tbuckley/cabot-search huggingface dataset:
Subcortical Brain Development in Autism and Fragile X Syndrome: Evidence for Dynamic, Age- and Disorder-Specific Trajectories in Infancy
Authors: Mark D. Shen, Meghan R. Swanson, Jason J. Wolff, Jed T. Elison, Jessica B. Girault, Sun Hyung Kim, Rachel G. Smith, Michael M. Graves, Leigh Anne H. Weisenfeld, Lisa Flake, Leigh MacIntyre, Julia L. Gross, Catherine A. Burrows, Vladimir S. Fonov, D. Louis Collins, Alan C. Evans, Guido Gerig, Robert C. McKinstry, Juhi Pandey, Tanya St. John, Lonnie Zwaigenbaum, Annette M. Estes, Stephen R. Dager, Robert T. Schultz, Martin A. Styner, Kelly N. Botteron, Heather C. Hazlett, Joseph Piven
Journal: American Journal of Psychiatry (2022)

Objective: Previous research has demonstrated that the amygdala is enlarged in children with autism spectrum disorder (ASD). However, the precise onset of this enlargement during infancy, how it relates to later diagnostic behaviors, whether the timing of enlargement in infancy is specific to the amygdala, and whether it is specific to ASD (or present in other neurodevelopmental disorders, such as fragile X syndrome) are all unknown. Methods: Longitudinal MRIs were acquired at 6–24 months of age in 29 infants with fragile X syndrome, 58 infants at high likelihood for ASD who were later diagnosed with ASD, 212 high-likelihood infants not diagnosed with ASD, and 109 control infants (1,099 total scans). Results: Infants who developed ASD had typically sized amygdala volumes at 6 months, but exhibited significantly faster amygdala growth between 6 and 24 months, such that by 12 months the ASD group had significantly larger amygdala volume (Cohen’s d=0.56) compared with all other groups. Amygdala growth rate between 6 and 12 months was significantly associated with greater social deficits at 24 months when the infants were diagnosed with ASD. Infants with fragile X syndrome had a persistent and significantly enlarged caudate volume at all ages between 6 and 24 months (d=2.12), compared with all other groups, which was significantly associated with greater repetitive behaviors. Conclusions: This is the first MRI study comparing fragile X syndrome and ASD in infancy, demonstrating strikingly different patterns of brain and behavior development. Fragile X syndrome–related changes were present from 6 months of age, whereas ASD-related changes unfolded over the first 2 years of life, starting with no detectable group differences at 6 months. Increased amygdala growth rate between 6 and 12 months occurs prior to social deficits and well before diagnosis. This gradual onset of brain and behavior changes in ASD, but not fragile X syndrome, suggests an age- and disorder-specific pattern of cascading brain changes preceding autism diagnosis.
A novel IgG-based FLT3xCD3 bispecific antibody for the treatment of AML and B-ALL
Authors: Naveen K Mehta, Martin Pfluegler, Kristan Meetze, Bochong Li, Isabelle Sindel, Fabian Vogt, Melanie Marklin, Jonas S Heitmann, Joseph Kauer, Lukas Osburg, Latifa Zekri, Hans-Jörg Bühring, Stefanie Mueller, Sebastian Hörner, Patrick A Baeuerle, Jennifer S Michaelson, Gundram Jung, Helmut R Salih
Journal: Journal for ImmunoTherapy of Cancer (2022)

In lymphoid malignancies, the introduction of chimeric antigen receptor T (CAR-T) cells and bispecific antibodies (bsAbs) has achieved remarkable clinical success. However, such immunotherapeutic strategies are not yet established for acute myeloid leukemia (AML), the most common form of acute leukemia in adults. Common targets in AML such as CD33, CD123, and CLEC12A are highly expressed on both AML blasts and on normal myeloid cells and hematopoietic stem cells (HSCs), thereby raising toxicity concerns. In B-cell acute lymphoblastic leukemia (B-ALL), bsAbs and CAR-T therapy targeting CD19 and CD22 have demonstrated clinical success, but resistance via antigen loss is common, motivating the development of agents focused on alternative targets. An attractive emerging target is FLT3, a proto-oncogene expressed in both AML and B-ALL, with low and limited expression on myeloid dendritic cells and HSCs.We developed and characterized CLN-049, a T cell-activating bsAb targeting CD3 and FLT3, constructed as an IgG heavy chain/scFv fusion. CLN-049 binds the membrane proximal extracellular domain of the FLT3 protein tyrosine kinase, which facilitates the targeting of leukemic blasts regardless of FLT3 mutational status. CLN-049 was evaluated for preclinical safety and efficacy in vitro and in vivo.CLN-049 induced target-restricted activation of CD4+ and CD8+ T cells. AML cell lines expressing a broad range of surface levels of FLT3 were efficiently lysed on treatment with subnanomolar concentrations of CLN-049, whereas FLT3-expressing hematopoietic progenitor cells and dendritic cells were not sensitive to CLN-049 killing. Treatment with CLN-049 also induced lysis of AML and B-ALL patient blasts by autologous T cells at the low effector-to-target ratios typically observed in patients with overt disease. Lysis of leukemic cells was not affected by supraphysiological levels of soluble FLT3 or FLT3 ligand. In mouse xenograft models, CLN-049 was highly active against human leukemic cell lines and patient-derived AML and B-ALL blasts.CLN-049 has a favorable efficacy and safety profile in preclinical models, warranting evaluation of its antileukemic activity in the clinic.
