tbuckley/cabot-search huggingface dataset:
Screening for <i>Helicobacter pylori</i> to Prevent Gastric Cancer—Reply
Authors: Yi-Chia Lee, Amy Ming-Fang Yen, Tony Hsiu-Hsi Chen
Journal: JAMA (2025)

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Validated Integration of Tumor Deposits in N Staging for Prognostication in Colon Cancer
Authors: Richard Sassun, Annaclara Sileo, Jyi Cheng Ng, Tommaso Violante, Ibrahim Gomaa, Jay Mandrekar, Kristen K. Rumer, Nicholas P. McKenna, David W. Larson
Journal: JAMA Surgery (2025)

Importance Tumor deposits have prognostic value in colon cancer, but the current American Joint Committee on Cancer (AJCC) staging only considers them if there are no concurrent positive lymph nodes. Objective To devise a staging system for colon cancer by integrating counts of tumor deposits with positive lymph nodes while retaining the current AJCC staging framework. Design, Setting, and Participants This retrospective cohort study examines data from a large-volume, tertiary care center database (January 2010 through March 2023 with follow-up until December 2023) and the population-based National Cancer Database (January 2010 through December 2020 with follow-up until December 2021). Participants were adults (age 18-75 years) with stage III colon adenocarcinoma who underwent chemotherapy, and had a specified positive lymph node count and tumor deposit count were selected. Exposure A real positive lymph nodes count was developed and used to derive Sassun-Mayo N/tumor, lymph node, and metastasis (TNM) stages that were compared with the AJCC N/TNM stages. Main Outcomes and Measures Receiver operating characteristic (ROC) curves and Kaplan-Meier analyses for 3-year overall survival were performed to assess the efficiency of the 2 staging systems. The concordance index was used for validation using the National Cancer Database. Results From a total patient number of 11 162 (institutional) and 848 704 (national), the final patient numbers were 788 and 77 790, respectively. The institutional database patients had a mean (SD) age of 58.5 (11.5) years; there were 433 male patients (54.9%) and 355 female (45.1%). The national database patients had a mean (SD) age of 59.3 (10.6) years; there were 40 315 male patients (51.8%) and 37 475 female (48.2%). ROC curve areas were improved using the Sassun-Mayo stages (3-year death for AJCC TMN, 0.63 [95% CI, 0.57-0.69] vs 0.66 [95% CI, for 0.60-0.72] for Sassun-Mayo TNM). Kaplan-Meier curves revealed visible overlaps among AJCC N stages, which were absent in the Sassun-Mayo N stages. The concordance index in the Sassun-Mayo N/TNM stages was 0.611 and 0.616, respectively, while in the AJCC N/TNM stages, it was 0.598 and 0.606, respectively. Patients upstaged from N1 to N2 (n = 10 307; 13.2%) had a 3-year overall survival rate nearly identical to that of AJCC N2a patients. Additionally, 3001 patients (3.9%) were upstaged from N2a to N2b, indicating that 13 308 patients (17.1%) with stage III colon cancer across cohorts were understaged. Conclusions and Relevance This study found that Sassun-Mayo N/TNM staging provided superior overall survival stratification compared with the current AJCC staging, suggesting that their implementation could improve prognostication in colon cancer.
