tbuckley/cabot-search huggingface dataset:
Maternal and neonatal outcomes of pregnancies after metabolic bariatric surgery: a retrospective population-based study
Authors: Pierre Bel Lassen, Anne-Isabelle Tropeano, Armelle Arnoux, Estelle Lu, Louis Romengas, Sandrine Katsahian, Bérénice Ségrestin, Bénédicte Lelièvre, Delphine Mitanchez, Géraldine Gascoin, Tigran Poghosyan, Andrea Lazzati, Barbara Heude, Jacky Nizard, Sébastien Czernichow, Cécile Ciangura, Claire Rives-Lange
Journal: The Lancet Regional Health - Europe (2025)
Long‐term results of the FIL MCL0208 trial of lenalidomide maintenance versus observation after ASCT in MCL patients
Authors: Rita Tavarozzi, Simone Ferrero, Andrea Evangelista, Elisa Genuardi, Daniela Drandi, Michael Mian, Manuela Zanni, Federica Cavallo, Alice Di Rocco, Vittorio Stefoni, Chiara Pagani, Alessandro Re, Barbara Botto, Monica Balzarotti, Vittorio R. Zilioli, Maria Gomes da Silva, Luca Arcaini, Anna L. Molinari, Filippo Ballerini, Andrés J. M. Ferreri, Benedetta Puccini, Carlo Visco, Piero M. Stefani, Mario Luppi, Ivana Casaroli, Caterina Stelitano, Giovannino Ciccone, Umberto Vitolo, Maurizio Martelli, Sergio Cortelazzo, Marco Ladetto
Journal: HemaSphere (2025)
Low‐risk MDS—A spotlight on precision medicine for <i>SF3B1‐</i>mutated patients
Authors: Shoshana Burke, Onima Chowdhury, Kevin Rouault‐Pierre
Journal: HemaSphere (2025)

Abstract A deep understanding of the biological mechanisms driving the pathogenesis of myelodysplastic neoplasms (MDS) is essential to develop comprehensive therapeutic approaches that will benefit patient's disease management and quality of life. In this review, we focus on MDS harboring mutations in the splicing factor SF3B1 . Clones harboring this mutation arise from the most primitive hematopoietic compartment and expand throughout the entire myeloid lineage, exerting distinct effects at various stages of differentiation. Supportive care, particularly managing anemia, remains essential in SF3B1 ‐mutated MDS. While SF3B1 mutations are frequently linked with ring sideroblasts and iron overload due to impaired erythropoiesis, the current therapeutic landscape fails to adequately address the underlying disease biology, particularly in transfusion‐dependent patients, where further iron overload contributes to increased morbidity and mortality. Novel agents such as Luspatercept and Imetelstat have shown promise, but their availability remains restricted and their long‐term efficacy is to be investigated. Spliceosome modulators have failed to deliver and inhibitors of inflammatory pathways, including TLR and NF‐κB inhibitors, are still under investigation. This scarcity of effective and disease‐modifying therapies highlights the unmet need for new approaches tailored to the molecular and genetic abnormalities in SF3B1 ‐mutated MDS. Emerging strategies targeting metabolic mis‐splicing (e.g., COASY ) with vitamin B5, pyruvate kinase activators, and inhibitors of oncogenic pathways like MYC and BCL‐2 represent potential future avenues for treatment, but their clinical utility remains to be fully explored. The current limitations in treatment underscore the urgency of developing novel, more effective therapies for patients with SF3B1 ‐mutated MDS.