Reply to ‘Paracetamol use in pregnancy — neglecting context promotes misinterpretation’
Authors: Ann Z. Bauer, Shanna H. Swan, David Kriebel, Zeyan Liew, Hugh S. Taylor, Carl-Gustaf Bornehag, Anderson M. Andrade, Jørn Olsen, Rigmor H. Jensen, Rod T. Mitchell, Niels E. Skakkebaek, David M. Kristensen
Journal: Nature Reviews Endocrinology (2022)
Is the UK's covid inquiry at risk of forgetting about children and young people?
Authors: Robert C Hughes, Michael Absoud, Sunil S Bhopal
Journal: BMJ (2022)

This study was performed to establish the normal values and range of variability for three- and five-segment regional ejection fraction analysis. In addition, file conversion was utilized to compare global values produced by different vendors' systems. Global values show considerable differences between systems (15%-20% in most cases) which indicate the need for standardization and correction when comparing data. For regional analysis, with a mean global value of 60.6%, the mean regional ejection fractions varied from 47% to 81%. Interobserver variation of the regional parameters was between 2% and 6% (standard error of estimate) for a group of 50 "normals" (global ejection fraction &gt;50%) with least variability in the apex and maximum in the septal segment. Intraobserver variability was between 1% and 4% with the same pattern. In a mixed population (global ejection fraction 10%–85%) all parameters exhibited more variability, and paying strict attention to patient positioning for repeat studies appears to have little effect on reducing this variation.
Prognostic Utility of the Ki-67 Labeling Index in Follicular Thyroid Tumors: a 20-Year Experience from a Tertiary Thyroid Center
Authors: L. Samuel Hellgren, Adam Stenman, Johan O. Paulsson, Anders Höög, Catharina Larsson, Jan Zedenius, C. Christofer Juhlin
Journal: Endocrine Pathology (2022)

Follicular thyroid tumors pose a diagnostic challenge on the preoperative level, as the discrimination between follicular thyroid carcinoma (FTC) and adenoma (FTA) demands careful histopathological investigation. Moreover, prognostication of FTCs is mostly based on tumor size and extent of invasive properties, while immunohistochemical markers pinpointing high-risk cases are lacking. We have routinely established a Ki-67 labeling index for follicular thyroid tumors since 1999. To assess the potential value of Ki-67 as an adjunct tool to (1) correctly separate FTCs from FTAs and (2) help identify poor-prognosis FTCs, we collected histopathological and clinical data from 818 follicular thyroid tumors with a histological Ki-67 labeling index established in clinical routine practice (516 FTAs, 252 FTCs, and 50 follicular thyroid tumors of uncertain malignant potential (FT-UMPs)). The Ki-67 labeling index was higher in FTCs (mean 5.8%) than in FTAs (mean 2.6%) (P < 0.001), and a receiver operating characteristic curve analysis revealed a cut-off value of 4% to separate FTC from FTA with a sensitivity and specificity of 65% and 83%, respectively. Similarly, a Ki-67 labeling index above 4% was found to identify FTCs that later metastasized from clinically indolent FTCs with a sensitivity and specificity of 80% and 48%, respectively. Ki-67 constituted an independent predictor of future FTC metastases/recurrence and death of disease, and a value > 4% was a reliable prognostic marker within individual pT staging groups. We conclude that Ki-67 is a potentially valuable marker for the prognostication of FTCs, and future implementation in the histopathological assessments of follicular thyroid tumors could be beneficial if reproduced in international series.
