tbuckley/cabot-search huggingface dataset:
Large scale multi-omic analysis identifies anatomic differences and immunogenic potential in subtypes of leiomyosarcoma
Authors: Galina Lagos, Roman Groisberg, Andrew Elliott, Don S. Dizon, Andreas Seeber, Geoffrey Thomas. Gibney, Margaret von Mehren, Kenneth Cardona, Michael J. Demeure, Richard F. Riedel, Vaia Florou, Alexander J. Chou, Jaime F. Modiano, Abhijeet Kumar, Moh'd M. Khushman, Gina Z. D'Amato, Andrea P. Espejo Freire, Bradley DeNardo, Jonathan C. Trent
Journal: Clinical Cancer Research (2025)

Abstract Purpose: Comprehensive molecular profiling was used to define the genomic and immune landscapes of leiomyosarcomas (LMS) by anatomic subtype, which have not been completely characterized. Design: 1115 LMS samples, categorized into uterine (uLMS), retroperitoneal (rpLMS), or other (oLMS), underwent DNA/RNA sequencing (Caris Life Sciences). Genomic/transcriptomic profiles were compared across subtypes. Immune profiling was compared to melanoma (n=1255), an immunogenic tumor. Insurance claims data were used to infer real-world outcomes with immune checkpoint inhibitors (ICI) in LMS. Results: uLMS (n=701) were molecularly distinct from rpLMS (n=166) and oLMS (n=248). RB1 mutations and MAP2K4 copy number amplification were more common in non-uLMS. MED12 mutations were almost exclusive to uLMS. Traditional ICI response biomarkers (i.e. PD-L1) didn’t vary by anatomic site. Non-uLMS demonstrated upregulated immune-related gene sets, including interferon and inflammatory response pathways, and higher immune cell infiltration, especially CD8+ T cells and B cells (&amp;gt;2-fold increase, p&amp;lt;0.0001). LMS had lower immune cell abundance and T-cell inflamed scores (TIS) compared to melanoma, though 11% of oLMS samples had high TIS scores. In a real-world cohort (n=138), 29% of LMS patients receiving ICI were treated &amp;gt;6 months, indicating potential clinical benefit. Conclusion: Comprehensive profiling suggested that uLMS represents a molecularly distinct disease from non-uLMS. While traditional ICI response biomarkers were similar across anatomic subtypes, uLMS were immune cold compared to non-uLMS. Signals for ICI responsiveness, such as high TIS and immune cell abundance, in some tumors suggest that further research into immunotherapies for LMS is warranted.
T-bet+ CXCR3+ B cells drive hyperreactive B-T cell interactions in multiple sclerosis
Authors: Ivan Jelcic, Reza Naghavian, Imran Fanaswala, Will Macnair, Cinzia Esposito, Daniela Calini, Yanan Han, Zoe Marti, Catarina Raposo, Jacobo Sarabia Del Castillo, Pietro Oldrati, Daniel Erny, Veronika Kana, Galina Zheleznyakova, Faiez Al Nimer, Björn Tackenberg, Ina Reichen, Mohsen Khademi, Fredrik Piehl, Mark D Robinson, Ilijas Jelcic, Mireia Sospedra, Lucas Pelkmans, Dheeraj Malhotra, Richard Reynolds, Maja Jagodic, Roland Martin
Journal: Cell Reports Medicine (2025)
CD4+ anti-TGF-β CAR T cells and CD8+ conventional CAR T cells exhibit synergistic antitumor effects
Authors: Diwei Zheng, Le Qin, Jiang Lv, Meihui Che, Bingjia He, Yongfang Zheng, Shouheng Lin, Yuekun Qi, Ming Li, Zhaoyang Tang, Bin-Chao Wang, Yi-Long Wu, Robert Weinkove, Georgia Carson, Yao Yao, Nathalie Wong, James Lau, Jean Paul Thiery, Dajiang Qin, Bin Pan, Kailin Xu, Zhenfeng Zhang, Peng Li
Journal: Cell Reports Medicine (2025)
Safety and efficacy of combined treatment with tumor-infiltrating lymphocytes and oncolytic adenovirus TILT-123 in metastatic melanoma
Authors: Tine J Monberg, Santeri A Pakola, Benedetta Albieri, Eva Ellebaek, Marco Donia, Rikke L Eefsen, Troels H Borch, Tatiana V Kudling, Torben Lorentzen, Helle W Hendel, Cecilie Vestergaard, Cathrine Lorentzen, Rikke B Holmstroem, Victor Arias, Amir Khammari, Claudia Kistler, João M Santos, James H A Clubb, Lyna Haybout, Marie C W Westergaard, Özcan Met, Dafne C A Quixabeira, Elise Jirovec, Riikka Havunen, Suvi Sorsa, Victor Cervera-Carrascon, Brigitte Dreno, Akseli Hemminki, Inge Marie Svane
Journal: Cell Reports Medicine (2025)
On‐Demand Removal of Rapid Hemostatic Sponge for Non‐Compressible Hemorrhage Through Disrupting Ionic Bonds
Authors: Pengcheng Zhang, Chuan Yu, Zhuofan Hu, Yijin Li, Guangming Wan, Keyong Tang, Xialian Fan
