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352. Supplementary Figures 1 - 9 from High Fidelity Patient-Derived Xenografts for Accelerating Prostate Cancer Discovery and Drug Development

Author

Yuzhuo Wang, Colin C. Collins, Martin E. Gleave, Stanislav V. Volik, Larry Goldenberg, James Morris, Peter W. Gout, Michael Cox, Mark Rubin, Himisha Beltran, Manju Sharma, Ladan Fazli, Antonio Hurtado-Coll, Shawn Anderson, Robert H. Bell, Lina Jong, Fan Mo, Sonal Brahmbhatt, Rebecca Wu, Anne Haegert, Xin Dong, Yuwei Wang, Hui Xue, Alexander W. Wyatt, and Dong Lin

Abstract

PDF file - 1579K, Supplementary Figure 1: Histopathological similarity between tumor lines and matched patient tumors. Supplementary Figure 2: Growth curves, host plasma PSA levels and response to castration/Bicalutmide in the tumor lines. Supplementary Figure 3: Similarity of genome copy number between tumor lines and matched patient tumors. Supplementary Figure 4: Conservation of genome copy number after multiple generations of serial passaging. Supplementary Figure 5: Molecular characteristics of transplantable tumour lines. Supplementary Figure 6: Androgen withdrawal leads to the development of castrate-resistant lines. Supplementary Figure 7: Characterization of the neuroendocrine prostate cancer phenotype in LTL331R. Supplementary Figure 8: Evidence of adaptive response to castration in LTL331. Supplementary Figure 9: Genes potentially predisposing LTL331 to neuroendocrine transdifferentiation represent candidate molecular markers for risk stratification.

Published
2023
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353. Supplementary Table 3 from High Fidelity Patient-Derived Xenografts for Accelerating Prostate Cancer Discovery and Drug Development

Author

Yuzhuo Wang, Colin C. Collins, Martin E. Gleave, Stanislav V. Volik, Larry Goldenberg, James Morris, Peter W. Gout, Michael Cox, Mark Rubin, Himisha Beltran, Manju Sharma, Ladan Fazli, Antonio Hurtado-Coll, Shawn Anderson, Robert H. Bell, Lina Jong, Fan Mo, Sonal Brahmbhatt, Rebecca Wu, Anne Haegert, Xin Dong, Yuwei Wang, Hui Xue, Alexander W. Wyatt, and Dong Lin

Abstract

XLSX file - 12K, Supplementary Table 3: Clinical information of grafted cases.

Published
2023
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355. Data from High Fidelity Patient-Derived Xenografts for Accelerating Prostate Cancer Discovery and Drug Development

Author

Yuzhuo Wang, Colin C. Collins, Martin E. Gleave, Stanislav V. Volik, Larry Goldenberg, James Morris, Peter W. Gout, Michael Cox, Mark Rubin, Himisha Beltran, Manju Sharma, Ladan Fazli, Antonio Hurtado-Coll, Shawn Anderson, Robert H. Bell, Lina Jong, Fan Mo, Sonal Brahmbhatt, Rebecca Wu, Anne Haegert, Xin Dong, Yuwei Wang, Hui Xue, Alexander W. Wyatt, and Dong Lin

Abstract

Standardized and reproducible preclinical models that recapitulate the dynamics of prostate cancer are urgently needed. We established a bank of transplantable patient-derived prostate cancer xenografts that capture the biologic and molecular heterogeneity currently confounding prognostication and therapy development. Xenografts preserved the histopathology, genome architecture, and global gene expression of donor tumors. Moreover, their aggressiveness matched patient observations, and their response to androgen withdrawal correlated with tumor subtype. The panel includes the first xenografts generated from needle biopsy tissue obtained at diagnosis. This advance was exploited to generate independent xenografts from different sites of a primary site, enabling functional dissection of tumor heterogeneity. Prolonged exposure of adenocarcinoma xenografts to androgen withdrawal led to castration-resistant prostate cancer, including the first-in-field model of complete transdifferentiation into lethal neuroendocrine prostate cancer. Further analysis of this model supports the hypothesis that neuroendocrine prostate cancer can evolve directly from adenocarcinoma via an adaptive response and yielded a set of genes potentially involved in neuroendocrine transdifferentiation. We predict that these next-generation models will be transformative for advancing mechanistic understanding of disease progression, response to therapy, and personalized oncology. Cancer Res; 74(4); 1272–83. ©2013 AACR.