The ecosystem of health decision making: from fragmentation to synergy
Authors: Holger J Schünemann, Marge Reinap, Thomas Piggott, Erki Laidmäe, Kristina Köhler, Mariliis Pōld, Brendalynn Ens, Alar Irs, Elie A Akl, Carlos A Cuello, Maicon Falavigna, Michelle Gibbens, Luciana Neamtiu, Elena Parmelli, Mouna Jameleddine, Lisa Pyke, Ilse Verstijnen, Pablo Alonso-Coello, Peter Tugwell, Yuan Zhang, Zuleika Saz-Parkinson, Tanja Kuchenmüller, Lorenzo Moja
Journal: The Lancet Public Health (2022)

Clinicians, patients, policy makers, funders, programme managers, regulators, and science communities invest considerable amounts of time and energy in influencing or making decisions at various levels, using systematic reviews, health technology assessments, guideline recommendations, coverage decisions, selection of essential medicines and diagnostics, quality assurance and improvement schemes, and policy and evidence briefs. The criteria and methods that these actors use in their work differ (eg, the role economic analysis has in decision making), but these methods frequently overlap and exist together. Under the aegis of WHO, we have brought together representatives of different areas to reconcile how the evidence that influences decisions is used across multiple health system decision levels. We describe the overlap and differences in decision-making criteria between different actors in the health sector to provide bridging opportunities through a unifying broad framework that we call theory of everything. Although decision-making activities respond to system needs, processes are often poorly coordinated, both globally and on a country level. A decision made in isolation from other decisions on the same topic could cause misleading, unnecessary, or conflicted inputs to the health system and, therefore, confusion and resource waste.
Targeting hepatic kisspeptin receptor ameliorates nonalcoholic fatty liver disease in a mouse model
Authors: Stephania Guzman, Magdalena Dragan, Hyokjoon Kwon, Vanessa de Oliveira, Shivani Rao, Vrushank Bhatt, Katarzyna M. Kalemba, Ankit Shah, Vinod K. Rustgi, He Wang, Paul R. Bech, Ali Abbara, Chioma Izzi-Engbeaya, Pinelopi Manousou, Jessie Y. Guo, Grace L. Guo, Sally Radovick, Waljit S. Dhillo, Fredric E. Wondisford, Andy V. Babwah, Moshmi Bhattacharya
Journal: Journal of Clinical Investigation (2022)

Nonalcoholic fatty liver disease (NAFLD), the most common liver disease, has become a silent worldwide pandemic. The incidence of NAFLD correlates with the rise in obesity, type 2 diabetes, and metabolic syndrome. A hallmark featureof NAFLD is excessive hepatic fat accumulation or steatosis, due to dysregulated hepatic fat metabolism, which can progress to nonalcoholic steatohepatitis (NASH), fibrosis, and cirrhosis. Currently, there are no approved pharmacotherapies to treat this disease. Here, we have found that activation of the kisspeptin 1 receptor (KISS1R) signaling pathway has therapeutic effects in NAFLD. Using high-fat diet–fed mice, we demonstrated that a deletion of hepatic Kiss1r exacerbated hepatic steatosis. In contrast, enhanced stimulation of KISS1R protected against steatosis in wild-type C57BL/6J mice and decreased fibrosis using a diet-induced mouse model of NASH. Mechanistically, we found that hepatic KISS1R signaling activates the master energy regulator, AMPK, to thereby decrease lipogenesis and progression to NASH. In patients with NAFLD and in high-fat diet–fed mice, hepatic KISS1/KISS1R expression and plasma kisspeptin levels were elevated, suggesting a compensatory mechanism to reduce triglyceride synthesis. These findings establish KISS1R as a therapeutic target to treat NASH.
