tbuckley/cabot-search huggingface dataset:
Abstract We106: Long Non-Coding RNA <i>LIPTER</i> Regulates Lipid Metabolism of Human Cardiomyocytes and Preserves Cardiac Function
Authors: Lei Han, Dayang Huang, Cheng Wang, Sheng Liu, Jun Wan, Lei Yang
Journal: Circulation Research (2024)

Background: Recently, long non-coding RNAs (lncRNAs) have emerged as novel human-specific (i.e. non-conserved) regulators of cardiovascular development and disease, which possess diverse functions through interacting with other molecules, including DNA, RNA, protein, and lipid. We identified a human lncRNA, LIPTER, which mediates lipid droplet (LD) transport to regulate lipid metabilism of human cardiomyocytes (CMs). Mechanistically, LIPTER binds phospholipids PA and PI4P on the LD membranes and the MYH10 protein, connecting LDs to the cytoskeleton and facilitating LD transport to mitochondria. LIPTER deficiencies led to prominent LD accumulation, mitochondrial dysfunction, and death of human iPS cell-derived CMs. Since downregulation of LIPTER and enahnced LD accumulation are associated with cardiac dysfunction and heart failure in patients with metabolic disorders, such as obesity and diabetes mellitus, we thereby seek to explore the preclinical potential of LIPTER for the therapy of human metabolic disorder associated cardiac dysfunction and heart failure. Hypothesis: We hypothesize that transgenic overexpression of the human lncRNA LIPTER in mouse heart could attenuate metabolic syndrome-associated myocardium lipid accumulation and cardiac dysfunction, as well as prevent isoproterenol-induced heart failure through increasing the fatty acid oxidation (FAO) of mouse heart. Goals: To evaluate the preclinical potential of human lncRNA LIPTER for the therapy of cardiac dysfunction and heart failure by using mouse cardiac dysfunction and heart failure models. Methods: We established a LIPTER transgenic overexpression mouse line (LIPTER Tg ). Both WT and LIPTER Tg mice were fed with high fat diet for 10 months to induce cardiac lipid accumulation and dysfunction. Additionally, heart failure was induced by the chronic isoproterenol administration. After treatment, mice were subjected to histological and molecular analyses. Results: We found LIPTER Tg significantly enhanced FAO of mouse heart, reduced cardiac lipid accumulation and fibrosis, and alleviated cardiac dysfunction of high-fat-diet fed mice, as well as preserved cardiac function of mice post isoproterenol administration. Conclusions: We unveil a crucial role of human lncRNA LIPTER in regulating lipid metabolism of human CMs and testify its clinical potential for treating cardiac dysfunction and heart failure.
Abstract We100: Altering cardiac impulse propagation and generation by local flash photolysis of caged Ca <sup>2+</sup>
Authors: Kentaro Mochizuki, Shoko Tamura, Yuma Morishita, Yoshinori Harada, Hideo Tanaka
Journal: Circulation Research (2024)

Calcium ion (Ca 2+ ) is one of key components in the heart excitation and conduction, and its overload is known to induce abnormal impulse propagation and generation, enabling to lead lethal arrhythmias. However, unknown is how large area of Ca 2+ -overload in a cardiac tissue is required to provoke such abnormalities. By utilizing UV-photolysis of caged Ca 2+ , we investigated whether the increase of Ca 2+ concentration ([Ca 2+ ]) at the local on a cardiomyocytes monolayer alters its spatiotemporal impulse patterns, and also assessed its dependence on area-sizes of the Ca 2+ -overload. The monolayers of cardiomyocytes isolated from neonatal rats were prepared on quartz-substrates (φ27 mm) with 2 days incubation, then treated with a fluorescent indicator of Ca 2+ (Fluo-8/AM: 5 µM) and a caged Ca 2+ (DMNPE-4/AM: 5 - 50 µM). Its excitation manner and impulse propagation were monitored as fluorescence images by a macro-zoom microscope (image size: ~1,500 mm 2 , frame rate: 400 frame/s). Under monitoring, UV light (λ: 365 nm) for flash photolysis of caged Ca 2+ was irradiated to a limited area (diameters of 3 - 9 mm) on the cell layer, with and without electrical pacing. Under periodical excitation by pacing, the delay of impulse propagation was detected at UV-irradiated area on the monolayer. The delay was enhanced with an increase of [Ca 2+ ] under the photolysis, but gradually dissolved with a decay of [Ca 2+ ] after stopping UV irradiation. Under non-pacing, on the other hand, it was found that abnormal impulses were generated from the UV-irradiated area as a result of increase of [Ca 2+ ]. Probabilities about the abnormal impulses showed a linear relationship with the area size of UV-photolysis. Also, we confirmed that the abnormal impulses by the UV-photolysis provoked a reentry-like excitation manner when the electrical conductivity of cardiomyocytes was further degraded by an administration of carbenoxolone. In conclusion, we demonstrated altering impulse propagation/generation of cardiomyocytes monolayer by the local frash photolysis of caged Ca 2+ , and investigated its dependence on spatial conditions of the overload region. The target of this study will be shifted to whole hearts as one on next steps in order to provide the statistical insight in arrhythmogenesis. This research was partially supported by JSPS(18K19459, 22K18174) and JST-CREST(JPMJCR 1925).
Abstract We109: AAV9-Mediated Overexpression of Mixed Lineage Kinase 3 After Transaortic Constriction Improves Left Ventricular Function
Authors: Suchita Pande, Gregory Martin, Robert Blanton
Journal: Circulation Research (2024)