Published
2023
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356. Supplementary Table 1 from High Fidelity Patient-Derived Xenografts for Accelerating Prostate Cancer Discovery and Drug Development

Author

Yuzhuo Wang, Colin C. Collins, Martin E. Gleave, Stanislav V. Volik, Larry Goldenberg, James Morris, Peter W. Gout, Michael Cox, Mark Rubin, Himisha Beltran, Manju Sharma, Ladan Fazli, Antonio Hurtado-Coll, Shawn Anderson, Robert H. Bell, Lina Jong, Fan Mo, Sonal Brahmbhatt, Rebecca Wu, Anne Haegert, Xin Dong, Yuwei Wang, Hui Xue, Alexander W. Wyatt, and Dong Lin

Abstract

XLSX file - 10K, Supplementary Table 1: Growth inhibition of transplantable tumor lines after Bicalutamide treatment.

Published
2023
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357. Supplementary Methods and References from TIF1γ Suppresses Tumor Progression by Regulating Mitotic Checkpoints and Chromosomal Stability

Author

Laurent Bartholin, Stéphanie Sentis, Ulrich Valcourt, Alain Puisieux, Stéphane Ansieau, Caroline Moyret-Lalle, Pascal Bernard, Geneviève Fourel, Guillaume Devailly, Bastien Kaniewski, Sylvie Martel, Vanessa Arfi, Nicolas Chuvin, Lindsay B. Alcaraz, David F. Vincent, Johann Gout, and Roxane M. Pommier

Abstract

Description of additional methods and procedures used in the study. Also includes Supplementary References.

Published
2023
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358. Supplementary Table 2 from High Fidelity Patient-Derived Xenografts for Accelerating Prostate Cancer Discovery and Drug Development

Author

Yuzhuo Wang, Colin C. Collins, Martin E. Gleave, Stanislav V. Volik, Larry Goldenberg, James Morris, Peter W. Gout, Michael Cox, Mark Rubin, Himisha Beltran, Manju Sharma, Ladan Fazli, Antonio Hurtado-Coll, Shawn Anderson, Robert H. Bell, Lina Jong, Fan Mo, Sonal Brahmbhatt, Rebecca Wu, Anne Haegert, Xin Dong, Yuwei Wang, Hui Xue, Alexander W. Wyatt, and Dong Lin

Abstract

XLSX file - 37K, Supplementary Table 2: Gene expression signature associated with predisposition to neuroendocrine transdifferentiation.

Published
2023
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362. Evolutionary conservation of the fidelity of transcription

Author

Claire Chung, Bert M. Verheijen, Zoe Navapanich, Eric G. McGann, Sarah Shemtov, Guan-Ju Lai, Payal Arora, Atif Towheed, Suraiya Haroon, Agnes Holczbauer, Sharon Chang, Zarko Manojlovic, Stephen Simpson, Kelley W. Thomas, Craig Kaplan, Peter van Hasselt, Marc Timmers, Dorothy Erie, Lin Chen, Jean-Franćois Gout, and Marc Vermulst

Subjects
Multidisciplinary, General Physics and Astronomy, General Chemistry, General Biochemistry, Genetics and Molecular Biology
Abstract

Accurate transcription is required for the faithful expression of genetic information. However, relatively little is known about the molecular mechanisms that control the fidelity of transcription, or the conservation of these mechanisms across the tree of life. To address these issues, we measured the error rate of transcription in five organisms of increasing complexity and found that the error rate of RNA polymerase II ranges from 2.9 × 10−6 ± 1.9 × 10−7/bp in yeast to 4.0 × 10−6 ± 5.2 × 10−7/bp in worms, 5.69 × 10−6 ± 8.2 × 10−7/bp in flies, 4.9 × 10−6 ± 3.6 × 10−7/bp in mouse cells and 4.7 × 10−6 ± 9.9 × 10−8/bp in human cells. These error rates were modified by various factors including aging, mutagen treatment and gene modifications. For example, the deletion or modification of several related genes increased the error rate substantially in both yeast and human cells. This research highlights the evolutionary conservation of factors that control the fidelity of transcription. Additionally, these experiments provide a reasonable estimate of the error rate of transcription in human cells and identify disease alleles in a subunit of RNA polymerase II that display error-prone transcription. Finally, we provide evidence suggesting that the error rate and spectrum of transcription co-evolved with our genetic code.

