tbuckley/cabot-search huggingface dataset:
Response Trajectories and Temporal Trends of Viloxazine Treatment for Young People With ADHD
Authors: Chia-Ling Yu, Yu-Chen Kao, Trevor Thompson, Brendon Stubbs, Ping-Tao Tseng, Chih-Wei Hsu, Fu-Chi Yang, Yu-Kang Tu, Tien-Wei Hsu, Chih-Sung Liang
Journal: JAMA Network Open (2024)

Importance Viloxazine is a novel nonstimulant medication approved for the treatment of attention-deficit/hyperactivity disorder (ADHD). Objectives To investigate the whether viloxazine is associated with effective and acceptable outcomes when treating children and adolescents with ADHD and to evaluate these outcomes’ associations with viloxazine doses and duration of treatment. Data Sources The MEDLINE, Cochrane Central Register of Controlled Trials (CENTRAL), Embase, PsycINFO, and ClinicalTrial.gov databases were searched from database inception to June 23, 2024. Study Selection Two reviewers independently screened for double-blind, fixed-dose randomized clinical trials (RCTs) that compared viloxazine with placebo for pediatric patients with ADHD. Data Extraction and Synthesis The study followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses reporting guideline. Data extraction was completed independently by 2 authors and cross-checked for errors. Random-effects pairwise and dose-response meta-analyses were conducted. Main Outcomes and Measures The primary outcome was the improvement of ADHD symptoms (measured by ADHD Rating Scale–5), and the secondary outcomes were all-cause discontinuation, dropout due to adverse effects, and serious adverse effects. Results A total of 5 dose-response RCTs were included, with 1560 participants (1011 [64.8%] male; mean [SD] age, 10.6 [6.7] years). Viloxazine was associated with better outcomes in ADHD treatment compared with placebo (mean difference, 5.47 points; 95% CI, 4.03-6.91 points). The dose-response curve was bell-shaped, suggesting that doses greater than 400 mg or greater than 7 mg/kg might not be associated with more efficacy. The temporal trends analysis showed ascent curves tapering off at approximately weeks 4 to 6. The curve for 100 mg/d declined more rapidly, while the curves for 200 mg/d and 400 mg/d declined more gradually. The overall discontinuation rate due to adverse effects was 4.15% in the viloxazine group (45 of 1084), while viloxazine compared with placebo was associated with 2.48-fold higher risk of discontinuation due to adverse effects (risk ratio, 2.48; 95% CI, 1.26-4.88). Conclusions and relevance In this meta-analysis, viloxazine was associated with better efficacy in treating children and adolescents with ADHD than placebo. A moderate dose (200-400 mg or 6-8 mg/kg) may provide optimal treatment outcomes. Future studies are warranted to assess the long-term effect of viloxazine. Viloxazine was relatively well tolerated for children and adolescents with ADHD.
Disaggregating Asian American Data to Enhance Medical Education and Patient Care
Authors: Mytien Nguyen, Dowin Boatright, Tonya L. Fancher
Journal: JAMA Network Open (2024)

Patricia Mae G. Santos, MD, MS; Carlos Irwin A. Oronce, MD, PhD; Kanan Shah, MD; Fumiko Chino, MD; Mylin A. Torres, MD; Reshma Jagsi, MD, DPhil; Curtiland Deville Jr, MD; Neha Vapiwala, MD
Solid tumor immunotherapy using NKG2D-based adaptor CAR T cells
Authors: Jana Obajdin, Daniel Larcombe-Young, Maya Glover, Fahima Kausar, Caroline M Hull, Katie R Flaherty, Ge Tan, Richard E Beatson, Phoebe Dunbar, Roberta Mazza, Camilla Bove, Chelsea Taylor, Andrea Bille, Katelyn M Spillane, Domenico Cozzetto, Alessandra Vigilante, Anna Schurich, David M Davies, John Maher
Journal: Cell Reports Medicine (2024)