Journal: Advanced Healthcare Materials (2025)

Abstract Self‐expanding hemostatic sponge plays an important role in the control of non‐compressible hemorrhage in deep wound. After hemostasis is accomplished, the sponge adheres to the wound via blood clots, posing a considerable challenge in wound debridement. A kind of protocatechualdehyde modified chitosan/sodium alginate composite hemostatic sponge with on‐demand removal performance is designed in this study. After absorbing blood, the compression sponge rapidly expands and compresses the damaged blood vessels. The physical compression of the hemostatic sponge and the chemical adhesion of catechol is used to promote rapid hemostasis of the wound. The composite hemostatic sponge demonstrated outstanding hemostasis performance in both mouse liver and rat femoral artery bleeding model. Notably, after complete hemostasis of the rat femoral artery, the composite sponge is rapidly removed from the wound by rinsing it with a suitable concentration of Sodium carbonate (Na 2 CO 3 ) solution. This composite hemostatic sponge featuring the on‐demand removal capability demonstrates outstanding application potential for non‐compressible hemorrhage in deep wounds and provides a novel way for constructing removable hemostatic sponges.
Immune-featured stromal niches associate with response to neoadjuvant immunotherapy in oral squamous cell carcinoma
Authors: Yu-Tong Liu, Hai-Ming Liu, Jian-Gang Ren, Wei Zhang, Xin-Xin Wang, Zi-Li Yu, Qiu-Yun Fu, Xue-Peng Xiong, Jun Jia, Bing Liu, Gang Chen
Journal: Cell Reports Medicine (2025)
High-dimensional analysis of injured patients reveals distinct circulating proteomic profiles in plasma vs. whole blood resuscitation
Authors: Hamed Moheimani, Xuejing Sun, Mehves Ozel, Jennifer L Darby, Erika P Ong, Tunde Oyebamiji, Upendra K Kar, Mark H Yazer, Matthew D Neal, Francis X Guyette, Stephen R Wisniewski, Bryan A Cotton, Jeremy W Cannon, Martin A Schreiber, Ernest E Moore, Nicholas Namias, Joseph P Minei, Christopher D Barrett, Jishnu Das, Jason L Sperry, Timothy R Billiar
Journal: Cell Reports Medicine (2025)
Identifying Younger Postmenopausal Women With Osteoporosis Using USPSTF-Recommended Osteoporosis Risk Assessment Tools
Authors: Henry W. Zheng, Alex A. T. Bui, Kristine E. Ensrud, Nicole C. Wright, JoAnn E. Manson, Nelson B. Watts, Karen C. Johnson, Aladdin H. Shadyab, Carolyn J. Crandall
Journal: JAMA Network Open (2025)

Importance For younger postmenopausal women, clinical guidelines recommend using osteoporosis risk prediction tools to identify candidates with low bone mineral density (BMD). However, the performance of these tools is not well quantified. Objective To examine the performance of Osteoporosis Risk Assessment Instrument (ORAI) and Osteoporosis Index of Risk (OSIRIS), compared with Osteoporosis Self-Assessment Tool (OST), in identifying the presence of osteoporotic BMD in younger postmenopausal women. Design, Setting, and Participants This cross-sectional study used data from the Women’s Health Initiative Bone Density Substudy, which was conducted at 3 clinical centers in Tucson and Phoenix, Arizona; Pittsburgh, Pennsylvania; and Birmingham, Alabama. Participants were healthy postmenopausal women aged 50 to 64 years with BMD measurements evaluated using the 3 risk prediction tools: OSIRIS, ORAI, and OST. Risk factors and other participant characteristics were compared across osteoporosis status. Data were collected from October 1993 to December 1998 and analyzed between September 23, 2023, and April 10, 2024. Exposures The primary exposures were OSIRIS, ORAI, and OST risk scores. Main Outcomes and Measures Primary outcome was osteoporosis defined by BMD T score of –2.5 or lower at 1 or more of 3 anatomical locations: femoral neck, total hip, and/or lumbar spine. The tools were evaluated via area under the receiver operating characteristic curve (AUC) at published score cutoffs and at alternate cutoffs. Results Among 6067 included participants (mean [SD] age at baseline, 57.7 [4.1] years), the prevalence of osteoporosis was 14.1% (n = 857) at any 1 of 3 anatomical sites. AUC for identifying osteoporosis at any site was 0.633 (95% CI, 0.633-0.634) for OSIRIS, 0.663 (95% CI, 0.663-0.664) for ORAI, and 0.654 (95% CI, 0.654-0.655) for OST. Conclusions and Relevance In this cross-sectional study, 3 guideline-recommended osteoporosis risk assessment tools had fair to moderate discrimination in identifying osteoporosis defined by lowest BMD at any 1 of 3 skeletal sites. Screening is essential to reducing individual and societal burden of osteoporosis and related fractures, and this study showed a gap in identifying younger postmenopausal women using common clinical risk factors.