An International Multicenter, Retrospective Cohort Study of 203 Patients with Pediatric Androgenetic Alopecia
Authors: Tyan Shin Lee, Mara O'Connor, Leslie Castelo-Soccio, Dawn Eichenfield, Danny Lee, Amy S Paller, Manuel Valdebran, Jenna Vroman, Angela Yang, Grace L Lee, Megan Craddock, Cathryn Sibbald
Journal: Journal of the American Academy of Dermatology (2025)
RETRACTION: Decellularized Scaffolds with Double‐Layer Aligned Microchannels Induce the Oriented Growth of Bladder Smooth Muscle Cells: Toward Urethral and Ureteral Reconstruction
Journal: Advanced Healthcare Materials (2025)

Abstract RETRACTION : Q. Cheng, L. Zhang, J. Zhang, X. Zhou, B. Wu, D. Wang, T. Wei, M. Shafiq, S. Li, D. Zhi, Y. Guan, K. Wang, and D. Kong, “Decellularized Scaffolds with Double‐Layer Aligned Microchannels Induce the Oriented Growth of Bladder Smooth Muscle Cells: Toward Urethral and Ureteral Reconstruction,” Advanced Healthcare Materials 12, no. 26 (2023): 2300544, https://doi.org/10.1002/adhm.202300544 . The above article, published online on 28 August 2023 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor‐in‐Chief, Uta Goebel; and Wiley‐VCH GmbH. The retraction has been agreed upon following an investigation into concerns raised by a third party, which revealed inappropriate duplication of image sections and/or formatting artefacts in Figures 2B, 5A, and 7C, as well as errors in Figure S8 and its quantifications. The authors have stated that these image alterations were performed to enhance the visual appearance of the images and do not impact the clinical and scientific findings outlined in the paper. Nevertheless, due to the number and the level of inconsistencies identified in the published figures, the editors considered the conclusions substantially compromised and decided to retract the article.
Mitochondrial dysfunction and mitophagy blockade contribute to renal osteodystrophy in chronic kidney disease-mineral bone disorder
Authors: Shun-Neng Hsu, Louise A Stephen, Kanchan Phadwal, Scott Dillon, Roderick Carter, Nicholas M Morton, Ineke Luijten, Katie Emelianova, Anish K Amin, Vicky E Macrae, Tom C Freeman, Yu-Juei Hsu, Katherine A Staines, Colin Farquharson
Journal: Kidney International (2025)
A risk score to predict kidney survival in patients with autosomal recessive polycystic kidney disease at the age of two months
Authors: Kathrin Burgmaier, Samuel Kilian, Klaus Arbeiter, Bahriye Atmis, Olivia Boyer, Anja Buescher, Ismail Dursun, Florian Erger, Marc Fila, Matthias Galiano, Ibrahim Gokce, Karsten Haeffner, Dieter Haffner, Nakysa Hooman, Guenter Klaus, Jens König, Bärbel Lange-Sperandio, Matko Marlais, Laura Massella, Djalila Mekahli, Monika Miklaszewska, Gordana Miloševski-Lomić, Lukasz Obrycki, Bruno Ranchin, Barbara Seitz, Stella Stabouli, Yilmaz Tabel, Katarzyna Taranta-Janusz, Lutz Thorsten Weber, Marcus Weitz, Elke Wühl, Alev Yilmaz, Jörg Dötsch, Franz Schaefer, Max Christoph Liebau
Journal: Kidney International (2025)
A 2.5D Transfer Deep Learning Model Based on Artificial Intelligence for Differentiating Lymphoma and Tuberculous Lymphadenitis in HIV/AIDS Patients
Authors: Chang Song, Chun-Yan Zhao, Kai Li, Yan-Rong Lin, Shu-Lin Song, Chao-Yan Xu, Hang-Biao Qiang, Zhou-Hua Xie, Qing-Dong Zhu
Journal: Journal of Infection (2025)
Cholesterol Functionalized Nanoparticles Are Effective against <i>Helicobacter pylori</i>, the Gastric Bug: A Proof‐of‐Concept Study
Authors: Ana Sofia Pinho, Renato Pereira, Mariana Pereira, Akhilesh Rai, Lino Ferreira, Maria Cristina Lopes Martins, Paula Parreira
Journal: Advanced Healthcare Materials (2025)

Abstract Helicobacter pylori chronic infection is the highest risk factor for the development of gastric cancer, being this Gram‐negative bacterium classified as carcinogenic. The mounting resistance of H. pylori to antibiotics calls for innovative therapeutic strategies. Here, the proof‐of‐concept studies that support the development of a “trojan horse” therapeutic strategy based on cholesterol‐grafted nanoparticles (Chol‐NP) to counteract H. pylori infection are depicted. The bacterium ability to specifically recognize and bind to surface grafted cholesterol is demonstrated by its adhesion to cholesterol(Chol)‐functionalized self‐assembled monolayers (SAMs) on gold substrates (2D Chol‐SAMs) in a concentration dependent manner, with optimal Chol‐SAMs prepared with 25% Chol‐polyethylene glycol (PEG)‐thiol in solution (75% tetra(ethylene glycol)‐thiol). These results further show that cholesterol functionalized gold nanoparticles (3D Chol‐SAMs, Chol‐NP) eradicate H. pylori at a minimum bactericidal concentration of 125 µg mL −1 . Chol‐NP kill H. pylori through internalization and membrane rupture, as observed by transmission electron microscopy (TEM). Chol‐NP are cytocompatible (human gastric adenocarcinoma (AGS) cell line), non‐hemolytic and innocuous to bacteria representative of the gut microbiota ( Escherichia coli and Lactobacillus acidophilus ). This study supports the further development of cholesterol functionalized biomaterials as an advanced and targeted treatment for H. pylori infection.
Retraction Notice to: Lentivirus Mediated Delivery of Neurosin Promotes Clearance of Wild-type α-Synuclein and Reduces the Pathology in an α-Synuclein Model of LBD
Authors: Brian Spencer, Sarah Michael, Jay Shen, Kori Kosberg, Edward Rockenstein, Christina Patrick, Anthony Adame, Eliezer Masliah
Journal: Molecular Therapy (2025)
Recommendations for implementing the Hevolution Alliance for Aging Biomarkers initiative
Authors: Toshiko Tanaka, Felipe Sierra, Vadim N. Gladyshev, Tony Wyss-Coray, Ana Maria Cuervo, Viviana Perez, Luigi Ferrucci, David B. Allison, John R. Beard, Daniel W Belsky, Heike A. Bischoff-Ferrari, Eileen M. Crimmins, Jens Eckstein, Linda P. Fried, Vadim N. Gladyshev, William Greene, Steve Horvath, Rose Anne Kenny, Stephen B. Kritchevsky, Louise Lafortune, Andrea B. Maier, Terrie E. Moffitt, Sophia Pathai, Parminder Raina, Joanne Ryan, Jonathan C. Silverstein, Yousin Suh
Journal: Nature Aging (2025)
The MI-CLAIM-GEN checklist for generative artificial intelligence in health
Authors: Brenda Y. Miao, Irene Y. Chen, Christopher Y. K. Williams, Jaysón Davidson, Augusto Garcia-Agundez, Shenghuan Sun, Travis Zack, Suchi Saria, Rima Arnaout, Giorgio Quer, Hossein J. Sadaei, Ali Torkamani, Brett Beaulieu-Jones, Bin Yu, Milena Gianfrancesco, Atul J. Butte, Beau Norgeot, Madhumita Sushil
Journal: Nature Medicine (2025)
Oncogenic TFE3 fusions drive OXPHOS and confer metabolic vulnerabilities in translocation renal cell carcinoma
Authors: Jiao Li, Kaimeng Huang, Meha Thakur, Fiona McBride, Ananthan Sadagopan, Daniel S Gallant, Prateek Khanna, Yasmin Nabil Laimon, Bingchen Li, Razan Mohanna, Maolin Ge, Cary N Weiss, Mingkee Achom, Qingru Xu, Sayed Matar, Gwo-Shu Mary Lee, Kun Huang, Miao Gui, Chin-Lee Wu, Kristine M Cornejo, Toni K Choueiri, Birgitta A Ryback, Sabina Signoretti, Liron Bar-Peled, Srinivas R Viswanathan
Journal: Nature Metabolism (2025)
Loss of Endothelial TRPC1 Induces Aortic Hypercontractility and Hypertension
Authors: Yifei Zhu, Yuan Chu, Yihui Lan, Sheng Wang, Yizhi Zhang, Yuan Liu, Xianfeng Wang, Fan Yu, Xin Ma
Journal: Circulation Research (2025)

BACKGROUND: The increasing prevalence of obesity-related cardiovascular diseases demands a better understanding of the contribution of different cell types to vascular function for developing new treatment strategies. Previous studies have established a fundamental role of TRPC1 (transient receptor potential channel canonical family member 1) in blood vessels. However, little is known about its functional roles within different cell types. METHODS: We generated endothelial-specific TRPC1-deficient and knockin mice and analyzed their changes in vascular function under physiological and pathologically obese state. Wire myography, Ca 2+ image, blood pressure measurements, RNA-sequencing analysis, liquid chromatography–mass spectrometry, immunoblotting, ELISA, luciferase reporter assay, and morphometric assessments were performed to unravel phenotype and molecular changes in response to the absence or presence of endothelial TRPC1. RESULTS: Loss of endothelial TRPC1 reduced endothelial-dependent relaxation and exaggerated endothelial-dependent contraction in mouse aorta. As expected, loss of endothelial TRPC1 amplified blood pressure and decreased acetylcholine-induced intracellular Ca 2+ concentration rise in the aorta. In endothelial-specific TRPC1-deficient mouse arteries, the mRNA profile identified upregulation of c-Fos. Blockade of c-Fos rescued the impaired vasomotor tone in the aorta of mice deficient in endothelial TRPC1. Endothelial TRPC1-regulated nitric oxide/endothelin-1 production is involved in vascular c-Fos expression. Moreover, knockin of endothelial TRPC1 ameliorated enhanced endothelial-dependent contraction and hypertension in obese mice which is related to alleviated endothelial endothelin-1/c-Fos production and smooth muscle contraction. CONCLUSIONS: Our results identify endothelial TRPC1 as a previously unclear regulator of vascular changes and blood pressure in both physiological and pathologically obese state, and it is associated with nitric oxide/endothelin-1/c-Fos signaling.
Induced Cytokinesis Generates Highly Proliferative Mononuclear Cardiomyocytes at the Expense of Contractility
Authors: Nicholas T. Lam, Ngoc Uyen Nhi Nguyen, Waleed M. Elhelaly, Ching-Cheng Hsu, Ivan Menendez-Montes, Feng Xiao, Shah R. Ali, Nelson Vo, Nathan Briard, Lobna El-Feky, Qamar M. Omari, Alisson C. Cardoso, Yan Liu, Mahmoud Salama Ahmed, Shujuan Li, Suwannee Thet, Chao Xing, Lior Zangi, Hesham A. Sadek
Journal: Circulation (2025)

BACKGROUND: Cytokinesis is the last step in the eukaryotic cell cycle, which physically separates a mitotic cell into 2 daughter cells. A few days after birth in mouse cardiomyocytes, DNA synthesis occurs without cytokinesis, leading to the majority of cardiomyocytes becoming binucleated instead of generating 2 daughter cells with 1 nucleus each. This results in cell cycle arrest of cardiomyocytes, and the mouse heart is no longer able to regenerate. A longstanding unanswered question is whether binucleation of cardiomyocytes is a result of cytokinesis failure. METHODS: To address this, we generated several transgenic mouse models to determine whether forced induction of cardiomyocyte cytokinesis generates mononucleated cardiomyocytes and restores the endogenous regenerative properties of the myocardium. We focused on 2 complementary regulators of cytokinesis: Plk1 (polo-like kinase 1) and Ect2 (epithelial cell-transformation sequence 2). RESULTS: We found that cardiomyocyte-specific transgenic overexpression of constitutively active Plk1(T210D) promotes mitosis and cytokinesis in adult hearts, whereas overexpression of Ect2 alone promotes only cytokinesis. Cardiomyocyte-specific overexpression of both Plk1(T210D) and Ect2 concomitantly (double transgenic) prevents binucleation of cardiomyocytes postnatally and results in widespread cardiomyocyte mitosis, cardiac enlargement, contractile failure, and death before 2 weeks of age. Similarly, doxycycline-inducible cardiomyocyte-specific overexpression of both proteins (inducible double transgenic) in the adult heart results in reversible widespread cardiomyocyte mitosis and contractile failure. Transient induction of both genes in adult mice improves left ventricular systolic function after myocardial infarction. CONCLUSIONS: These results collectively demonstrate that cytokinesis failure mediates cardiomyocyte multinucleation and cell cycle exit of postnatal cardiomyocytes, but may be a protective mechanism to preserve the contractile function of the myocardium.