SOCIAL DETERMINANTS OF MORTALITY FROM COVID-19, A RETROSPECTIVE STUDY OF 6,000 PATIENTS
Authors: Mujahed Abualfoul, Yi Zhao, Victor Canela, Lawrence M. Hoang, Sri Naga Pavani Prathivada, Michael Vu, Lucas Wang, Priyanka Acharya, Manavjot Singh Sidhu
Journal: Journal of the American College of Cardiology (2022)
Efficacy of Acceptance and Commitment Therapy in Daily Life in Early Psychosis: Results from the Multi-Center INTERACT Randomized Controlled Trial
Authors: Inez Myin-Germeys, Evelyne van Aubel, Thomas Vaessen, Henrietta Steinhart, Annelie Klippel, Ginette Lafit, Wolfgang Viechtbauer, Tim Batink, Ruud van Winkel, Mark van der Gaag, Therese van Amelsvoort, Machteld Marcelis, Frederike Schirmbeck, Lieuwe de Haan, Ulrich Reininghaus
Journal: Psychotherapy and Psychosomatics (2022)

&lt;b&gt;&lt;i&gt;Introduction/Objective:&lt;/i&gt;&lt;/b&gt; This study aimed to investigate efficacy of Acceptance and Commitment Therapy in Daily Life (ACT-DL), combining face-to-face therapy with an Ecological Momentary Intervention (EMI), in addition to treatment as usual (TAU) for psychotic distress, in comparison to TAU. &lt;i&gt;Methods&lt;/i&gt;: Individuals aged 15–65 years with clinically established ultra-high risk or first episode of psychosis were randomly assigned to TAU or ACT-DL+TAU. ACT-DL+TAU consisted of 8 ACT-sessions augmented with an EMI-app. The primary outcome was psychotic distress assessed with the Comprehensive Assessment scale of At Risk Mental State (CAARMS) at post-intervention and 6- and 12-month follow-up. Secondary outcomes were functioning, symptom severity, and momentary psychotic distress. We performed multivariate mixed models according to intent-to-treat principles. &lt;b&gt;&lt;i&gt;Results:&lt;/i&gt;&lt;/b&gt; Between June 1, 2015 and December 31, 2018, 668 participants were referred, of whom 148 were randomized to ACT-DL+TAU (&lt;i&gt;n&lt;/i&gt; = 71) or TAU (&lt;i&gt;n&lt;/i&gt; = 77). One hundred and fifteen (78%) provided primary outcome data at least at one follow-up assessment. There was no evidence of greater reduction in the primary outcome measure CAARMS distress in ACT-DL+TAU compared to TAU (χ&lt;sup&gt;2&lt;/sup&gt;(3) = 2.36; &lt;i&gt;p&lt;/i&gt; = 0.50). However, out of the tested secondary outcomes, global functioning (χ&lt;sup&gt;2&lt;/sup&gt;(3) = 9.05; &lt;i&gt;p&lt;/i&gt; = 0.033), and negative symptoms (χ&lt;sup&gt;2&lt;/sup&gt;(3) = 19.91; p&amp;#x3c;0.001) improved in ACT-DL+TAU compared to TAU, as did momentary psychotic distress (χ&lt;sup&gt;2&lt;/sup&gt;(3) = 21.56; &lt;i&gt;p&lt;/i&gt; &amp;#x3c; 0.001). &lt;b&gt;&lt;i&gt;Conclusions:&lt;/i&gt;&lt;/b&gt; INTERACT did not support a significant effect of ACT-DL over TAU on the primary outcome measure of psychotic distress as assessed with the CAARMS. Although significant improvements were found for some secondary outcome measures, further replication studies are needed to confirm the strength and specificity of these effects.