Notes from the field: The Inflation Reduction Act and Enbrel
Authors: Charles L Bennett, Jason B Gibbons, Chadi Nabhan, Kenneth R Carson, June M McKoy, Kevin B Knopf, Gerald Anderson
Journal: Arthritis & Rheumatology (2025)

Disclosure Form Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
Author Correction: Intratumoral oncolytic herpes virus G47∆ for residual or recurrent glioblastoma: a phase 2 trial
Authors: Tomoki Todo, Hirotaka Ito, Yasushi Ino, Hiroshi Ohtsu, Yasunori Ota, Junji Shibahara, Minoru Tanaka
Journal: Nature Medicine (2025)
Nrf3-Mediated Mitochondrial Superoxide Promotes Cardiomyocyte Apoptosis and Impairs Cardiac Functions by Suppressing Pitx2
Authors: Qishan Chen, Ancheng Zheng, Xiaolei Xu, Zhenning Shi, Mei Yang, Shasha Sun, Leyu Wang, Yumeng Wang, Haige Zhao, Qingzhong Xiao, Li Zhang
Journal: Circulation (2025)

BACKGROUND: Myocardial infarction (MI) elicits mitochondria reactive oxygen species (ROS) production and cardiomyocyte (CM) apoptosis. Nrf3 (nuclear factor erythroid 2-related factor 3) has an established role in regulating redox signaling and tissue homeostasis. Here, we aimed to evaluate the role and mechanism of Nrf3 in injury-induced pathological cardiac remodeling. METHODS: Global (Nrf3-KO) and CM-specific (Nrf3 △CM ) Nrf3 knockout mice were subjected to MI or ischemia/reperfusion injury, followed by functional and histopathological analysis. Primary neonatal mouse and rat ventricular myocytes and CMs derived from human induced pluripotent stem cells were used to evaluate the impact of Nrf3 on CM apoptosis and mitochondrial ROS production. Chromatin immunoprecipitation sequencing and immunoprecipitation–mass spectrometry analysis were used to uncover potential targets of Nrf3. MitoParaquat administration and CM-specific adeno-associated virus vectors were used to further confirm the i n vivo relevance of the identified signal pathways. RESULTS: Nrf3 was expressed mainly in CMs in healthy human hearts, and an increased level of Nrf3 was observed in CMs within the border zone of infarcted human hearts and murine cardiac tissues after MI. Both global and CM-specific Nrf3 knockout significantly decreased injury-induced mitochondrial ROS production, CM apoptosis, and pathological cardiac remodeling, consequently improving cardiac functions. In addition, cardiac-specific Nrf3 overexpression reversed the ameliorative cardiac phenotypes observed in Nrf3-KO mice. Functional studies showed that Nrf3 promoted neonatal mouse ventricular myocyte, neonatal rat ventricular myocyte, and CMs derived from human induced pluripotent stem cell apoptosis by increasing mitochondrial ROS production. Critically, augmenting mitochondrial ROS with MitoParaquat blunted the beneficial effects of Nrf3 deletion on cardiac function and remodeling. Mechanistically, a redox regulator Pitx2 (paired-like homeodomain transcription factor 2) was identified as one of the main target genes of Nrf3. Specifically, Nrf3 binds to Pitx2 promoter, where it increases DNA methylation through recruiting heterogeneous nuclear ribonucleoprotein K and DNA-methyltransferase 1 complex, thereby inhibiting Pitx2 expression. CM-specific knockdown of Pitx2 blunted the beneficial effects of Nrf3 deletion on cardiac function and remodeling, and cardiac-specific Pitx2 overexpression attenuated MI-induced mitochondrial ROS production and CM apoptosis, as well as preserved cardiac functions after MI. CONCLUSIONS: Nrf3 promotes injury-induced CM apoptosis and deteriorates cardiac functions by increasing mitochondrial ROS production through suppressing Pitx2 expression. Targeting the Nrf3–Pitx2–mitochondrial ROS signal axis may therefore represent a novel therapeutic approach for MI treatment.