Introduction: Mixed-lineage kinase 3 (MLK3) is a cGMP-dependent protein kinase 1α (PKG1α) substrate, preserving left ventricular (LV) function without affecting blood pressure (BP). MLK3 kinase-dependent effects maintain LV function, while kinase-independent signalling regulates BP. Thus, enhancing MLK3 kinase activity may improve LV function in heart failure (HF) while circumventing PKG1-induced hypotension. No MLK3-activation strategies exist currently, thus hindering progress in MLK3 research and potential therapeutics. Hypothesis: Augmenting MLK3 after pressure overload by transaortic constriction (TAC) would prevent LV hypertrophy and dysfunction in mice. Goal: To test the effect of adeno-associated virus 9 (AAV9)-mediated MLK3 overexpression on LV function, when administered in the setting of pre-existing LV hypertrophy and dysfunction. Methods: Male mice 12 weeks of age underwent 26G TAC or sham surgery. At day 5 post-TAC we administered by retro-orbital injection AAV9 encoding MLK3 or TdTomato negative control, each under control of the CM-specific cTNT promoter (AAV-MLK3: n=12 TAC, 7 sham; AAV-TdTomato: n=10 Tac, 8 sham. At day 28 post-AAV9 injection, we measured cardiac structure and function by echocardiography, invasive LV hemodynamics, and organ weights. Results: Echocardiography 5 days post-TAC confirmed TAC-induced LV hypertrophy and reduced systolic function prior to AAV9 treatment. At day 28, AAV-MLK3-treated TAC mice demonstrated improved LV ejection fraction and fractional shortening compared with TAC-AAV-Td controls, indicating improved systolic function. MLK3-treated TAC mice maintained higher LV systolic pressure post-TAC vs. Td controls, further indicating improved cardiac performance. Diastolic indices, including ratio of mitral E/A inflow velocities, tau, and LV relaxation rate were also improved in AAV-MLK3 TAC versus AAV-Td controls. AAV9-MLK3 administration had no effect on LV wall thickness or on LV or whole heart mass normalized to tibia length. MLK3 expression was increased 3-fold in AAV9-MLK3 TAC LVs compared with AAV9-Td controls. Conclusion: AAV9-mediated MLK3 overexpression after the onset of LV hypertrophy and dysfunction improves LV function in mice.
Abstract We108: Adipocyte Enhancer Binding Protein 1 (AEBP1) Inhibition as a Potential Anti-Fibrotic Therapy in Heart Failure
Authors: Thirupura S Shankar, Joseph Visker, Junedh Amrute, Georgiy Polishchuk, J Ty Lunde, JING LING, Peter Ferrin, Rana Hamouche, Dominik Feigle, Dallen Calder, Frank Sachse, Christos Kyriakopoulos, Eleni Maneta, Harini Srinivasan, ELENI TSELIOU, Sutip Navankasattusas, Craig Selzman, Sihem Boudina, Thomas Seidel, Kory Lavine, Stavros Drakos
Journal: Circulation Research (2024)

Introduction: Cardiac fibrosis is one of the major hallmarks of heart failure (HF) progression. Fibrosis is initiated as a repair mechanism following any kind of cardiac injury including a heart attack, inflammation, hypertension, etc. Briefly, fibroblasts are activated to form myofibroblasts that secrete collagen. Persistent fibroblast activation leads to excess collagen deposition leading to tissue stiffening and impaired contractility and thereby HF. To date, there is no anti-fibrotic therapy used in HF patients. Using bulk and snRNA sequencing data performed on myocardial tissue from HF patients, we identified adipocyte enhancer binding protein (AEBP1) to be significantly upregulated in activated fibroblasts. AEBP1 has been shown to play a crucial role in fibroblast activation following injury in the kidney, liver, and lungs. AEBP1 inhibition resulted in fibrosis attenuation in these organs. However, its role in cardiac fibrosis is not well understood. Hypothesis: We hypothesize that AEBP1 is crucial for cardiac fibroblast activation and AEBP1 inhibition will prevent collagen secretion and lead to improved cardiac function. Methods: Human cardiac fibroblasts (HCF) from non-failing donors were used for in vitro experiments. AdV-CMV-AEBP1 was used for AEBP1 overexpression (OE) and AdV-CMV-shAEBP1 was used to knockdown (KD) AEBP1 in vitro. AAV9-CMV-shAEBP1 was used for in vivo KD of AEBP1 in mice following myocardial infarction (MI). Human myocardial slices from n=6 HF patients were used and AdV-CMV-shAEBP1 was used to knockdown AEBP1 in human samples. Results and Discussion: AEBP1 OE in HCF resulted in fibroblast activation and collagen secretion (n=6, p=0.002). Contrarily, loss of AEBP1 significantly prevented fibroblast activation, evident from a reduction in transgelin (SM22) (n=6, p=0.02) and collagen (COL1A1) protein levels (n=6, p=0.01). AEBP1 KD in a mouse model of acute cardiac fibrosis resulted in reduced fibrosis and improved cardiac function (n=6, 12% absolute improvement compared to untreated mice, relative improvement in ejection fraction, p=0.02). Tissue culture studies of human HF myocardium showed a significant improvement in cardiac structure evident from reduced cardiomyocyte hypertrophy (n=6 HF patients, p=0.05) and reduced fibrosis (n=6, p&lt;0.0001) following AEBP1 KD. Overall, we show that AEBP1 plays a critical role in fibrogenesis, and its inhibition has the potential to attenuate fibrosis in acute and chronic HF.
Abstract We119: Treatment of Viral Myocarditis by Targeting the TRIM29-PERK Axis-Mediated ER Stress Immune Response
Authors: Junying Wang, Wenting Lu, Jerry Zhang, Yong Du, Mingli Fang, Ao Zhang, Gabriel Sungcad, Samantha Chon, Zhiqiang Zhang, Junji Xing
Journal: Circulation Research (2024)

Viral myocarditis, an inflammatory disease of the myocardium, is a significant cause of sudden death in children and young adults. The current coronavirus disease 19 pandemic emphasizes the need to understand the pathogenesis mechanisms and potential treatment strategies for viral myocarditis. Here, we found that TRIM29 was highly induced by cardiotropic viruses and promoted protein kinase RNA-like endoplasmic reticulum kinase (PERK)-mediated endoplasmic reticulum (ER) stress, apoptosis, and reactive oxygen species (ROS) responses that promote viral replication in cardiomyocytes in vitro . TRIM29 deficiency protected mice from viral myocarditis by promoting cardiac antiviral functions and reducing PERK-mediated inflammation and immunosuppressive monocytic myeloid-derived suppressor cells (mMDSC) in vivo . Mechanistically, TRIM29 interacted with PERK to promote SUMOylation of PERK to maintain its stability, thereby promoting PERK-mediated signaling pathways. Finally, we demonstrated that the PERK inhibitor GSK2656157 mitigated viral myocarditis by disrupting the TRIM29-PERK connection, thereby bolstering cardiac function, enhancing cardiac antiviral responses, and curbing inflammation and immunosuppressive mMDSC in vivo . Our findings offer insight into how cardiotropic viruses exploit TRIM29-regulated PERK signaling pathways to instigate viral myocarditis, suggesting that targeting the TRIM29-PERK axis could mitigate disease severity.
Assessing the role of bacterial innate and adaptive immunity as barriers to conjugative plasmids
Authors: Berit Siedentop, Carlota Losa Mediavilla, Roger D Kouyos, Sebastian Bonhoeffer, Hélène Chabas
Journal: Molecular Biology and Evolution (2024)