Published
2023
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363. IFNγ binding to extracellular matrix prevents fatal systemic toxicity

Author

Josephine Kemna, Evelyne Gout, Leon Daniau, Jessica Lao, Kristoffer Weißert, Sandra Ammann, Ralf Kühn, Matthias Richter, Christine Molenda, Anje Sporbert, Dario Zocholl, Robert Klopfleisch, Hugues Lortat-Jacob, Peter Aichele, Thomas Kammertoens, Thomas Blankenstein, Institut de biologie structurale (IBS - UMR 5075), Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche Interdisciplinaire de Grenoble (IRIG), Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Grenoble Alpes (UGA), Molecular Epidemiology Research Group, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), 13125 Berlin, Germany, Institute for Immunodeficiency, Fakultät für Biologie = Faculty of Biology [Freiburg], Albert-Ludwigs-Universität Freiburg, Center of Chronic Immunodeficiency, University Medical Center and University of Freiburg, Charité - UniversitätsMedizin = Charité - University Hospital [Berlin], and Institute of Veterinary Pathology

Subjects
MESH: Signal Transduction, MESH: Cytokines, Cancer Research, MESH: Interferon-gamma, [SDV]Life Sciences [q-bio], Immunology, Immunology and Allergy, MESH: Animals, MESH: Neoplasms, MESH: Extracellular Matrix, Technology Platforms, MESH: Mice
Abstract

Interferon-γ (IFNγ) is an important mediator of cellular immune responses, but high systemic levels of this cytokine are associated with immunopathology. IFNγ binds to its receptor (IFNγR) and to extracellular matrix (ECM) via four positively charged C-terminal amino acids (KRKR), the ECM-binding domain (EBD). Across evolution, IFNγ is not well conserved, but the EBD is highly conserved, suggesting a critical function. Here, we show that IFNγ lacking the EBD (IFNγΔKRKR) does not bind to ECM but still binds to the IFNγR and retains bioactivity. Overexpression of IFNγΔKRKR in tumors reduced local ECM binding, increased systemic levels and induced sickness behavior, weight loss and toxicity. To analyze the function of the EBD during infection, we generated IFNγΔKRKR mice lacking the EBD by using CRISPR–Cas9. Infection with lymphocytic choriomeningitis virus resulted in higher systemic IFNγΔKRKR levels, enhanced sickness behavior, weight loss and fatal toxicity. We conclude that local retention of IFNγ is a pivotal mechanism to protect the organism from systemic toxicity during prolonged immune stimulation.

Published
2023
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364. The radiologically isolated syndrome: revised diagnostic criteria