Atrial Translocation of <i>Porphyromonas gingivalis</i> Exacerbates Atrial Fibrosis and Atrial Fibrillation
Authors: Shunsuke Miyauchi, Miki Kawada-Matsuo, Hisako Furusho, Hiromi Nishi, Ayako Nakajima, Pham Trong Phat, Fumie Shiba, Masae Kitagawa, Kazuhisa Ouhara, Noboru Oda, Takehito Tokuyama, Yousaku Okubo, Sho Okamura, Taiichi Takasaki, Shinya Takahashi, Toru Hiyama, Hiroyuki Kawaguchi, Hitoshi Komatsuzawa, Mutsumi Miyauchi, Yukiko Nakano
Journal: Circulation (2025)

BACKGROUND: Recent studies have indicated an association between periodontitis and atrial fibrillation (AF), although the underlying mechanisms remain unclear. Porphyromonas gingivalis is a causative agent of periodontal disease and is highly pathogenic. This study focused on P gingivalis and aimed to investigate the relationship among periodontitis, atrial translocation of P gingivalis , and atrial fibrosis and AF. METHODS: An experiment was conducted using P gingivalis –infected C57BL/6J mice, in which P gingivalis was inoculated into the pulp of the molars. Immunohistochemistry was used to visualize the localization of P gingivalis , and loop-mediated isothermal amplification was employed to detect P gingivalis DNA in the left atrium. AF inducibility was examined by intracardiac stimulation. Moreover, left atrial appendage specimens were obtained from 68 patients with AF. A periodontal examination was conducted before the surgery, and the periodontal epithelial surface area and periodontal inflamed surface area, which are quantitative indices used to determine the clinical severity of periodontitis, were measured. The bacterial number of P gingivalis in human atrial tissue was analyzed via quantitative polymerase chain reaction. Atrial fibrosis was assessed using Azan-Mallory staining. RESULTS: The translocation path of P gingivalis from the dental granuloma to the left atrium via the circulatory system was demonstrated by immunohistochemistry and loop-mediated isothermal amplification in P gingivalis –infected mice, which showed a higher degree of atrial fibrosis (21.9% versus 16.3%; P =0.0003) and a higher AF inducibility (30.0% versus 5.0%; P =0.04) than the control mice. Upregulation of GAL3 (galectin 3) and transforming growth factor-beta 1 in the left atrium was observed in P gingivalis –infected mice. Moreover, immunohistochemistry revealed that P gingivalis was also present in human atrial tissue. The number of P gingivalis in the human atrial tissue was positively correlated with periodontal epithelial surface area (ρ=0.35; P =0.004), periodontal inflamed surface area (ρ=0.52, P &lt;0.0001), and the degree of atrial fibrosis (ρ=0.38; P =0.002). CONCLUSIONS: P gingivalis translocation to the left atrium correlates with the clinical severity of periodontitis, which may exacerbate atrial fibrosis and AF. Atrial translocation of P gingivalis is a potential pathway explaining the causal relationship between periodontitis and AF.