Generation of human tonsil epithelial organoids as an ex vivo model for SARS-CoV-2 infection
Authors: Han Kyung Kim, Hyeryeon Kim, Myoung Kyu Lee, Woo Hee Choi, Yejin Jang, Jin Soo Shin, Jun-Yeol Park, Dong Hyuck Bae, Seong-In Hyun, Kang Hyun Kim, Hyun Wook Han, Byungho Lim, Gildon Choi, Meehyein Kim, Young Chang Lim, Jongman Yoo
Journal: Biomaterials (2022)
ASSOCIATION BETWEEN CIRCULATING KETONE BODIES AND CARDIOVASCULAR OUTCOMES AMONG PARTICIPANTS OF THE MULTI-ETHNIC STUDY OF ATHEROSCLEROSIS (MESA)
Authors: Parag Anilkumar Chevli, Elad Shemesh, Tareq Islam, Charles German, Michael Blaha, James Otvos, Fatima Rodriguez, Joseph Yeboah, Michael D. Shapiro
Journal: Journal of the American College of Cardiology (2022)
Sodium–Glucose Cotransporter 2 Inhibitors and Risk of Bladder and Renal Cancer: Scandinavian Cohort Study
Authors: Peter Ueda, Henrik Svanström, Anders Hviid, Björn Eliasson, Ann-Marie Svensson, Stefan Franzén, Soffia Gudbjörnsdottir, Kristian Hveem, Christian Jonasson, Viktor Wintzell, Mads Melbye, Björn Pasternak
Journal: Diabetes Care (2022)
IMPACT OF PRE-EXISTING PULMONARY HYPERTENSION ON ALL-CAUSE MORTALITY AND REHOSPITALIZATION IN PATIENTS WITH SEVERE MITRAL REGURGITATION UNDERGOING MITRACLIP THERAPY: A SYSTEMATIC REVIEW AND META-ANALYSIS
Authors: Anan Abu Rmilah, Abdalla Kara Balla, Mohammad Abdelhafez, Maen Assali, Soban Ahmad, Omar Latif, Ikram-Ul Haq, Hossam Alzu’Bi, Ahmad Al-Abdouh, Suhaib jaber, Mayra Guerrero
Journal: Journal of the American College of Cardiology (2022)
Combination cancer immunotherapy targeting TNFR2 and PD-1/PD-L1 signaling reduces immunosuppressive effects in the microenvironment of pancreatic tumors
Authors: Xiaozhen Zhang, Mengyi Lao, Jian Xu, Yi Duan, Hanshen Yang, Muchun Li, Honggang Ying, Lihong He, Kang Sun, Chengxiang Guo, Wen Chen, Haitao Jiang, Xiaoyu Zhang, Xueli Bai, Tingbo Liang
Journal: Journal for ImmunoTherapy of Cancer (2022)

Backgrounds In advanced pancreatic ductal adenocarcinoma (PDAC), immune therapy, including immune checkpoint inhibitors, has limited efficacy, encouraging the study of combination therapy. Methods Tumor necrosis factor receptor 2 (TNFR2) was analyzed via immunohistochemistry, immunofluorescence, western blotting, and ELISAs. The in vitro mechanism that TNFR2 regulates programmed cell death 1 ligand 1 (PD-L1) was investigated using immunofluorescence, immunohistochemistry, flow cytometry, western blotting, and chromatin immunoprecipitation (ChIP). In vivo efficacy and mechanistic studies, using C57BL/6 mice and nude mice with KPC cell-derived subcutaneous and orthotopic tumors, employed antibodies against TNFR2 and PD-L1. Survival curves were constructed for the orthotopic model and a genetically engineered PDAC model (LSL-Kras G12D/+ ; LSL-Trp53 R172H/+ ; Pdx1-Cre). Mass cytometry, immunohistochemistry, and flow cytometry analyzed local and systemic alterations in the immunophenotype. Results TNFR2 showed high expression and is a prognostic factor in CD8+ T cell-enriched pancreatic cancer. TNFR2 promotes tumorigenesis and progression of pancreatic cancer via dual effect: suppressing cancer immunogenicity and partially accelerating tumor growth. TNFR2 positivity correlated with PD-L1, and in vitro and in vivo, it could regulate the expression of PDL1 at the transcription level via the p65 NF-κB pathway. Combining anti-TNFR2 and PD-L1 antibodies eradicated tumors, prolonged overall survival in pancreatic cancer, and induced strong antitumor immune memory and secondary prevention by reducing the infiltration of Tregs and tumor-associated macrophages and inducing CD8+ T cell activation in the PDAC microenvironment. Finally, the antitumor immune response derived from combination therapy is mainly dependent on CD8+ T cells, partially dependent on CD4+ T cells, and independent of natural killer cells. Conclusions Anti-TNFR2 and anti-PD-L1 combination therapy eradicated tumors by inhibiting their growth, relieving tumor immunosuppression, and generating robust memory recall.