Author

Lebrun-Frénay, Christine, Okuda, Darin, Siva, Aksel, Landes-Chateau, Cassandre, Azevedo, Christina, Mondot, Lydiane, Carra-Dallière, Clarisse, Zephir, Helene, Louapre, Celine, Durand-Dubief, Françoise, Le Page, Emmanuelle, Bensa, Caroline, Ruet, Aurélie, Ciron, Jonathan, Laplaud, David, Casez, Olivier, Mathey, Guillaume, de Seze, Jerome, Zeydan, Burcu, Makhani, Naila, Tutuncu, Melih, Levraut, Michael, Cohen, Mikael, Thouvenot, Eric, Pelletier, Daniel, Kantarci, Orhun, Sehaki, Sabrina, Devys-Meyer, Nathalie, Bereau, Mathieu, Cappe, Chrystelle, Brochet, Bruno, Ouallet, Jean-Christophe, Kounkou, Katy-Kim, Defer, Gilles, Branger, Pierre, Taithe, Frédéric, Dumont, Emilie, Lescieux, Edwige, Fromont, Agnès, Protin, Alexia, Kane, Maty Diop, Hautecoeur, Patrick, Outteryck, Olivier, Vermersch, Patrick, Boucher, Julie, Petit, Julie, Kasonde, Irène Tabellah, de Vilmarrest, Aymeric, Magy, Laurent, Nicol, Marie, Malbezin, Muriel, Olaiz, Javier, Rigaud-Bully, Claire, Debard, Nadine, Cotton, Sandra Vukusic François, Ionescu, Iuliana, Abdelalli, Amalle, Pelletier, Jean, Audoin, Bertrand, Maarouf, Adil, Di Lelio, Bernadette, Ayrignac, Xavier, Labauge, Pierre, Pinna, Frédéric, Guillemin, Francis, Debouverie, Marc, Ziegler, Amandine, Wiertlevski, Sandrine, Bresch, Saskia, Callier, Céline, David, Elodie, Castelnovo, Giovanni, Papeix, Caroline, Maillart, Elisabeth, Lubetzki, Catherine, Zehrouni, Karima, Fontaine, Bertrand, Giannesini, Claire, Hodel, Jérôme, Wahab, Abir, Zedet, Mickaël, Fagniez, Ombeline, Laage, Clémence, Pottier, Corinne, Slesari, Iuliana, Sampaio, Mathilde, Rabois, Emilie, Castex, Cédric, Hebant, Benjamin, Guillaume, Maxime, Vimont, Christine, Gout, Olivier, Guegen, Antoine, Michel, Laure, Muraz, Romain, Le Port, Damien, Leray, Emmanuelle, Henry, Carole, de Broucker, Thomas, Collongues, Nicolas, Berthe, Carole, Biotti, Damien, Freitas, Noellie, Visneux, Vincent, Forestier, Mélanie, Beltran, Stéphane, Meunier, Géraldine, Servan, Jérôme, Pico, Fernando, Chatagner, Virginie, Radji, Fatai, Morel, Nathalie, Grosset-Jeannin, Deborah, Ungureanu, Aurelian, Boyer, Latine, Suchet, Laurent, Lebrun-Frenay, Christine, Centre Hospitalier Universitaire de Nice (CHU Nice), Université Côte d'Azur (UCA), Unité de Recherche Clinique de la Côte d’Azur (URRIS UR2CA), Centre Hospitalier Universitaire de Nice (CHU Nice)-Université Côte d'Azur (UCA), University of Texas Southwestern Medical Center [Dallas], Cerrahpasa Faculty of Medicine, Istanbul University, University of Southern California (USC), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), CHU Lille, Lille Neurosciences & Cognition - U 1172 (LilNCog), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Sorbonne Université (SU), Hôpital neurologique et neurochirurgical Pierre Wertheimer [CHU - HCL], Hospices Civils de Lyon (HCL), CHU Pontchaillou [Rennes], Centre d'Investigation Clinique [Rennes] (CIC), Université de Rennes (UR)-Hôpital Pontchaillou-Institut National de la Santé et de la Recherche Médicale (INSERM), Fondation Ophtalmologique Adolphe de Rothschild [Paris], Neurocentre Magendie : Physiopathologie de la Plasticité Neuronale (U1215 Inserm - UB), Université de Bordeaux (UB)-Institut François Magendie-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Bordeaux [Bordeaux], Institut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), CIC Plurithématique de Nantes, Institut National de la Santé et de la Recherche Médicale (INSERM)-Ministère des Affaires sociales et de la Santé-Direction générale de l'offre de soins (DGOS)-Centre hospitalier universitaire de Nantes (CHU Nantes), Centre hospitalier universitaire de Nantes (CHU Nantes), Centre de Recherche en Transplantation et Immunologie - Center for Research in Transplantation and Translational Immunology (U1064 Inserm - CR2TI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Nantes Université - UFR de Médecine et des Techniques Médicales (Nantes Univ - UFR MEDECINE), Nantes Université - pôle Santé, Nantes Université (Nantes Univ)-Nantes Université (Nantes Univ)-Nantes Université - pôle Santé, Nantes Université (Nantes Univ)-Nantes Université (Nantes Univ), Translational Research in Autoimmunity and Inflammation Group (TIMC-T-RAIG), Translational Innovation in Medicine and Complexity / Recherche Translationnelle et Innovation en Médecine et Complexité - UMR 5525 (TIMC ), VetAgro Sup - Institut national d'enseignement supérieur et de recherche en alimentation, santé animale, sciences agronomiques et de l'environnement (VAS)-Centre National de la Recherche Scientifique (CNRS)-Université Grenoble Alpes (UGA)-Institut polytechnique de Grenoble - Grenoble Institute of Technology (Grenoble INP ), Université Grenoble Alpes (UGA)-VetAgro Sup - Institut national d'enseignement supérieur et de recherche en alimentation, santé animale, sciences agronomiques et de l'environnement (VAS)-Centre National de la Recherche Scientifique (CNRS)-Université Grenoble Alpes (UGA)-Institut polytechnique de Grenoble - Grenoble Institute of Technology (Grenoble INP ), Université Grenoble Alpes (UGA), Centre Hospitalier Universitaire [Grenoble] (CHU), Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), Adaptation, mesure et évaluation en santé. Approches interdisciplinaires (APEMAC), Université de Lorraine (UL), CHU Strasbourg, CIC Strasbourg (Centre d’Investigation Clinique Plurithématique (CIC - P) ), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Nouvel Hôpital Civil de Strasbourg-Hôpital de Hautepierre [Strasbourg], Mayo Clinic [Rochester], Yale School of Medicine [New Haven, Connecticut] (YSM), Service de Neurologie [CHU Nimes] (Pôle NIRR), Hôpital Universitaire Carémeau [Nîmes] (CHU Nîmes), Centre Hospitalier Universitaire de Nîmes (CHU Nîmes)-Centre Hospitalier Universitaire de Nîmes (CHU Nîmes), Institut de Génomique Fonctionnelle (IGF), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM), and None