A Novel Hidden Protein p-414aa Encoded by <i>circSETD2(14,15</i> ) Inhibits Vascular Remodeling
Authors: Si-Fan Wang, Li-Yun Yang, An-Qi Zhao, Zhao-Yi Wang, Sen Wang, Miao Gong, Ming-Qi Zheng, Gang Liu, Shu-Yan Yang, Jia-Jie Lin, Shao-Guang Sun
Journal: Circulation (2025)

BACKGROUND: Phenotypic switching of vascular smooth muscle cells (VSMCs), leading to neointimal hyperplasia, is a fundamental cause of vascular remodeling diseases such as atherosclerosis and hypertension. Novel hidden proteins encoded by circular RNAs play crucial roles in disease progression, yet their involvement in vascular remodeling diseases has not been comprehensively studied. This study identifies a novel protein derived from a circular RNA in VSMCs and demonstrates its potential role in regulating vascular remodeling. METHODS: Cell proliferation assays were performed to investigate the effects of circSETD2(14,15 ) on VSMC proliferation. Techniques such as vector construction, immunoprecipitation–mass spectrometry, and dual-luciferase reporter gene were used to confirm that circSETD2(14,15 ) encoded a novel protein, p-414aa. The interaction between p-414aa and HuR (human antigen R) was validated with techniques such as coimmunoprecipitation, mass spectrometry, and proximity ligation assay. Through experiments including RNA sequencing and RNA immunoprecipitation, the interaction between HuR and C-FOS (C-Fos proto-oncogene) mRNA was revealed. The role of p-414aa in neointimal hyperplasia was assessed with a carotid artery ligation model in male mice. RESULTS: Overexpression of circSETD2(14,15 ) inhibits VSMC phenotypic switching. The novel protein p-414aa, encoded by circSETD2(14,15 ), interacts with HuR to reduce C-FOS mRNA stability, thereby suppressing VSMC proliferation and ultimately inhibiting neointimal hyperplasia in male mice. CONCLUSIONS: We uncover a novel hidden protein derived from circSETD2(14,15 ), called p-414aa, that inhibits vascular remodeling. CircSETD2(14,15 ) and p-414aa may serve as potential therapeutic targets for vascular remodeling diseases.
Optimal Vasopressin Initiation in Septic Shock
Authors: Alexandre Kalimouttou, Jason N. Kennedy, Jean Feng, Harvineet Singh, Suchi Saria, Derek C. Angus, Christopher W. Seymour, Romain Pirracchio
Journal: JAMA (2025)

Norepinephrine is the first-line vasopressor for patients with septic shock. When and whether a second agent, such as vasopressin, should be added is unknown. To derive and validate a reinforcement learning model to determine the optimal initiation rule for vasopressin in adult, critically ill patients receiving norepinephrine for septic shock. Reinforcement learning was used to generate the optimal rule for vasopressin initiation to improve short-term and hospital outcomes, using electronic health record data from 3608 patients who met the Sepsis-3 shock criteria at 5 California hospitals from 2012 to 2023. The rule was evaluated in 628 patients from the California dataset and 3 external datasets comprising 10 217 patients from 227 US hospitals, using weighted importance sampling and pooled logistic regression with inverse probability weighting. Clinical, laboratory, and treatment variables grouped hourly for 120 hours in the electronic health record. The primary outcome was in-hospital mortality. The derivation cohort (n = 3608) included 2075 men (57%) and had a median (IQR) age of 63 (56-70) years and Sequential Organ Failure Assessment (SOFA) score at shock onset of 5 (3-7 [range, 0-24, with higher scores associated with greater mortality]). The validation cohorts (n = 10 217) were 56% male (n = 5743) with a median (IQR) age of 67 (57-75) years and a SOFA score of 6 (4-9). In validation data, the model suggested vasopressin initiation in more patients (87% vs 31%), earlier relative to shock onset (median [IQR], 4 [1-8] vs 5 [1-14] hours), and at lower norepinephrine doses (median [IQR], 0.20 [0.08-0.45] vs 0.37 [0.17-0.69] µg/kg/min) compared with clinicians' actions. The rule was associated with a larger expected reward in validation data compared with clinician actions (weighted importance sampling difference, 31 [95% CI, 15-52]). The adjusted odds of hospital mortality were lower if vasopressin initiation was similar to the rule compared with different (odds ratio, 0.81 [95% CI, 0.73-0.91]), a finding consistent across external validation sets. In adult patients with septic shock receiving norepinephrine, the use of vasopressin was variable. A reinforcement learning model developed and validated in several observational datasets recommended more frequent and earlier use of vasopressin than average care patterns and was associated with reduced mortality.