NKG2D ligands (NKG2DLs) are broadly expressed in cancer. To target these, we describe an adaptor chimeric antigen receptor (CAR) termed NKG2D/Dap10-12. Herein, T cells are engineered to co-express NKG2D with a fusion protein that comprises Dap10 joined to a Dap12 endodomain. NKG2D/Dap10-12 T cells elicit compelling efficacy, eradicating or controlling NKG2DL-expressing tumors in several established xenograft models. Importantly, durable responses, long-term survival, and rejection of tumor re-challenge are reproducibly achieved. Efficacy is markedly superior to a clinical stage CAR analog, comprising an NKG2D-CD3ζ fusion. Structure-function analysis using an extended CAR panel demonstrates that potency is dependent on membrane proximity of signaling units, high NKG2D cell surface expression, adaptor structure, provision of exogenous Dap10, and inclusion of one rather than three immune tyrosine activation motifs per signaling unit. Potent therapeutic impact of NKG2D/Dap10-12 T cells is also underpinned by enhanced oxidative phosphorylation, reduced senescence, and transcriptomic re-programming for increased ribosomal biogenesis.
Polycomb group protein Mel18 inhibits hematopoietic stem cell self-renewal through repressing the transcription of self-renewal and proliferation genes
Authors: Wenjie Cai, Xicheng Liu, Sergio Barajas, Shiyu Xiao, Sasidhar Vemula, Hongxia Chen, Yuxia Yang, Christopher Bochers, Danielle Henley, Sheng Liu, Yuzhi Jia, Michelle Hong, Tiffany M. Mays, Maegan L. Capitano, Huiping Liu, Peng Ji, Zhonghua Gao, Diego Pasini, Jun Wan, Feng Yue, Leonidas C. Platanias, Rongwen Xi, Sisi Chen, Yan Liu
Journal: Leukemia (2024)
An unconventional purine connection
Authors: Fabio Grassi
Journal: The Journal of Experimental Medicine (2024)

Xu et al. (https://doi.org/10.1084/jem.20240354) define NAD-induced cell death via purinergic P2RX7 receptor in type 1 unconventional T cells, particularly intrahepatic MAIT cells that are pivotal in liver homeostasis. Therefore, P2RX7 is a potential target to modulate unconventional T cells in immunopathological conditions and cancer.
Hepatic glucose production rises with the histological severity of metabolic dysfunction-associated steatohepatitis
Authors: Silvia Sabatini, Partho Sen, Fabrizia Carli, Samantha Pezzica, Chiara Rosso, Erminia Lembo, Ornella Verrastro, Ann Daly, Olivier Govaere, Simon Cockell, Tuulia Hyötyläinen, Geltrude Mingrone, Elisabetta Bugianesi, Quentin M Anstee, Matej Orešič, Amalia Gastaldelli
Journal: Cell Reports Medicine (2024)
Autologous transplantation of P63+ lung progenitor cells in patients with bronchiectasis: A randomized, single-blind, controlled trial
Authors: Jiayang Yan, Weipan Zhang, Yun Feng, Xuefei Liu, Lingyun Niu, Yi Guo, Ling Zhou, Mengmeng Shi, Caixia Di, Qiurui Zhang, Xiaofei Wang, Jianping Zhou, Ranran Dai, Lei Ni, Zhiyao Bao, Tianli Yan, Yun Hu, Ping Wang, Ting Zhang, Min Zhou, Wei Zuo, Jieming Qu
Journal: Cell Reports Medicine (2024)
Hospitalization Following Outpatient Diagnosis of Respiratory Syncytial Virus in Adults
Authors: Suzanne N. Landi, Diana C. Garofalo, Maya Reimbaeva, Amie M. Scott, Lili Jiang, Katherine Cappell, David Lewandowski, Machaon Bonafede, Kaylen Brzozowski, Zuzanna Drebert, Mike Temple, Margaret Tawadrous, Glenn C. Pixton, Niki Alami, Scott P. Kelly, Negar Aliabadi, Elizabeth Begier, Joshua T. Swan
Journal: JAMA Network Open (2024)