Subjects
[SCCO.NEUR]Cognitive science/Neuroscience, diagnostic criteria, radiologically isolated syndrome, Neurology (clinical), prognosis, multiple sclerosis, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, MRI
Abstract

The radiologically isolated syndrome (RIS) was defined in 2009 as the presence of asymptomatic, incidentally identified demyelinating-appearing white matter lesions in the CNS within individuals lacking symptoms typical of multiple sclerosis (MS). The RIS criteria have been validated and predict the transition to symptomatic MS reliably. The performance of RIS criteria that require fewer MRI lesions is unknown. 2009-RIS subjects, by definition, fulfil three to four of four criteria for 2005 dissemination in space (DIS) and subjects fulfilling only one or two lesions in at least one 2017 DIS location were identified within 37 prospective databases. Univariate and multivariate Cox regression models were used to identify predictors of a first clinical event. Performances of different groups were calculated. Seven hundred and forty-seven subjects (72.2% female, mean age 37.7 ± 12.3 years at the index MRI) were included. The mean clinical follow-up time was 46.8 ± 45.4 months. All subjects had focal T2 hyperintensities suggestive of inflammatory demyelination on MRI; 251 (33.6%) fulfilled one or two 2017 DIS criteria (designated as Groups 1 and 2, respectively), and 496 (66.4%) fulfilled three or four 2005 DIS criteria representing 2009-RIS subjects. Group 1 and 2 subjects were younger than the 2009-RIS group and were more likely to develop new T2 lesions over time (P < 0.001). Groups 1 and 2 were similar regarding survival distribution and risk factors for transition to MS. At 5 years, the cumulative probability for a clinical event was 29.0% for Groups 1 and 2 compared to 38.7% for 2009-RIS (P = 0.0241). The presence of spinal cord lesions on the index scan and CSF-restricted oligoclonal bands in Groups 1–2 increased the risk of symptomatic MS evolution at 5 years to 38%, comparable to the risk of development in the 2009-RIS group. The presence of new T2 or gadolinium-enhancing lesions on follow-up scans independently increased the risk of presenting with a clinical event (P < 0.001). The 2009-RIS subjects or Groups 1 and 2 with at least two of the risk factors for a clinical event demonstrated better sensitivity (86.0%), negative predictive value (73.1%), accuracy (59.8%) and area under the curve (60.7%) compared to other criteria studied. This large prospective cohort brings Class I evidence that subjects with fewer lesions than required in the 2009 RIS criteria evolve directly to a first clinical event at a similar rate when additional risk factors are present. Our results provide a rationale for revisions to existing RIS diagnostic criteria.

Published
2023
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365. A thousand-genome panel retraces the global spread and adaptation of a major fungal crop pathogen

Author

Feurtey, Alice, Lorrain, Cécile, McDonald, Megan C, Milgate, Andrew, Solomon, Peter S, Warren, Rachael, Puccetti, Guido, Scalliet, Gabriel, Torriani, Stefano F F, Gout, Lilian, Marcel, Thierry C, Suffert, Frédéric, Alassimone, Julien, Lipzen, Anna, Yoshinaga, Yuko, Daum, Christopher, Barry, Kerrie, Grigoriev, Igor V, Goodwin, Stephen B, Genissel, Anne, Seidl, Michael F, Stukenbrock, Eva H, Lebrun, Marc-Henri, Kema, Gert H J, McDonald, Bruce A, Croll, Daniel, Sub Bioinformatics, Theoretical Biology and Bioinformatics, Sub Bioinformatics, and Theoretical Biology and Bioinformatics

Subjects
Chemistry(all), Physiological, Acclimatization, Resistance, General Physics and Astronomy, Physics and Astronomy(all), General Biochemistry, Genetics and Molecular Biology, Virulence/genetics, Plant-pathogens, Genetics, 2.1 Biological and endogenous factors, 2.2 Factors relating to the physical environment, Life Science, Humans, Adaptation, Aetiology, Plant Diseases, Mycosphaerella-graminicola, Multidisciplinary, Virulence, Biochemistry, Genetics and Molecular Biology(all), Populations, Genomics, General Chemistry, Adaptation, Physiological, Plant Diseases/microbiology, Laboratorium voor Phytopathologie, Infectious Diseases, Genes, Laboratory of Phytopathology, Zero Hunger, EPS, Infection, Biotechnology
Abstract