Brentuximab vedotin monotherapy is a feasible and effective treatment for older patients with classical Hodgkin lymphoma unsuitable for curative chemotherapy: Results from the prospective GHSG–NLG phase II BVB trial
Authors: Alexander Fosså, Daniel Molin, Paul J. Bröckelmann, Gundolf Schneider, Ulf Schnetzke, Johan Linderoth, Peter M. H. Kamper, Sirpa M. Leppä, Julia Meissner, Valdete Schaub, Kjersti Lia, Michael Fuchs, Peter Borchmann, Boris Böll
Journal: HemaSphere (2025)
Integrated Analysis of the Anoikis‐Related Signature Identifies Rac Family Small GTPase 3 as a Novel Tumor‐Promoter Gene in Hepatocellular Carcinoma
Authors: Dong Wu, Ze‐Kun Liu, Ying Sun, Chu‐Heng Gou, Run‐Ze Shang, Meng Lu, Ren‐Yu Zhang, Hao‐Lin Wei, Can Li, Ying Shi, Cong Zhang, Yu‐Tong Wang, Ding Wei, Zhi‐Nan Chen, Huijie Bian
Journal: MedComm (2025)

ABSTRACT Anoikis resistance in hepatocellular carcinoma (HCC) cells boosts survival and metastasis. This study aimed to establish an anoikis‐related genes (ARGs)‐based model for predicting HCC patients’ outcomes and investigate the clinicopathological significance and function of crucial ARGs. The transcriptional expression patterns for HCC cohorts were compiled from TCGA, GEO and ICGC. Univariate and LASSO multivariate analyses were performed to screen for prognostic ARGs. Gain‐ and loss‐of‐function studies, RNA sequencing, and mass spectrometry were employed to elucidate the underlying mechanisms of ARGs in HCC. We established a five‐gene ARGs risk model for HCC prognosis, with an AUC value of 0.812 for 1‐year survival. Among the five genes, Rac family small GTPase 3 (RAC3) was upregulated in HCC relative to adjacent normal tissues and negatively correlated to overall survival and disease‐free survival of patients with HCC. Silence of RAC3 in HCC cells resulted in an increased cell apoptosis and diminished cell proliferation and invasion. Mechanistically, we uncovered that RAC3 binding with SOX6 propelled the advancement of HCC cells through NNMT‐mediated stimulation of the cAMP/MAPK/Rap1 signaling. In particular, EHop‐016, a small molecule inhibitor targeting RAC3, significantly suppressed HCC progression.
Bioactive hemostatic materials: a new strategy for promoting wound healing and tissue regeneration
Authors: Zhengyuan Liu, Junnan Xu, Xing Wang
Journal: MedComm (2025)

Abstract Wound healing remains a critical global healthcare challenge, with an annual treatment cost exceeding $50 billion worldwide. Over the past decade, significant advances in wound care have focused on developing sophisticated biomaterials that promote tissue regeneration and prevent complications. Despite these developments, there remains a crucial need for multifunctional wound healing materials that can effectively address the complex, multiphase nature of wound repair while being cost effective and easily applicable in various clinical settings. This review systematically analyzes the latest developments in wound healing materials, examining their chemical composition, structural design, and therapeutic mechanisms. We comprehensively evaluate various bioactive components, including natural polymers, synthetic matrices, and hybrid composites, along with their different forms, such as hydrogels, powders, and smart dressings. Special attention is given to emerging strategies in material design that integrate multiple therapeutic functions, including sustained drug delivery, infection prevention, and tissue regeneration promotion. The insights provided in this review illuminate the path toward next‐generation wound healing materials, highlighting opportunities for developing more effective therapeutic solutions that can significantly improve patient outcomes and reduce healthcare burden.
ATP11B Modulates Microglial Lipid Metabolism and Alleviates Alzheimer's Disease Pathology
Authors: Yuchen Zhang, Shibo Zhang, Xuyu Zhao, Peiru Wu, Yiwei Ying, Lingling Wu, Junyi Zhuang, Zixin Chen, Yufan Chao, Xin Dong, Robert Chunhua Zhao, Jiao Wang
Journal: MedComm (2025)

ABSTRACT Abnormal lipid metabolism in microglia leads to the formation of pathological lipid droplets (LDs), a phenomenon also observed in neurodegenerative diseases such as Alzheimer's disease (AD). The abnormal accumulation of LDs disrupts normal cellular function and exacerbates the pathological process of AD. ATP11B is a P4‐ATPase and the expression of Atp11b changes in the brain of patients with AD and diseases of lipid metabolism. The present study aimed to explore the regulatory role of ATP11B in microglial lipid metabolism and assess the potential of ATP11B as a therapeutic target for AD. Atp11b deficiency caused excessive fatty acid uptake and activated the PPAR signaling pathway, resulting in abnormal synthesis of neutral lipids and mitochondrial energy metabolism in microglia. Further results showed that Atp11b deficiency led to the accumulation of pathological LDs in microglia and AD mice. Conversely, overexpression of Atp11b alleviated exploratory behavior impairment, learning and memory impairment, LD accumulation, beta‐amyloid (Aβ) deposition, and inflammatory response in the brain of AD mice. These findings provide important clues for a better understanding of the pathogenesis of AD and for developing novel therapeutic strategies.