Importance Respiratory syncytial virus (RSV) is a leading cause of acute respiratory tract infections among adults and is estimated to cause approximately 159 000 hospitalizations among adults aged 65 years and older in the US each year. Estimates of hospitalization among adults with outpatient medically attended RSV (MA-RSV) infections are required to design interventional studies that aim to prevent hospitalization. Objective To assess absolute risk of 28-day, all-cause hospitalization following outpatient MA-RSV infections in adults. Design, Setting, and Participants In this cohort study, data from 3 different deidentified databases containing electronic health records (EHR) linked to closed claims data (Optum’s deidentified Integrated Claims-Clinical dataset, TriNetX Linked, and Veradigm Network EHR [VNEHR] database linked with claims) were analyzed separately across 6 RSV years (October 1, 2016, to September 30, 2022) in adults with commercial or government insurance. Outpatient (eg, clinics and emergency departments) MA-RSV infections were identified based on clinical laboratory data or RSV-specific International Statistical Classification of Diseases, Tenth Revision, Clinical Modification ( ICD-10-CM ) diagnosis codes. Data were analyzed from March 2023 to April 2024. Main Outcomes and Measures The main outcome was all-cause 28-day hospitalization following outpatient MA-RSV infections among all adults and a high-risk subgroup (defined as age ≥65 years or with asthma, chronic obstructive pulmonary disease [COPD], or congestive heart failure [CHF]). Results In this cohort study of 67 239 MA-RSV infections in adults (2771 from Optum, 7442 from TriNetX, and 57 026 from VNEHR), most occurred among females (62%-67%) and comorbidity prevalences were 20.0% to 30.5% for COPD, 14.6% to 24.4% for CHF, 14.6% to 24.4% for asthma; 14.0% to 54.5% of individuals were aged 65 years or older. The proportion hospitalized was 6.2% (95% CI, 5.3%-7.1%) in Optum, 6.0% (95% CI, 5.4% to 6.5%) in TriNetX, and 4.5% (95% CI, 4.3%-4.6%) in VNEHR. Among the high-risk subgroup, the proportion hospitalized was 7.6% (95% CI, 6.5%-8.9%) in Optum, 8.5% (95% CI, 7.6%-9.4%) in TriNetX, and 6.5% (95% CI, 6.2%-6.8%) in VNEHR. Conclusions and Relevance In this cohort study of adults with outpatient MA-RSV infections from 3 large deidentified US databases across 6 RSV seasons, approximately 1 in 20 adults experienced all-cause hospitalization within 28 days. The results of this study highlight the public health need for RSV prevention and treatment.
Molecular adaptation to neoadjuvant immunotherapy in triple-negative breast cancer
Authors: Carsten Denkert, Andreas Schneeweiss, Julia Rey, Thomas Karn, Akira Hattesohl, Karsten E Weber, Sivaramakrishna Rachakonda, Michael Braun, Jens Huober, Paul Jank, Hans-Peter Sinn, Dirk-Michael Zahm, Bärbel Felder, Claus Hanusch, Julia Teply-Szymanski, Frederik Marmé, Tanja Fehm, Jörg Thomalla, Bruno V Sinn, Thorsten Stiewe, Michal Marczyk, Jens-Uwe Blohmer, Marion van Mackelenbergh, Christian Schem, Peter Staib, Theresa Link, Volkmar Müller, Elmar Stickeler, Daniel G Stover, Christine Solbach, Otto Metzger-Filho, Christian Jackisch, Charles E Geyer, Peter A Fasching, Lajos Pusztai, Valentina Nekljudova, Michael Untch, Sibylle Loibl
Journal: Cell Reports Medicine (2024)
Sepsis pathogenesis and outcome are shaped by the balance between the transcriptional states of systemic inflammation and antimicrobial response
Authors: Rachel Brandes-Leibovitz, Anca Riza, Gal Yankovitz, Andrei Pirvu, Stefania Dorobantu, Adina Dragos, Ioana Streata, Isis Ricaño-Ponce, Aline de Nooijer, Florentina Dumitrescu, Nikolaos Antonakos, Eleni Antoniadou, George Dimopoulos, Ioannis Koutsodimitropoulos, Theano Kontopoulou, Dimitra Markopoulou, Eleni Aimoniotou, Apostolos Komnos, George N Dalekos, Mihai Ioana, Evangelos J Giamarellos-Bourboulis, Irit Gat-Viks, Mihai G Netea
Journal: Cell Reports Medicine (2024)
Cold-induced thermogenesis requires neutral-lipase-mediated intracellular lipolysis in brown adipocytes
Authors: Etienne Mouisel, Anaïs Bodon, Christophe Noll, Stéphanie Cassant-Sourdy, Marie-Adeline Marques, Remy Flores-Flores, Elodie Riant, Camille Bergoglio, Pierre Vezin, Sylvie Caspar-Bauguil, Camille Fournes-Fraresso, Geneviève Tavernier, Khalil Acheikh Ibn Oumar, Pierre Gourdy, Denis P Blondin, Pierre-Damien Denechaud, André C Carpentier, Dominique Langin
Journal: Cell Metabolism (2024)
Erratum: “Impact of Skin Care Products on Phthalates and Phthalate Replacements in Children: The ECHO-FGS”
Authors: Michael S. Bloom, Juliana M. Clark, John L. Pearce, Pamela L. Ferguson, Roger B. Newman, James R. Roberts, William A. Grobman, Anthony C. Sciscione, Daniel W. Skupski, Kelly Garcia, John E. Vena, Kelly J. Hunt
Journal: Environmental Health Perspectives (2024)
NOTCH1 drives sexually dimorphic immune responses in hepatocellular carcinoma
Authors: Katherine E. Lindblad, Romain Donne, Ian Liebling, Marina Barcena-Varela, Anthony Lozano, Marina Ruiz de Galarreta, Maxime Dhainaut, Nesteene J. Param, Bruno Giotti, Sarah Cappuyns, Takahiro Kodama, Yulei Wang, Alice O. Kamphorst, Alexander M. Tsankov, Amaia Lujambio
Journal: Cancer Discovery (2024)