Human activity impacts the evolutionary trajectories of many species worldwide. Global trade of agricultural goods contributes to the dispersal of pathogens reshaping their genetic makeup and providing opportunities for virulence gains. Understanding how pathogens surmount control strategies and cope with new climates is crucial to predicting the future impact of crop pathogens. Here, we address this by assembling a global thousand-genome panel of Zymoseptoria tritici, a major fungal pathogen of wheat reported in all production areas worldwide. We identify the global invasion routes and ongoing genetic exchange of the pathogen among wheat-growing regions. We find that the global expansion was accompanied by increased activity of transposable elements and weakened genomic defenses. Finally, we find significant standing variation for adaptation to new climates encountered during the global spread. Our work shows how large population genomic panels enable deep insights into the evolutionary trajectory of a major crop pathogen., Nature Communications, 14 (1), ISSN:2041-1723

Published
2023
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367. Improving the decision to switch from first- to second-line therapy in multiple sclerosis: A dynamic scoring system

Author

Camille Sabathé, Romain Casey, Sandra Vukusic, Emmanuelle Leray, Guillaume Mathey, Jérôme De Sèze, Jonathan Ciron, Sandrine Wiertlewski, Aurélie Ruet, Jean Pelletier, Hélène Zéphir, Laure Michel, Christine Lebrun-Frenay, Xavier Moisset, Eric Thouvenot, Jean-Philippe Camdessanché, Serge Bakchine, Bruno Stankoff, Abdullatif Al Khedr, Philippe Cabre, Elisabeth Maillart, Eric Berger, Olivier Heinzlef, Karolina Hankiewicz, Thibault Moreau, Olivier Gout, Bertrand Bourre, Abir Wahab, Pierre Labauge, Alexis Montcuquet, Gilles Defer, Aude Maurousset, Nicolas Maubeuge, Dalia Dimitri Boulos, Haïfa Ben Nasr, Chantal Nifle, Olivier Casez, David-Axel Laplaud, Yohann Foucher, Université de Nantes, Université de Tours, Inserm, UMR1246 Sphere, Nantes, Centre d'Investigation Clinique [Rennes] (CIC), Université de Rennes (UR)-Hôpital Pontchaillou-Institut National de la Santé et de la Recherche Médicale (INSERM), Département Méthodes quantitatives en santé publique (METIS), École des Hautes Études en Santé Publique [EHESP] (EHESP), Recherche sur les services et le management en santé (RSMS), Université de Rennes (UR)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Pôle de Neurosciences Cliniques, Service de Neurologie, APHM, Hôpital de la Timone, Aix-Marseille University, Marseille, France, Centre de résonance magnétique biologique et médicale (CRMBM), Aix Marseille Université (AMU)-Assistance Publique - Hôpitaux de Marseille (APHM)-Centre National de la Recherche Scientifique (CNRS), Centre hospitalier universitaire de Poitiers (CHU Poitiers), Recherche en Pharmaco-épidémiologie et Recours aux Soins (REPERES), and Université de Rennes (UR)-École des Hautes Études en Santé Publique [EHESP] (EHESP)

Subjects
Multiple sclerosis, Neurology, Epidemiology, Second-line treatment, Neurology (clinical), Treatment response, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

Background: In relapsing-remitting multiple sclerosis (RRMS), early identification of suboptimal responders can prevent disability progression. Objective: We aimed to develop and validate a dynamic score to guide the early decision to switch from first- to second-line therapy. Methods: Using time-dependent propensity scores (PS) from a French cohort of 12,823 patients with RRMS, we constructed one training and two validation PS-matched cohorts to compare the switched patients to second-line treatment and the maintained patients. We used a frailty Cox model for predicting individual hazard ratios (iHRs). Results: From the validation PS-matched cohort of 348 independent patients with iHR ⩽ 0.69, we reported the 5-year relapse-free survival at 0.14 (95% confidence interval (CI) 0.09–0.22) for the waiting group and 0.40 (95% CI 0.32–0.51) for the switched group. From the validation PS-matched cohort of 518 independent patients with iHR > 0.69, these values were 0.37 (95% CI 0.30–0.46) and 0.44 (95% CI 0.37–0.52), respectively. Conclusions: By using the proposed dynamic score, we estimated that at least one-third of patients could benefit from an earlier switch to prevent relapse.