Nano‐Topography Enhanced Topological‐Cell‐Analysis in Radiation‐Therapy
Authors: Francesca Pagliari, Maria‐Francesca Spadea, Pierre Montay‐Gruel, Anggraeini Puspitasari‐Kokko, Joao Seco, Luca Tirinato, Angelo Accardo, Francesco De Angelis, Francesco Gentile
Journal: Advanced Healthcare Materials (2025)

Abstract Radiotherapy (RT) is a cancer treatment technique that involves exposing cells to ionizing radiation, including X‐rays, electrons, or protons. RT offers promise to treat cancer, however, some inherent limitations can hamper its performance. Radio‐resistance, whether innate or acquired, refers to the ability of tumor cells to withstand treatment, making it a key factor in RT failure. This perspective hypothesizes that nanoscale surface topography can impact on the topology of cancer cells network under radiation, and that this understanding can possibly advance the assessment of cell radio‐resistance in RT applications. An experimental plan is proposed to test this hypothesis, using cancer cells exposed to various RT forms. By examining the influence of 2D surface and 3D scaffold nanoscale architecture on cancer cells, this approach diverges from traditional methodologies, such as clonogenic assays, offering a novel viewpoint that integrates fields such as tissue engineering, artificial intelligence, and nanotechnology. The hypotheses at the base of this perspective not only may advance cancer treatment but also offers insights into the broader field of structural biology. Nanotechnology and label‐free Raman phenotyping of biological samples are lenses through which scientists can possibly better elucidate the structure‐function relationship in biological systems.
Sprint running mechanics are associated with hamstring strain injury: a 6-month prospective cohort study of 126 elite male footballers
Authors: Christopher Bramah, Samantha Rhodes, Alexandra Clarke-Cornwell, Thomas Dos’Santos
Journal: British Journal of Sports Medicine (2025)

Objective To investigate the association between sprint running biomechanics and sprint-related hamstring strain injury (HSI) in elite male football players. Methods This prospective cohort study recruited 126 professional male football players from eight clubs in the English football league, who were followed across a 6-month period. Maximal velocity sprint running videos (240 fps) were collected from five teams during preseason (June to August) and three teams during the in-season period (October to March) and subsequently assessed using the Sprint Mechanics Assessment Score (S-MAS) by a single, blinded assessor. Sprint-related HSI within the previous 12 months and any new MRI-confirmed sprint-related HSI were reported by club medical staff. Incidence rate ratios were calculated using a Poisson regression model to determine the association between S-MAS and new sprint-related HSIs. Results There were 23 players with a previous sprint-related HSI and 17 new HSIs during the follow-up period, with 14 sprint-related injuries. S-MAS values were significantly greater among players with a previous HSI (median difference (MD): 1, p=0.007, 95% CI: 0 to 3) and those sustaining a new sprint-related HSI (MD: 2, p=0.006, 95% CI: 1 to 3) compared with uninjured players. Adjusting for age and previous injury found a significant association between the S-MAS and prospective sprint-related HSIs, with an adjusted incidence rate ratio of 1.33 (95% CI: 1.01 to 1.76) for each one-point increase in S-MAS. Conclusions This is the first study to identify an association between sprint running kinematics and prospective sprint-related HSI in elite male football players. Sprint running mechanics assessed using the S-MAS were associated with both past and future HSIs, with a 33% increase in the risk of a new HSI with every one-point increase in S-MAS. Given the association to injury, evaluating sprint mechanics within rehabilitation and injury prevention may be warranted.