Hepatocellular carcinoma presents strong sexual dimorphism, being two to three times more frequent in males than in females; however, the role of sex in response to immunotherapies in HCC remains unknown. We demonstrate that NOTCH1, an understudied oncogene in HCC, elicits sexually dimorphic antitumor immunity and response to FDA-approved immunotherapies. Surprisingly, males harboring NOTCH1-driven tumors displayed enhanced antitumor immune responses, which, in mice, were mediated by dendritic and T cells. Conversely, females harboring NOTCH1-driven tumors presented immune evasion and resistance to immunotherapies through a defect in dendritic cell (DC)-mediated priming and activation of CD8+ T cells in mice, which was restored therapeutically with CD40 agonism. Mechanistically, the sexually dimorphic immunity was mediated by genes in the sex chromosomes but not by sex hormones. Together, our study unravels an unexpected association between NOTCH1 and sex in cancer immunity and highlights the potential of restoring the DC-CD8+ T-cell axis with CD40 agonism to improve outcomes. Significance: Although HCC presents strong sexual dimorphism, the role of sex in response to immunotherapies remains elusive. With a novel HCC mouse model and validation in patients with HCC, we demonstrate that NOTCH1 disrupts antitumor immunity specifically in females through a mechanism mediated by sex chromosome genes, which is reversed with CD40 agonism. See related commentary by Zhu and Koltsova, p. 452.
PKN2 is a dependency of the mesenchymal-like cancer cell state
Authors: Shane T. Killarney, Gabriel Mesa, Rachel Washart, Benjamin Mayro, Kerry Dillon, Suzanne E. Wardell, Madeline Newlin, Min Lu, Areej Abu Rmaileh, Nicky Liu, Donald P. McDonnell, Ann Marie Pendergast, Kris C. Wood
Journal: Cancer Discovery (2024)

Cancer cells exploit a mesenchymal-like transcriptional state (MLS) to survive drug treatments. Although the MLS is well characterized, few therapeutic vulnerabilities targeting this program have been identified. In this study, we systematically identify the dependency network of mesenchymal-like cancers through an analysis of gene essentiality scores in ∼800 cancer cell lines, nominating a poorly studied kinase, PKN2, as a top therapeutic target of the MLS. Coessentiality relationships, biochemical experiments, and genomic analyses of patient tumors revealed that PKN2 promotes mesenchymal-like cancer growth through a PKN2-SAV1-TAZ signaling mechanism. Notably, pairing genetic PKN2 inhibition with clinically relevant targeted therapies against EGFR, KRAS, and BRAF suppresses drug resistance by depleting mesenchymal-like drug-tolerant persister cells. These findings provide evidence that PKN2 is a core regulator of the Hippo tumor suppressor pathway and highlight the potential of PKN2 inhibition as a generalizable therapeutic strategy to overcome drug resistance driven by the MLS across cancer contexts. Significance: This work identifies PKN2 as a core member of the Hippo signaling pathway, and its inhibition blocks YAP/TAZ-driven tumorigenesis. Furthermore, this study discovers PKN2-TAZ as arguably the most selective dependency of mesenchymal-like cancers and supports specific inhibition of PKN2 as a provocative strategy to overcome drug resistance in diverse cancer contexts. See related commentary by Shen and Tan, p. 458.
The histological growth patterns in liver metastases from colorectal cancer display differences in lymphoid, myeloid, and mesenchymal cells
Authors: Gemma Garcia‐Vicién, Núria Ruiz, Patrick Micke, José Carlos Ruffinelli, Kristel Mils, María Bañuls, Natalia Molina, Miguel A. Pardo, Laura Lladó, Artur Mezheyeuski, David G. Molleví
Journal: MedComm (2024)