Prognostic factors for polyp recurrence in chronic rhinosinusitis with nasal polyps
Authors: Junqin Bai, Julia H. Huang, Caroline P.E. Price, Jacob M. Schauer, Lydia A. Suh, Regan Harmon, David B. Conley, Kevin C. Welch, Robert C. Kern, Stephanie Shintani-Smith, Anju T. Peters, Whitney W. Stevens, Atsushi Kato, Robert P. Schleimer, Bruce K. Tan
Journal: Journal of Allergy and Clinical Immunology (2022)
CARDIAC CACHEXIA IS ASSOCIATED WITH A PROLONGED HOSPITAL STAY, HIGHER MORTALITY AND NO INCREASE RISK FOR 30-DAY READMISSION AFTER CHF EXACERBATION
Authors: Mohamad Alhoda Mohamad Alahmad, Prakash Acharya, Abdulrahman Morad, Kamal Gupta
Journal: Journal of the American College of Cardiology (2022)
Breathing Rhythm and Pattern and Their Influence on Emotion
Authors: Sufyan Ashhad, Kaiwen Kam, Christopher A. Del Negro, Jack L. Feldman
Journal: Annual Review of Neuroscience (2022)

Breathing is a vital rhythmic motor behavior with a surprisingly broad influence on the brain and body. The apparent simplicity of breathing belies a complex neural control system, the breathing central pattern generator (bCPG), that exhibits diverse operational modes to regulate gas exchange and coordinate breathing with an array of behaviors. In this review, we focus on selected advances in our understanding of the bCPG. At the core of the bCPG is the preBötzinger complex (preBötC), which drives inspiratory rhythm via an unexpectedly sophisticated emergent mechanism. Synchronization dynamics underlying preBötC rhythmogenesis imbue the system with robustness and lability. These dynamics are modulated by inputs from throughout the brain and generate rhythmic, patterned activity that is widely distributed. The connectivity and an emerging literature support a link between breathing, emotion, and cognition that is becoming experimentally tractable. These advances bring great potential for elucidating function and dysfunction in breathing and other mammalian neural circuits.
INFLUENCE OF SYSTEMIC LUPUS ERYTHEMATOUS ON 30-DAY READMISSION FOR HEART FAILURE: AN INSIGHT FROM NATIONAL READMISSION DATABASE
Authors: Smriti Khanal, Iriagbonse R. Asemota, Prajwal Shrestha, Bharosa Sharma, Emmanuel Akuna, Raquel Soon-Shiong, Dennis Danso Kumi, Muhammad Usman, Muhammad U. Almani
Journal: Journal of the American College of Cardiology (2022)
<i>USF1</i>/<i>CD90</i> signaling in maintaining glioblastoma stem cells and tumor-associated macrophages adhesion
Authors: Yuanshuai Zhou, Xingjun Meng, Wen He, Xinying Li, Rongchuan Zhao, Caihua Dong, Detian Yuan, Jiao Yang, Ruobing Zhang, Guohua Shi, Yulun Huang, Jiangang Liu, Jianping Liu, Songbai Liu, Peng Fu, Minxuan Sun
Journal: Neuro-Oncology (2022)

Abstract Background Glioblastoma stem cells (GSCs) and their interplay with tumor-associated macrophages (TAMs) are responsible for malignant growth and tumor recurrence of glioblastoma multiforme (GBM), but the underlying mechanisms are largely unknown. Methods Cell viability, stemness, migration, and invasion were measured in GSCs after the knockdown of upstream stimulating factor 1 (USF1). Luciferase assay and chromatin immunoprecipitation qPCR were performed to determine the regulation of CD90 by USF1. Immunohistochemistry and immunofluorescent staining were used to examine the expression of USF1 and GSC markers, as well as the crosstalk between GSCs and TAMs. In addition, the interaction between GSCs and TAMs was confirmed using in vivo GBM models. Results We show that USF1 promotes malignant glioblastoma phenotypes and GSCs-TAMs physical interaction by inducing CD90 expression. USF1 predicts a poor prognosis for glioma patients and is upregulated in patient-derived GSCs and glioblastoma cell lines. USF1 overexpression increases the proliferation, invasion, and neurosphere formation of GSCs and glioblastoma cell lines, while USF1 knockdown exerts an opposite effect. Further mechanistic studies reveal that USF1 promotes GSC stemness by directly regulating CD90 expression. Importantly, CD90 of GSCs functions as an anchor for physical interaction with macrophages. Additionally, the USF1/CD90 signaling axis supports the GSCs and TAMs adhesion and immunosuppressive feature of TAMs, which in turn enhance the stemness of GSCs. Moreover, the overexpression of CD90 restores the stemness property in USF1 knockdown GSCs and its immunosuppressive microenvironment. Conclusions Our findings indicate that the USF1/CD90 axis might be a potential therapeutic target for the treatment of glioblastoma.