Immunosuppressive JAG2<sup>+</sup> tumor‐associated neutrophils hamper PD‐1 blockade response in ovarian cancer by mediating the differentiation of effector regulatory T cells
Authors: Chenyang Wang, Moran Yang, Yujing Zhong, Kankan Cao, Xueling Wang, Chen Zhang, Yiying Wang, Mengdi He, Jiaqi Lu, Guodong Zhang, Yan Huang, Haiou Liu
Journal: Cancer Communications (2025)

Abstract Background Tumor‐associated neutrophils (TANs) play a critical role in modulating immune responses and exhibit significant heterogeneity. Our previous study demonstrated that jagged canonical Notch ligand 2 (JAG2) + TANs were associated with an immunosuppressive microenvironment in high‐grade serous ovarian cancer (HGSOC), but the underlying mechanism remains unclear. This study aimed to elucidate the role of JAG2 + TANs in tumor immunosuppressive microenvironment in HGSOC. Methods HGSOC samples were collected, with 274 samples constituting two independent cohorts (training and validation cohorts) and an additional 30 samples utilized to establish patient‐derived tumor organoids (PDTOs). We characterized the number and phenotype of JAG2 + TANs by multiplex immunohistochemistry, flow cytometry, and single‐cell RNA sequencing (scRNA‐seq). We investigated the biological functions of JAG2 in immune evasion using in vitro co‐culture systems, flow cytometry, tumor‐bearing mouse models, and PDTOs. Results JAG2 + TANs expressed elevated levels of immunosuppressive molecules, including programmed cell death ligand 1 and CD14, and had independent prognostic value for the overall survival of patients with HGSOC. scRNA‐seq analysis revealed that JAG2 + TANs exhibited a terminally mature phenotype. The infiltration of JAG2 + TANs was positively correlated with the abundance of effector regulatory T cells (eTregs). Interaction with JAG2 + TANs skewed CD4 + T cells towards an eTreg phenotype, a process that was suppressed by the Notch inhibitor LY3039478 and induced by recombinant Jagged2. Furthermore, we demonstrated that JAG2 + TANs enhanced Notch signaling activation, ultimately promoting recombination signal binding protein for immunoglobulin kappa J region (RBPJ)‐induced differentiation of naïve CD4 + T cells into eTregs. Clinically, JAG2 + TANs could serve as a biomarker for assessing immunotherapy resistance in various solid tumors. Pharmacological targeting of Notch signaling with LY3039478 or JAG2 neutralization antibodies enhanced the efficacy of programmed cell death protein 1 (PD‐1) monoclonal antibodies (mAbs) in both xenograft and PDTO models. Conclusions The emergence of JAG2 + TANs is crucial for the differentiation of eTregs, which triggers immune evasion and resistance to anti‐PD‐1 therapy. Inhibiting Notch signaling with LY3039478 or JAG2 neutralization antibodies may overcome this anti‐PD‐1 resistance in HGSOC.
Pan‐cancer analysis shapes the understanding of cancer biology and medicine
Authors: Xiaoping Cen, Yuanyuan Lan, Jiansheng Zou, Ruilin Chen, Can Hu, Yahan Tong, Chen Zhang, Jingyue Chen, Yuanmei Wang, Run Zhou, Weiwei He, Tianyu Lu, Fred Dubee, Dragomirka Jovic, Wei Dong, Qingqing Gao, Man Ma, Youyong Lu, Yu Xue, Xiangdong Cheng, Yixue Li, Huanming Yang
Journal: Cancer Communications (2025)

Abstract Advances in multi‐omics datasets and analytical methods have revolutionized cancer research, offering a comprehensive, pan‐cancer perspective. Pan‐cancer studies identify shared mechanisms and unique traits across different cancer types, which are reshaping diagnostic and treatment strategies. However, continued innovation is required to refine these approaches and deepen our understanding of cancer biology and medicine. This review summarized key findings from pan‐cancer research and explored their potential to drive future advancements in oncology.