Colorectal liver metastases grow following different histologic growth patterns (HGPs), classified as desmoplastic and nondesmoplastic (dHGP, non-dHGP), being the latter associated with worst prognosis. This study aimed to investigate the tumor microenvironment (TME) between HGPs supporting different survival. Multiplexed immunohistochemical staining was performed with the Opal7 system in a 100-patients cohort to evaluate the tumor-liver interface with three different cell panels: lymphoid, myeloid, and carcinoma-associated fibroblasts. Differences between HGPs were assessed by Mann-Whitney
A predictive model based on quantitative fecal immunochemical test can stratify the risk of CRC in an organized screening program
Authors: Leonardo Frazzoni, Silvia Pecere, Cesare Hassan, Lorenzo Fuccio, Livio Enrico Del Vecchio, Carlo Fabbri, Arrigo Arrigoni, Paola Cassoni, Dario Mazzucco, Lorenzo Orione, Giulia Gibiino, Alessandro Repici, Cristiano Spada, Federico Iacopini, Carlo Senore, Giulio Antonelli
Journal: Clinical Gastroenterology and Hepatology (2024)
Immunomolecular and reactivity landscapes of gut IgA subclasses in homeostasis and inflammatory bowel disease
Authors: Sonia Tejedor Vaquero, Hadas Neuman, Laura Comerma, Xavi Marcos-Fa, Celia Corral-Vazquez, Mathieu Uzzan, Marc Pybus, Daniel Segura-Garzón, Joana Guerra, Lisa Perruzza, Roser Tachó-Piñot, Jordi Sintes, Adam Rosenstein, Emilie K. Grasset, Mar Iglesias, Monica Gonzalez Farré, Joan Lop, Maria Evangelina Patriaca-Amiano, Monica Larrubia-Loring, Pablo Santiago-Diaz, Júlia Perera-Bel, Pau Berenguer-Molins, Monica Martinez Gallo, Andrea Martin-Nalda, Encarna Varela, Marta Garrido-Pontnou, Fabio Grassi, Francisco Guarner, Saurabh Mehandru, Lucia Márquez-Mosquera, Ramit Mehr, Andrea Cerutti, Giuliana Magri
Journal: The Journal of Experimental Medicine (2024)

The human gut includes plasma cells (PCs) expressing immunoglobulin A1 (IgA1) or IgA2, two structurally distinct IgA subclasses with elusive regulation, function, and reactivity. We show here that intestinal IgA1+ and IgA2+ PCs co-emerged early in life, comparably accumulated somatic mutations, and were enriched within short-lived CD19+ and long-lived CD19− PC subsets, respectively. IgA2+ PCs were extensively clonally related to IgA1+ PCs and a subset of them presumably emerged from IgA1+ precursors. Of note, secretory IgA1 (SIgA1) and SIgA2 dually coated a large fraction of mucus-embedded bacteria, including Akkermansia muciniphila. Disruption of homeostasis by inflammatory bowel disease (IBD) was associated with an increase in actively proliferating IgA1+ plasmablasts, a depletion in long-lived IgA2+ PCs, and increased SIgA1+SIgA2+ gut microbiota. Such increase featured enhanced IgA1 reactivity to pathobionts, including Escherichia coli, combined with depletion of beneficial A. muciniphila. Thus, gut IgA1 and IgA2 emerge from clonally related PCs and show unique changes in both frequency and reactivity in IBD.
Dominant negative variants in <i>ITPR3</i> impair T cell Ca2+ dynamics causing combined immunodeficiency
Authors: Elena Blanco, Carme Camps, Sameer Bahal, Mohit D. Kerai, Matteo P. Ferla, Adam M. Rochussen, Adam E. Handel, Zainab M. Golwala, Helena Spiridou Goncalves, Susanne Kricke, Fabian Klein, Fang Zhang, Federica Zinghirino, Grace Evans, Thomas M. Keane, Sabrina Lizot, Maaike A.A. Kusters, Mildred A. Iro, Sanjay V. Patel, Emma C. Morris, Siobhan O. Burns, Ruth Radcliffe, Pradeep Vasudevan, Arthur Price, Olivia Gillham, Gabriel E. Valdebenito, Grant S. Stewart, Austen Worth, Stuart P. Adams, Michael Duchen, Isabelle André, David J. Adams, Giorgia Santili, Kimberly C. Gilmour, Georg A. Holländer, E. Graham Davies, Jenny C. Taylor, Gillian M. Griffiths, Adrian J. Thrasher, Fatima Dhalla, Alexandra Y. Kreins
Journal: The Journal of Experimental Medicine (2024)