Published
2023
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368. Safety and effectiveness of surgical excision of medium, large, and giant congenital melanocytic nevi:A systematic review and meta-analysis

Author

H. Antoine Gout, Anne C. Fledderus, Max M. Lokhorst, Suzanne G.M.A. Pasmans, Corstiaan C. Breugem, Oren Lapid, and Chantal M.A.M. van der Horst

Subjects
Surgery
Abstract

Background: Treatment indications of congenital melanocytic naevi (CMN) have shifted from the prevention of malignant transformation more towards the improvement of appearance and psychosocial health. Surgical excision is often preferred, but its safety and effectiveness remain unclear. Objective: To assess the outcomes of surgical excision of medium-to-giant CMN. Primary outcome: safety (complications). Secondary outcome: effectiveness (satisfaction and CMN core outcomes). Methods: PubMed, EMBASE, and CENTRAL were searched for studies on the excision of medium-to-giant CMN and/or CMN requiring reconstruction or serial excision. Meta-analyses of safety per patient were conducted, and pooled outcomes of safety and effectiveness were presented in summary-of-findings tables. Results: A total of 1444 studies were found, of which 22 were included, evaluating 643 eligible patients. Study quality varied, and reporting of baseline characteristics and outcomes was heterogeneous. Pooled proportions were overall 9.8% for major wound-related complications, 1.2% for minor wound-related complications, 1.2% for scar-related complications, and 4.3% for anatomical deformities. For large/giant CMN, complication rates were, respectively, 23.1%, 2.9%, 12.9%, and 2.4%; and for CMN with eyelid involvement, 0.5%, 3.3%, 0.4%, and 54.2%. Patients rated their satisfaction with the cosmetic outcome as 24.4% excellent, 71.0% good, and 4.6% poor/moderate. Physicians rated this as 18.3% excellent, 70.1% good, and 11.7% poor/moderate. Thirty-five other outcomes of effectiveness were summarized. However, many were rarely reported. Conclusions: Surgical excision of CMN appears to be safe and effective in many cases, depending on CMN size and location. Major wound-related complications and scar-related complications occurred more frequently with large/giant CMN, whereas anatomical deformities occurred with the majority of CMN with eyelid involvement.

Published
2023
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369. The fidelity of transcription in human cells

Author

Claire Chung, Bert M. Verheijen, Xinmin Zhang, Biao Huang, Aeowynn Coakley, Eric McGann, Emily Wade, Olivia Dinep-Schneider, Jessica LaGosh, Maria-Eleni Anagnostou, Stephen Simpson, Kelly Thomas, Mimi Ernst, Allison Rattray, Michael Lynch, Mikhail Kashlev, Berenice A. Benayoun, Zhongwei Li, Jeffrey Strathern, Jean-Francois Gout, and Marc Vermulst

Subjects
Multidisciplinary
Abstract

To determine the error rate of transcription in human cells, we analyzed the transcriptome of H1 human embryonic stem cells with a circle-sequencing approach that allows for high-fidelity sequencing of the transcriptome. These experiments identified approximately 100,000 errors distributed over every major RNA species in human cells. Our results indicate that different RNA species display different error rates, suggesting that human cells prioritize the fidelity of some RNAs over others. Cross-referencing the errors that we detected with various genetic and epigenetic features of the human genome revealed that the in vivo error rate in human cells changes along the length of a transcript and is further modified by genetic context, repetitive elements, epigenetic markers, and the speed of transcription. Our experiments further suggest that BRCA1, a DNA repair protein implicated in breast cancer, has a previously unknown role in the suppression of transcription errors. Finally, we analyzed the distribution of transcription errors in multiple tissues of a new mouse model and found that they occur preferentially in neurons, compared to other cell types. These observations lend additional weight to the idea that transcription errors play a key role in the progression of various neurological disorders, including Alzheimer’s disease.