Plasmids are ubiquitous mobile genetic elements, that can be either costly or beneficial for their bacterial host. In response to constant viral threat, bacteria have evolved various immune systems, such as the prevalent restriction modification (innate immunity) and CRISPR-Cas systems (adaptive immunity). At the molecular level, both systems also target plasmids, but the consequences of these interactions for plasmid spread are unclear. Using a modeling approach, we show that restriction modification and CRISPR-Cas are effective as barriers against the spread of costly plasmids, but not against beneficial ones. Consequently, bacteria can profit from the selective advantages that beneficial plasmids confer even in the presence of bacterial immunity. While plasmids that are costly for bacteria may persist in the bacterial population for a certain period, restriction modification and CRISPR-Cas can eventually drive them to extinction. Finally, we demonstrate that the selection pressure imposed by bacterial immunity on costly plasmids can be circumvented through a diversity of escape mechanisms and highlight how plasmid carriage might be common despite bacterial immunity. In summary, the population-level outcome of interactions between plasmids and defense systems in a bacterial population is closely tied to plasmid cost: Beneficial plasmids can persist at high prevalence in bacterial populations despite defense systems, while costly plasmids may face extinction.
Senescent CD8+ T cells: a novel risk factor in atrial fibrillation
Authors: Xiang Li, Yangyang Bao, Ning Zhang, Changjian Lin, Yun Xie, Yue Wei, Qingzhi Luo, Jingmeng Liu, Zimo Sha, Guanhua Wu, Taojie Zhou, Qiujing Chen, Tianyou Ling, Wenqi Pan, Lin Lu, Liqun Wu, Yang Dai, Qi Jin
Journal: Cardiovascular Research (2024)

Immune cell alterations may play a role in the development of atrial fibrillation (AF). Our objective was to comprehensively characterize immune cells in AF, and investigate the potential mechanisms.
Effect of Tele-ICU on Clinical Outcomes of Critically Ill Patients
Authors: Adriano J. Pereira, Danilo T. Noritomi, Maura Cristina dos Santos, Thiago D. Corrêa, Leonardo J. R. Ferraz, Guilherme P. P. Schettino, Eduardo Cordioli, Renata A. Morbeck, Lúbia C. Morais, Jorge I. F. Salluh, Luciano C. P. Azevedo, Rodrigo S. Biondi, Regis G. Rosa, Alexandre B. Cavalcanti, Otavio Berwanger, Ary Serpa Neto, Otavio T. Ranzani
Journal: JAMA (2024)

Importance Despite its implementation in several countries, there has not been a randomized clinical trial to assess whether telemedicine in intensive care units (ICUs) could improve clinical outcomes of critically ill patients. Objective To determine whether an intervention comprising daily multidisciplinary rounds and monthly audit and feedback meetings performed by a remote board-certified intensivist reduces ICU length of stay (LOS) compared with usual care. Design, Setting, and Participants A parallel cluster randomized clinical trial with a baseline period in 30 general ICUs in Brazil in which daily multidisciplinary rounds performed by board-certified intensivists were not routinely available. All consecutive adult patients (aged ≥18 years) admitted to the participating ICUs, excluding those admitted due to justice-related issues, were enrolled between June 1, 2019, and April 7, 2021, with last follow-up on July 6, 2021. Intervention Remote daily multidisciplinary rounds led by a board-certified intensivist through telemedicine, monthly audit and feedback meetings for discussion of ICU performance indicators, and provision of evidence-based clinical protocols. Main Outcomes and Measures The primary outcome was ICU LOS at the patient level. Secondary outcomes included ICU efficiency, in-hospital mortality, incidence of central line–associated bloodstream infections, ventilator-associated events, catheter-associated urinary tract infections, ventilator-free days at 28 days, patient-days receiving oral or enteral feeding, patient-days under light sedation, and rate of patients with oxygen saturation values under that of normoxemia, assessed using generalized linear mixed models. Results Among 17 024 patients (1794 in the baseline period and 15 230 in the intervention period), the mean (SD) age was 61 (18) years, 44.7% were female, the median (IQR) Sequential Organ Failure Assessment score was 6 (2-9), and 45.5% were invasively mechanically ventilated at admission. The median (IQR) time under intervention was 20 (16-21) months. Mean (SD) ICU LOS, adjusted for baseline assessment, did not differ significantly between the tele–critical care and usual care groups (8.1 [10.0] and 7.1 [9.0] days; percentage change, 8.2% [95% CI, −5.4% to 23.8%]; P = .24). Results were similar in sensitivity analyses and prespecified subgroups. There were no statistically significant differences in any other secondary or exploratory outcomes. Conclusions and Relevance Daily multidisciplinary rounds conducted by a board-certified intensivist through telemedicine did not reduce ICU LOS in critically ill adult patients. Trial Registration ClinicalTrials.gov Identifier: NCT03920501
Evaluating Complex Technological Innovations in Critical Care—Current Challenges and Future Directions
Authors: Kelly C. Vranas, Jeremy M. Kahn
Journal: JAMA (2024)

Adriano J. Pereira, MD, PhD; Danilo T. Noritomi, MD, PhD; Maura Cristina dos Santos, RN; Thiago D. Corrêa, MD, PhD; Leonardo J. R. Ferraz, MD, PhD; Guilherme P. P. Schettino, MD, PhD; Eduardo Cordioli, MD, PhD; Renata A. Morbeck, RN; Lúbia C. Morais, MD; Jorge I. F. Salluh, MD, PhD; Luciano C. P. Azevedo, MD, PhD; Rodrigo S. Biondi, MD, MSc; Regis G. Rosa, MD, PhD; Alexandre B. Cavalcanti, MD, PhD; Otavio Berwanger, MD, PhD; Ary Serpa Neto, MD, PhD; Otavio T. Ranzani, MD, PhD
Ventilator Weaning Strategies—Managing Interaction Between Randomized Treatments
Authors: Steven A. Webb, Lindsay R. Berry, Ary Serpa Neto
Journal: JAMA (2024)

Karen E. A. Burns, MD, MSc; Jessica Wong, MD, MPH; Leena Rizvi, BSc; Myriam Lafreniere-Roula, PhD; Kevin Thorpe, MMath; John W. Devlin, PharmD; Deborah J. Cook, MD; Andrew Seely, MD, PhD; Peter M. Dodek, MD, MHSc; Maged Tanios, MD, MPH; Thomas Piraino, RRT; Audrey Gouskos, MPH; Kenneth C. Kiedrowski, MEd; Phyllis Kay; Susan Mitchell; George W. Merner, BA; Michael Mayette, MD; Frederick D'Aragon, MD, MSc; Francois Lamontagne, MD, MSc; Bram Rochwerg, MD, MSc; Alexis Turgeon, MD, MSc; Ying Tung Sia, MD; Emmanuel Charbonney, MD, PhD; Pierre Aslanian, MD; Gerard J. Criner, MD; Robert C. Hyzy, MD; Jeremy R. Beitler, MD; Elias Baedorf Kassis, MD; Demetrios James Kutsogiannis, MD; Maureen O. Meade, MD, MSc; Janice Liebler, MD; Santhi Iyer-Kumar, MD; Jennifer Tsang, MD, PhD; Robert Cirone, MD; Carl Shanholtz, MD; Nicholas S. Hill, MD; Canadian Critical Care Trials Group; Kim Dawdy; Zana Mariano; Gyan Sandhu; Marlene Santos; Imrana Khalid; Kurtis Salway; Jennifer Hodder; Orla Smith; Jessica Hajj; Samantha Buchanan; Vivianne Severdija; Anna Medvetskaya; Sarah Enriquez; John Michaels; Kanthi Kavikondala; Irene Watpool; Rebecca Porteous; Kaitlyn Montroy; Sydney Miezitis; Jessica Haines; Heather Langlois; Jackie Bastianon; Saba Rawjani; Aaron Nesom; Brigette Gomes; Liane Leclair; Jay Greco; Marie-Hélène Masse; Joannie Marchand; Marie-Pier Bouchard; Elaine Carbonneau; Julie Belisle; Marilène Ladouceur ; Karine Grondin; France Clarke; Neala Hoad; Timothy Karachi; Tina Millen; Jennifer Leroux; Jean-Francois Naud; Isabelle Roy; Martin Faucher; Mélissa Bellefeuille; Danielle Tapps Tapps; Mylena Laplante; Cassandra Mailloux; Lea Durocher; Martine Lebrasseur; Marie-Eve Cantin; Dounia Boumahni; Fatna Benettaib Benettaib; Ali Ghamraoui; Maya Salamé; Karine-Candy Gagnon; David Bellemare; Joannie Blais; Marie-Claude Boulanger; Eve Cloutier; Olivier Costerousse; Hélène Côté; Emilie Couillard-Chénard; Marjorie Daigle; Charles Francoeur; Gabrielle Guilbault; Stéphanie Grenier; Francois Lauzier; Guillaume Leblanc; Shany Rodrigue; Isabelle St. Hilaire; Maude St. Onge; Antoine Tremblay; Patrica Thompson; Tayne Hewer; Cynthia Smit; Victoria Alcuaz; Lena Farina; Draga Jichici; Lori Hand; Claudia Poulin; Erick Duan; Mercedes Camargo-Penuela; Lisa Patterson; Jeremy Yue; Anthony (TJ) Fuagno; Mary M. Hayes; Abigail Pires; Grace Kersker; Fernando Martinez Guasch; Adriana Paz Mancia; Courtney Capobianco; Leslie Lussier; Hyunsoon Park; Kelvin Arreola; Kenneth Le; Son Nguyen; Kristi Peters-Fitzpatrick; Amy Blank; Joshua Cosa; Arin Marshall; Cedrik De La Pena; Francine McGonagle; Shubhra Srivastava-Malhotra; Sheril George; Heidi Shore-Brown; Lauren Miller; Linda Ayres; David Miller; Kristine Nelson; Carl Haas; Jose Victor Jimenez; Andy Weirauch; Alexis Serra; Ivan Garcia; Charmaine Wilson; Valerie Goodspeed; Julia (Dwyer) Crane; Andrew Toksoz-Exley; Krystal Capers; Andre De Souza Licht; Lynn Fukushima; Carese Lee; Daniel Motamedi; Thelma Harrington; Olga Kolesnik; Maura Deeley
Engineering Macrophage‐Derived Exosome to Deliver Pirfenidone: A Novel Approach to Combat Silicotic Pulmonary Fibrosis
Authors: Zhen Chen, Xiang Yun, Jiaqi Tian, Fei Li, Zitong Zhang, Jiahua Meng, Ning Li, Hongying Bian, Shuyin Duan, Lin Zhang
Journal: Advanced Healthcare Materials (2024)

Silicosis is a severe lung disease characterized by diffuse pulmonary fibrosis, for which there is currently no effective treatment. Pirfenidone (PFD) shows great antifibrotic potential but is clinically hindered by low bioavailability and gastrointestinal side effects. To address these limitations, this study develops a PFD delivery system (PFD-Exo) using J774A.1 macrophage-derived exosomes. Firstly, PFD is loaded via sonication, then PFD-Exo is characterized using Raman spectral imaging and UV absorption spectroscopy. Finally, in vitro and in vivo silicosis models are established to evaluate its antifibrotic effects. Results show that PFD-Exo outperforms free PFD in inhibiting TGF-β1-induced transdifferentiation of primary lung fibroblasts in vitro. In a mouse model of silicosis, PFD-Exo is found to be accumulated in the lungs following intratracheal administration and significantly ameliorates pulmonary inflammation and fibrosis while minimizing gastrointestinal side effects. Mechanistic studies reveal that PFD-Exo modulates the TGF-β signaling pathway by downregulating SMAD3 and upregulating SMAD7 and NOGGIN. In conclusion, this study provides the first evidence of macrophage-derived exosomes as an effective PFD delivery system for silicosis treatment and offers a promising strategy for other refractory pulmonary diseases.
Steering research on mRNA splicing in cancer towards clinical translation
Authors: Olga Anczukow, Frédéric H-T Allain, Brittany L Angarola, Douglas L Black, Angela N Brooks, Chonghui Cheng, Ana Conesa, Edie I Crosse, Eduardo Eyras, Ernesto Guccione, Sydney X Lu, Karla M Neugebauer, Priyanka Sehgal, Xiao Song, Zuzana Tothova, Juan Valcárcel, Kevin M Weeks, Gene W Yeo, Andrei Thomas-Tikhonenko
Journal: Nature reviews. Cancer (2024)