The importance of calcium (Ca2+) as a second messenger in T cell signaling is exemplified by genetic deficiencies of STIM1 and ORAI1, which abolish store-operated Ca2+ entry (SOCE) resulting in combined immunodeficiency (CID). We report five unrelated patients with de novo missense variants in ITPR3, encoding a subunit of the inositol 1,4,5-trisphosphate receptor (IP3R), which forms a Ca2+ channel in the endoplasmic reticulum (ER) membrane responsible for the release of ER Ca2+ required to trigger SOCE, and for Ca2+ transfer to other organelles. The patients presented with CID, abnormal T cell Ca2+ homeostasis, incompletely penetrant ectodermal dysplasia, and multisystem disease. Their predominant T cell immunodeficiency is characterized by significant T cell lymphopenia, defects in late stages of thymic T cell development, and impaired function of peripheral T cells, including inadequate NF-κB- and NFAT-mediated, proliferative, and metabolic responses to activation. Pathogenicity is not due to haploinsufficiency, rather ITPR3 protein variants interfere with IP3R channel function leading to depletion of ER Ca2+ stores and blunted SOCE in T cells.
3D printed drug-eluting stents: Toward personalized therapy for airway stenosis
Authors: Adva Krivitsky, Nevena Paunović, Karina Klein, Fergal Brian Coulter, Sarah Schleich, Agnieszka Anna Karol, Aline Bauer, Vadim Krivitsky, Victoria Lohmann, Paula Cendoya Carril, Yinyin Bao, Brigitte von Rechenberg, Cornelia Halin, André R Studart, Daniel Franzen, Jean-Christophe Leroux
Journal: Journal of Controlled Release (2024)

Airway stents are life-saving medical devices used to treat malignant or benign central airway stenoses. Unfortunately, these devices, typically manufactured from silicone alone and/or nitinol, can result in serious complications, such as stent migration, bacterial colonization, and tissue granulation, eventually forcing stent removal. Customized airway stents exhibit reduced migration and they can be tailored to address other complications by releasing drugs, such as the antibiotic levofloxacin and the antifibrotic drug nintedanib. Herein, the incorporation of these molecules in customized, bioresorbable 3D printed airway stents was investigated. Nintedanib (1.5 wt%) and levofloxacin (2.0 wt%) were incorporated in the polymer-based resin, which was used to 3D print tracheal stents with adequate mechanical and drug release properties. The drug-loaded stents were then deployed into rabbit tracheas and found to deliver the drugs locally with minimal systemic exposure. Drug activities were demonstrated by inhibition of bacterial colonization and reduced interleukin 8 (IL8) local expression. Although the application of these tracheal stents requires further exploration in larger animal models, this work paves the way for the rapid manufacturing of personalized medical devices with therapeutic functions.
Obesity-Specific improvement of lung cancer outcomes and immunotherapy efficacy with metformin
Authors: Randall J Smith, Robert Zollo, Sukumar Kalvapudi, Yeshwanth Vedire, Akhil Goud Pachimatla, Cara Petrucci, Garrison Shaller, Deschana Washington, Vethanayagam Rr, Stephanie N Sass, Aravind Srinivasan, Eric Kannisto, Sawyer Bawek, Prantesh Jain, Spencer Rosario, Joseph Barbi, Sai Yendamuri
Journal: JNCI Journal of the National Cancer Institute (2024)

Pre-clinical cancer studies ascribe promising anticancer properties to metformin. Yet, clinical findings vary, casting uncertainty on its therapeutic value for non-small cell lung cancer (NSCLC) patients. We hypothesized that metformin could benefit obese and overweight patients with NSCLC.