Near‐Infrared Imaging Agent ABSi‐148 Alleviates <i>CA IX</i>‐Mediated Hypoxic Fibrosis in Inflammation‐Cancer Transition
Authors: Zhi Cao, Jingmin Li, Weibin Hu, Jian Xu, Fengyun Zhao, Yishu Wang, Shuanglin Qin, Ming Liu, Ping Wang, Jingwei Duan, Wensheng Zhou, Zhaowei Ding, Shaohui Tang, Xiaodong Ma, Lisheng Wang
Journal: Advanced Healthcare Materials (2025)

Abstract Pancreatic ductal adenocarcinoma (PDAC) remains a formidable challenge due to its late diagnosis and intrinsic treatment resistance, exacerbates by its development from chronic inflammation to cancer transition (ICT). Here, this investigation aims to develop and evaluate ABSi‐148, a novel near‐infrared (NIR) agent targeting hypoxic carbonic anhydrase IX ( CA IX ), for its potential applications in ICT imaging and even PDAC treatment. ABSi‐148 is synthesized from 4‐(2‐Aminoethyl) benzene sulfonamide (ABS), a sulfonamide derivative, conjugating with MHI‐148 dye with merits of exceptional NIR‐emitting traits, high biocompatibility, and deep tissue penetration imaging capability. It selectively accumulates in CoCl 2 ‐induced pancreatic stellate cells and pancreatic cancer cells via binding with transmembrane CA IX in vitro. Meanwhile, ABSi‐148 effectively visualizes the early pancreatic lesion, and its long‐term administration inhibits the progression of hypoxia‐related fibrosis involved in pancreatic intraepithelial neoplasias (PanINs), and even PDAC progression in vivo. Besides, ABSi‐148 monitors treatment efficacy and localizes hypoxic tumor regions, enhancing survival in tamoxifen combined with caerulein‐induced KPC mice. Overall, ABSi‐148 emerges as a theranostic NIR agent for precise diagnosis and targeted therapy in ICT of PDAC, promising to alleviate tumor progression and enhancing outcomes.
Tranexamic acid-fatty alcohol polyoxyethylene ether conjugation/PVA foam for venous sclerotherapy via vascular damage and inhibiting plasmin system
Authors: Jizhuang Ma, Keda Zhang, Wenhan Li, Yu Ding, Yongfeng Chen, Xiaoyu Huang, Tong Yu, Di Song, Haoran Niu, Huichao Xie, Tianzhi Yang, Xiaoyun Zhao, Xinggang Yang, Pingtian Ding
Journal: Acta Pharmaceutica Sinica B (2025)
Alginate lyase immobilized Chlamydomonas algae microrobots: Minimal invasive therapy for biofilm penetration and eradication
Authors: Xiaoting Zhang, Huaan Li, Lu Liu, Yanzhen Song, Lishan Zhang, Jiajun Miao, Jiamiao Jiang, Hao Tian, Chang Liu, Fei Peng, Yingfeng Tu
Journal: Acta Pharmaceutica Sinica B (2025)
Computational drug repurposing: approaches, evaluation of in silico resources and case studies
Authors: Ziaurrehman Tanoli, Adrià Fernández-Torras, Umut Onur Özcan, Aleksandr Kushnir, Kristen Michelle Nader, Yojana Gadiya, Laura Fiorenza, Aleksandr Ianevski, Markus Vähä-Koskela, Mitro Miihkinen, Umair Seemab, Henri Leinonen, Brinton Seashore-Ludlow, Marianna Tampere, Adelinn Kalman, Flavio Ballante, Emilio Benfenati, Gary Saunders, Swapnil Potdar, Ismael Gómez García, Ricard García-Serna, Carmine Talarico, Andrea Rosario Beccari, Wesley Schaal, Andrea Polo, Susan Costantini, Enrico Cabri, Marc Jacobs, Jani Saarela, Alfredo Budillon, Ola Spjuth, Päivi Östling, Henri Xhaard, Jordi Quintana, Jordi Mestres, Philip Gribbon, Anton E Ussi, Donald C Lo, Martin de Kort, Krister Wennerberg, Maddalena Fratelli, Jordi Carreras-Puigvert, Tero Aittokallio
Journal: Nature Reviews Drug Discovery (2025)