Enrichment of CD7+CXCR3+ CAR T cells in infusion products is associated with durable remission in relapsed or refractory diffuse large B-cell lymphoma
Authors: R Bartolini, L Trueb, D Daoudlarian, V Joo, A Noto, R Stadelmann, B Gentner, C Fenwick, M Perreau, G Coukos, G Pantaleo, C Arber, M Obeid
Journal: Annals of Oncology (2025)

Chimeric antigen receptor (CAR) T-cell therapy is the standard of care for relapsed or refractory (R/R) diffuse large B-cell lymphoma (DLBCL). However, more than half of patients fail to achieve durable remission. Identifying predictive biomarkers within the CAR T-cell infusion product (IP) may guide strategies to improve clinical outcomes. This single-center observational study conducted at Lausanne University Hospital (CHUV), Switzerland, analyzed IPs from 13 patients with R/R DLBCL who underwent standard-of-care CAR T-cell therapy. A 39-marker mass cytometry panel was used to compare phenotypic and functional markers between long-term responders (R) and non-responders (NR). Unsupervised and supervised analytic approaches were applied to IP data, and longitudinal peripheral blood samples were collected over 30 days post-infusion to track CAR T-cell subpopulation dynamics. At a median follow-up of 13·5 months, median progression-free survival (PFS) was 13·3 months (95% CI 9·7-24·3) in R (n=8) versus 3·5 months (95% CI 0·5-5·4) in NR (n=5) (hazard ratio 56·67 [95% CI 7·3-439·3]; p=0·0001). A CD3+CXCR3+CD7+ CAR T-cell subpopulation-found in both CD4+ and CD8+ compartments-was significantly enriched in R. These cells showed increased expression of perforin, granzyme B, and NKG2D (restricted to CD8+ cells). In contrast, NR had a higher frequency of CXCR3+CD7+LAG3+ CAR T-cells. Surface expression of CD3, CD7, CXCR3, and NKG2D were higher in R, whereas LAG3, Ki67, and CD71 were elevated in NR. A predictive cut-off ratio of CD3+CXCR3+CD7+LAG3+CAR+ T-cells <0·83 and CD3+CXCR3+CD7+NKG2D+CAR+ T-cells >1·034 yielded a predictive accuracy of 0·92. Serum CXCL9 and CXCL10 concentrations did not differ between groups. Enrichment of CD7+CXCR3+ CAR T-cells alongside elevated NKG2D expression in R, in contrast to higher LAG3 and CD71 in NR, emerged as potentially robust correlates of therapeutic outcome. Although derived from a small, hypothesis-generating cohort, these findings suggest that targeted analysis of IP composition may inform the development of biomarker-driven strategies to optimize CAR T-cell products and improve the likelihood of durable remission in R/R DLBCL.
Leveraging nutritional rehabilitation and tuberculosis programmes to tackle tuberculosis and severe acute malnutrition in children
Authors: Bryan J Vonasek, Olivier Marcy, Jasmine Armour, Martina Casenghi, Cécile Cazes, Mohammod Jobayer Chisti, Marc d'Elbée, Helena Huerga, Cathy Hewison, Christina L Lancioni, Patrick S Lungu, Eric D McCollum, Victor Musiime, Tisungane Mvalo, James A Seddon, Andrew P Steenhoff, Tania A Thomas, Marco Tovar, Anca Vasiliu, Anthony Garcia-Prats, Chishala Chabala
Journal: The Lancet Child & Adolescent Health (2025)
Quick buys for prevention and control of noncommunicable diseases
Authors: Gauden Galea, Allison Ekberg, Angela Ciobanu, Marilys Corbex, Jill Farrington, Carina Ferreira-Bores, Daša Kokole, María Lasierra Losada, Maria Neufeld, Ivo Rakovac, Elena Tsoy, Kremlin Wickramasinghe, Julianne Williams, Martin McKee, David Stuckler
Journal: The Lancet Regional Health - Europe (2025)
Extracellular PHF-tau modulates astrocyte mitochondrial dynamics and mediates neuronal connectivity
Authors: Valentin Zufferey, Aatmika Barve, Enea Parietti, Luc Belinga, Audrey Bringaud, Yvan Varisco, Kerstin Fabbri, Francesca Capotosti, Paola Bezzi, Nicole Déglon, Pierre Marquet, Nicolas Preitner, Kevin Richetin
Journal: Translational Neurodegeneration (2025)

Abstract Background Tau is an intracellular protein that plays a crucial role in stabilizing microtubules. However, it can aggregate into various forms under pathological conditions and be secreted into the brain parenchyma. While the consequences of tau aggregation within neurons have been extensively studied, the effects of extracellular paired helical filaments of tau (ePHF-tau) on neurons and astrocytes are still poorly understood. Methods This study examined the effect of human ePHF-tau (2N4R) on primary cultures of rat neuroglia, focusing on changes in neurites or synapses by microscopy and analysis of synaptosome and mitochondria proteomic profiles after treatment. In addition, we monitored the behavior of mitochondria in neurons and astrocytes separately over three days using high-speed imaging and high-throughput acquisition and analysis. Results ePHF-tau was efficiently cleared by astrocytes within two days in a 3D neuron-astrocyte co-culture model. Treatment with ePHF-tau led to a rapid increase in synaptic vesicle production and active zones, suggesting a potential excitotoxic response. Proteomic analyses of synaptosomal and mitochondrial fractions revealed distinct mitochondrial stress adaptations: astrocytes exhibited elevated mitochondrial biogenesis and turnover, whereas neuronal mitochondria displayed only minor oxidative modifications. In a mixed culture model, overexpression of tau 1N4R specifically in astrocytes triggered a marked increase in mitochondrial biogenesis, coinciding with enhanced synaptic vesicle formation in dendrites. Similarly, astrocyte-specific overexpression of PGC1alpha produced a comparable pattern of synaptic vesicle production, indicating that astrocytic mitochondrial adaptation to ePHF-tau may significantly influence synaptic function. Conclusions These findings suggest that the accumulation of PHF-tau within astrocytes drives changes in mitochondrial biogenesis, which may influence synaptic regulation. This astrocyte-mediated adaptation to tauopathy highlights the potential role of astrocytes in modulating synaptic dynamics in response to tau stress, opening avenues for therapeutic strategies aimed at astrocytic mechanisms in the context of neurodegenerative diseases.
Single-cell spatial transcriptomic atlas of the whole mouse brain
Authors: Lei Han, Zhen Liu, Zehua Jing, Yuxuan Liu, Yujie Peng, Huizhong Chang, Junjie Lei, Kexin Wang, Yuanfang Xu, Wei Liu, Zihan Wu, Qian Li, Xiaoxue Shi, Mingyuan Zheng, He Wang, Juan Deng, Yanqing Zhong, Hailin Pan, Junkai Lin, Ruiyi Zhang, Yu Chen, Jinhua Wu, Mingrui Xu, Biyu Ren, Mengnan Cheng, Qian Yu, Xinxiang Song, Yanbing Lu, Yuanchun Tang, Nini Yuan, Suhong Sun, Yingjie An, Wenqun Ding, Xing Sun, Yanrong Wei, Shuzhen Zhang, Yannong Dou, Yun Zhao, Luyao Han, Qianhua Zhu, Junfeng Xu, Shiwen Wang, Dan Wang, Yinqi Bai, Yikai Liang, Yuan Liu, Mengni Chen, Chun Xie, Binshi Bo, Mei Li, Xinyan Zhang, Wang Ting, Zhenhua Chen, Jiao Fang, Shuting Li, Yujia Jiang, Xing Tan, Guolong Zuo, Yue Xie, Huanhuan Li, Quyuan Tao, Yan Li, Jianfeng Liu, Yuyang Liu, Mingkun Hao, Jingjing Wang, Huiying Wen, Jiabing Liu, Yizhen Yan, Hui Zhang, Yifan Sheng, Shui Yu, Xiaoyan Liao, Xuyin Jiang, Guangling Wang, Huanlin Liu, Congcong Wang, Ning Feng, Xin Liu, Kailong Ma, Xiangjie Xu, Tianyue Han, Huateng Cao, Huiwen Zheng, Yadong Chen, Haorong Lu, Zixian Yu, Jinsong Zhang, Bo Wang, Zhifeng Wang, Qing Xie, Shanshan Pan, Chuanyu Liu, Chan Xu, Luman Cui, Yuxiang Li, Shiping Liu, Sha Liao, Ao Chen, Qing-Feng Wu, Jian Wang, Zhiyong Liu, Yidi Sun, Jan Mulder, Huanming Yang, Xiaofei Wang, Chao Li, Jianhua Yao, Xun Xu, Longqi Liu, Zhiming Shen, Wu Wei, Yan-Gang Sun
Journal: Neuron (2025)
Anatomic Lung Resection is Associated with Improved Survival Compared with Wedge Resection for Stage IA (≤2 cm) Non-Small Cell Lung Cancer
Authors: Christopher W Seder, Shu-Ching Chang, Christopher W Towe, Varun Puri, Justin D Blasberg, Levi Bonnell, Felix G Fernandez, Robert H Habib, Benjamin D Kozower
Journal: Journal of Thoracic Oncology (2025)