Published
2023
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370. Responsabilité civile

Author

Gout, Olivier, Quézel-Ambrunaz, Christophe, Université Jean Moulin - Lyon 3 (UJML), Université de Lyon, Equipe de recherche Louis Josserand, Université de Lyon-Université de Lyon, Université Savoie Mont Blanc (USMB [Université de Savoie] [Université de Chambéry]), Centre de droit privé et public des obligations et de la consommation (CDPPOC), collaboration or project value, and Droit2HAL, Projet

Subjects
[SHS.DROIT]Humanities and Social Sciences/Law, [SHS.DROIT] Humanities and Social Sciences/Law, Responsabilité Civile
Abstract

International audience; novembre 2021 – octobre 2022

Published
2023

371. Bacillus subtilis YtpP and thioredoxin A are new players in the coenzyme-A-mediated defense mechanism against cellular stress

Author

Maria-Armineh Tossounian, Maria Baczynska, William Dalton, Sew Yeu Peak-Chew, Kipras Undzenas, George Korza, Valeriy Filonenko, Mark Skehel, Peter Setlow, and Ivan Gout

Subjects
Chemical Biology & High Throughput, coenzyme A, protein CoAlation, protein deCoAlation, mixed disulfide, oxidative stress, Bacillus subtilis, Bacillus megaterium, antioxidant, Physiology, Clinical Biochemistry, Cell Biology, Biochemistry & Proteomics, Molecular Biology, Biochemistry, Computational & Systems Biology
Abstract

Coenzyme A (CoA) is an important cellular metabolite that is critical for metabolic processes and the regulation of gene expression. Recent discovery of the antioxidant function of CoA has highlighted its protective role that leads to the formation of a mixed disulfide bond with protein cysteines, which is termed protein CoAlation. To date, more than 2000 CoAlated bacterial and mammalian proteins have been identified in cellular responses to oxidative stress, with the majority being involved in metabolic pathways (60%). Studies have shown that protein CoAlation is a widespread post-translational modification which modulates the activity and conformation of the modified proteins. The induction of protein CoAlation by oxidative stress was found to be rapidly reversed after the removal of oxidizing agents from the medium of cultured cells. In this study, we developed an enzyme-linked immunosorbent assay (ELISA)-based deCoAlation assay to detect deCoAlation activity from Bacillus subtilis and Bacillus megaterium lysates. We then used a combination of ELISA-based assay and purification strategies to show that deCoAlation is an enzyme-driven mechanism. Using mass-spectrometry and deCoAlation assays, we identified B. subtilis YtpP (thioredoxin-like protein) and thioredoxin A (TrxA) as enzymes that can remove CoA from different substrates. With mutagenesis studies, we identified YtpP and TrxA catalytic cysteine residues and proposed a possible deCoAlation mechanism for CoAlated methionine sulfoxide reducatse A (MsrA) and peroxiredoxin 5 (PRDX5) proteins, which results in the release of both CoA and the reduced form of MsrA or PRDX5. Overall, this paper reveals the deCoAlation activity of YtpP and TrxA and opens doors to future studies on the CoA-mediated redox regulation of CoAlated proteins under various cellular stress conditions.

Published
2023
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373. Supplementary Table S1 from BIRC6 Targeting as Potential Therapy for Advanced, Enzalutamide-Resistant Prostate Cancer

Author

Luk, Iris Sze Ue, primary, Shrestha, Raunak, primary, Xue, Hui, primary, Wang, Yuwei, primary, Zhang, Fang, primary, Lin, Dong, primary, Haegert, Anne, primary, Wu, Rebecca, primary, Dong, Xin, primary, Collins, Colin C., primary, Zoubeidi, Amina, primary, Gleave, Martin E., primary, Gout, Peter W., primary, and Wang, Yuzhuo, primary

Published
2023
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374. Supplementary figure S2 from BIRC6 Targeting as Potential Therapy for Advanced, Enzalutamide-Resistant Prostate Cancer

Author

Luk, Iris Sze Ue, primary, Shrestha, Raunak, primary, Xue, Hui, primary, Wang, Yuwei, primary, Zhang, Fang, primary, Lin, Dong, primary, Haegert, Anne, primary, Wu, Rebecca, primary, Dong, Xin, primary, Collins, Colin C., primary, Zoubeidi, Amina, primary, Gleave, Martin E., primary, Gout, Peter W., primary, and Wang, Yuzhuo, primary

Published
2023
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375. Supplementary Data from RINT1 Regulates SUMOylation and the DNA Damage Response to Preserve Cellular Homeostasis in Pancreatic Cancer

Author

Arnold, Frank, primary, Gout, Johann, primary, Wiese, Heike, primary, Weissinger, Stephanie E., primary, Roger, Elodie, primary, Perkhofer, Lukas, primary, Walter, Karolin, primary, Scheible, Jeanette, primary, Prelli Bozzo, Caterina, primary, Lechel, André, primary, