with junior and senior high school education, a very good self-perceived status, health insurance, knowing DOTS, and family members or friends with TB history had positive attitude of TB (P < 0.05). Residents living in urban areas, a primary school education or higher, occupation of teacher, doctor and workers, a very good self-perceived status, medical insurance, knowing DOTS, and family members or friends with TB history had positive practice of TB (P < 0.05). CONCLUSIONS: Favorable demographic (higher education levels, teachers or doctors) and socioeconomic (high income, living in urban area) factors are associated to better knowledge, attitudes and practices toward TB in Northwest China. Interventions to improve KAP at the community level are required to speed up the TB reduction rate, which may benefit to ensure the End TB Strategy will be achieved.

Clinical Characteristics of Overweight Patients With Acute Exacerbation Chronic Obstructive Pulmonary Disease (AECOPD).

INTRODUCTION: Low body weight in patients with COPD is associated with a poor prognosis and more comorbidities. However, the impact of increased body weight in patients with COPD remains controversial. The aim of this study was to explore the clinical features of overweight patients with AECOPD. METHODS: In this multicenter cross-sectional study, a total of 647 AECOPD patients were recruited. Finally, 269 normal weight and 162 overweight patients were included. Baseline characteristics and clinical and laboratory data were collected. The least absolute shrinkage and selection operator (LASSO) regression was performed to determine potential features, which were substituted into binary logistic regression to reveal overweight-associated clinical features. The nomogram and its associated curves were established to visualize and verify the logistic regression model. RESULTS: Six potential overweight-associated variables were selected by LASSO regression. Subsequently, a binary logistic regression model identified that the rates of type 2 diabetes (T2DM) and hypertension and levels of lymphocytes (LYM)%, and alanine aminotransferase (ALT) were independent variables of overweight in AECOPD patients. The C-index and AUC of the ROC curve of the nomogram were 0.671 and 0.666, respectively. The DCA curve revealed that the nomogram had more clinical benefits if the threshold was at a range of 0.22~0.78. CONCLUSIONS: Collectively, we revealed that T2DM and hypertension were more common, and LYM% and ALT were higher in AECOPD patients with overweight than those with normal weight. The result suggests that AECOPD patients with overweight are at risk for additional comorbidities, potentially leading to worse outcomes.

Case Report: Taking action or standing by: managing a preterm neonate at the risk of neonatal varicella by metagenomic next-generation sequencing.

Neonatal varicella is indeed a rare condition, and most infants born to mothers with varicella have a good prognosis. However, in exceptional cases, neonatal varicella can be life-threatening, particularly for preterm infants. Therefore, it is vital to make an early diagnosis or predict the risk of neonatal varicella to ensure prompt treatment and improve prognosis. This report made an effort to early predict neonatal vericalla by using metagenomic next-generation sequencing (mNGS) in a preterm infant who was at risk for vericalla infection. A preterm infant born from a mother with varicella with symptom onset at 8 days before delivery, putting the infant at risk for varicella infection. Importantly, the patient develop pneumonia and pneumothorax, and neonatal vericella was suspected. Fortunately, the use of mNGS for testing the varicella gene in the serum promptly ruled out varicella zoster virus (VZV) infection in the patient, as indicated by a negative mNGS result. Subsequent follow-up, which included a 14-day stay in the hospital followed by an additional 7 days at home, confirmed this finding. Throughout this period, the patient did not exhibit any rash or other symptoms associated with varicella. Therefore, the novel approach of using mNGS allows neonatologists to predict and promptly address potential neonatal infections. This early detection is crucial, as delayed diagnosis or treatment could pose life-threatening risks, as exemplified by the case of neonatal varicella. In such cases, neonatologists can take proactive measures instead of standing by for at-risk neonates. Furthermore, given the severity of neonatal varicella as a life-threatening condition, the early exclusion of subsequent varicella infection by mNGS can offer reassurance to both family members and healthcare professionals.

Racial and social-economic inequalities in systemic chemotherapy use among adult glioblastoma patients following surgery and radiotherapy.

Not all patients with glioblastoma multiforme (GBM) eligible for systemic chemotherapy after upfront surgery and radiotherapy finally receive it. The information on patients with GBM was retrieved from the surveillance, epidemiology, and end results database. Patients who underwent upfront surgery or biopsy and external beam radiotherapy between 2010 and 2019 were eligible for systemic chemotherapy. The available patient and tumor characteristics were assessed using multivariable logistic regression and chi-squared test. Out of the 16,682 patients eligible, 92.1% underwent systemic chemotherapy. The characteristics linked to the lowest systemic chemotherapy utilization included tumors of the brain stem/cerebellum (P = 0.01), former years of diagnosis (P = 0.001), ≥ 80 years of age (P < 0.001), Hispanic, Non-Hispanic Asian, Pacific Islander, or Black race (P < 0.001), non-partnered status (P < 0.001), and low median household income (P = 0.006). Primary tumor site, year of diagnosis, age, race, partnered status, and median household income correlated with the omission of systemic chemotherapy in GBM in adult patients.