Correlation Between N‐Glycan <scp>GnGnXF3</scp> and the Allergic Immune Response Against <i>Juniperus ashei</i> Pollen
Authors: Javier Álvarez, Nuria Parody, David Calzada, Tamara Aranda, Ana Renshaw, Sonia Serna, Niels Reichardt, Juan María Beitia, David González‐de‐Olano, Javier Dominguez‐Ortega, Jerónimo Carnés
Journal: Allergy (2025)

ABSTRACT Background Cupressaceae pollen increasingly causes respiratory allergies worldwide. Carbohydrates are abundant in extracts of these pollens, and the associated allergens are highly glycosylated. However, the contribution of saccharides to the allergenicity of these species remains unknown. Methods Juniperus ashei pollen extract was deglycosylated and characterised using SDS‐PAGE and immunoblotting. Additionally, N‐ and O‐glycans were purified from the extract, identified, used as inhibitors in IgE‐immunoblotting and further analysed via basophil activation tests. The interactions between IgE and J. ashei glycans were analysed using a glycan array. Purified Jun a 1 was treated with β‐N‐acetylglucosaminidase S and analysed using immunoblotting. The native pollen extract was used to immunise rabbits, and the IgG response was analysed using ELISA and glycan array. Results Deglycosylation of J. ashei proteins abolished the interaction between IgE and allergens. This effect primarily depends on N‐glycans. Purified N‐glycans triggered basophil activation in some patients. A biantennary N‐glycan with terminal GlcNAc, β‐1,2 xylose and core α‐1,3 fucose (GnGnXF3) was the most abundant glycan identified. The glycan array confirmed its interaction with IgE. The contribution of terminal N‐acetylglucosamines (GlcNAc) to IgE–Jun a 1 interaction was validated. Moreover, effective immunisation of rabbits with the native extract confirmed the immunogenicity of their N‐glycans. Conclusions The IgE– J. ashei allergen interaction is broadly controlled through N‐glycans different from MUXF3. GnGnXF3 exerts an immunogenic effect in humans and rabbits; terminal GlcNAc residues influence its recognition by IgE. These discoveries reinforce the role of N‐glycans in the allergic response to J. ashei .
Letter to the editor: effects of radiotherapy exposure on fruquintinib plus sintilimab treatment in refractory microsatellite stable metastatic colorectal cancer—a prospective observation study
Authors: Bi-Cheng Wang
Journal: Journal for ImmunoTherapy of Cancer (2025)

As an oncology physician, I appreciate the prospective study conducted by Cheng and colleagues, which investigates the survival benefits of advanced microsatellite stable (MSS) colorectal cancer patients treated with radiotherapy, fruquintinib, and sintilimab.[1][1] This trial compared the effects
Tumor mutational burden and survival on immune checkpoint inhibition in &gt;8000 patients across 24 cancer types
Authors: David R Gandara, Neeraj Agarwal, Shilpa Gupta, Samuel J Klempner, Miles C Andrews, Amit Mahipal, Vivek Subbiah, Ramez N Eskander, David P Carbone, Jonathan W Riess, Sarah Sammons, Jeremy Snider, Lilia Bouzit, Cheryl Cho-Phan, Megan Price, Gerald Li, Julia C F Quintanilha, Richard Sheng Poe Huang, Jeffrey S Ross, David Fabrizio, Geoffrey R Oxnard, Ryon P Graf
Journal: Journal for ImmunoTherapy of Cancer (2025)

Background There is uncertainty around clinical applicability of tumor mutational burden (TMB) across cancer types, in part because of inconsistency between TMB measurements from different platforms. The KEYNOTE 158 trial supported United States Food and Drug Administration (FDA) approval of the Foundation Medicine test (FoundationOneCDx) at TMB≥10 mut/Mb as a companion diagnostic (CDx) for single-agent pembrolizumab in second+line. Using a large real-world dataset with validated survival endpoint data, we evaluated clinical validity of TMB measurement by the test in over 8000 patients across 24 cancer types who received single-agent immune checkpoint inhibitor (ICI). Methods Patients with advanced-stage cancers from 24 cancer types treated with single-agent anti-PD(L)1 therapy in standard-of-care settings were included. Deidentified data from electronic health records from approximately 280 cancer treatment facilities were captured into a clinico-genomic database. This study used the TMB algorithm from the FDA-approved test supporting solid tumor CDx and composite mortality variable validated against the national death index: real-world overall survival (rwOS). Following a prespecified analysis plan, rwOS by TMB level was assessed using Cox PH models adjusted for Eastern Cooperative Oncology Group performance status, prior treatment, microsatellite instability, sex, age, opioid rx pretherapy, and socioeconomic assessment. Results 8440 patients met inclusion criteria. Adjusting for aforementioned factors, increasing TMB was significantly associated with rwOS across tumor types; HRs (95% CIs) relative to TMB&lt;5: TMB 5 to &lt;10: 0.95 (0.89 to 1.02), TMB 10 to &lt;20: 0.79 (0.73 to 0.85), TMB≥20: 0.52 (0.47 to 0.58). For individual cancer types with prespecified statistical power, adjusted rwOS comparing TMB≥10 vs TMB&lt;10 significantly favored TMB≥10 in 9 of 10 cancer types. In microsatellite stable subcohorts (except colorectal cancer), TMB≥10 remained associated with enriched ICI benefit. Exploratory assessments of patients receiving ICI+chemotherapy (n=4369) observed more favorable rwOS only in TMB≥20. Conclusions Across &gt;8000 patients treated with single-agent ICI, and within individual cancer types with sufficient power, elevated TMB based on the FDA-approved CDx was associated with more favorable rwOS compared with similar patients with lower TMB levels. This biomarker deserves further clinical investigation to potentially guide the use of immunotherapy in expanded clinical contexts.
Clofarabine induces tumor cell apoptosis, GSDME-related pyroptosis, and CD8<sup>+</sup>T-cell antitumor activity via the non-canonical P53/STING pathway
Authors: Jie Wu, Nian Liu, Jing Chen, Qian Tao, Can Lu, Qiuqiu Li, Xiang Chen, Cong Peng
Journal: Journal for ImmunoTherapy of Cancer (2025)

Background Clofarabine (Clo) is a Food and Drug Administration (FDA)-approved drug for the treatment of acute lymphoblastic leukemia; however, its effects on solid tumors remain largely unknown. Methods In vitro and in vivo experiments have demonstrated the cytotoxic effects of Clo on melanoma and lung cancer. The molecular mechanisms of Clo-induced tumor cell death were analyzed using western blotting, ELISA, reverse transcription-PCR, immunofluorescence, co-immunoprecipitation (CO-IP), short hairpin RNA, co-culture, chromatin immunoprecipitation, and flow cytometry. Clinical data sets were used to analyze the correlation between stimulator of interferon genes (STING)-NFκB signaling and immune infiltration. Results In this study, Clo significantly reduced the growth of melanoma and lung cancer cells. Furthermore, Clo treatment induced GSDME-mediated pyroptosis. Most importantly, Clo administration dramatically increased the cytotoxic activity of CD8 + T cells in vitro and in vivo. Mechanistically, the administration of Clo induced the interaction of P53 with STING, which activated the non-canonical STING-NFκB pathway; consequently, NF-κB directly bound to the promoter regions of its target genes, including CCL5, CXCL10, HLAs and BAX. This resulted in apoptosis, pyroptosis, and immunogenic cell death in tumor cells by Clo. Furthermore, Clo-induced GSDME-mediated pyroptosis partly assists in activating T cell immunity via CCL5 and CXCL10. The non-canonical STING-NF-κB pathway is the crucial signaling pathway that initiates and links apoptosis, pyroptosis, and immunogenic cell death. Conclusions Our study is the first to show that Clo, an FDA-approved drug, induces tumor cell apoptosis, GSDME-related pyroptosis, and CD8 + T-cell antitumor activity via the non-canonical P53-STING-NF-κB signaling pathway, providing a novel strategy for the clinical therapy of melanoma and lung cancer.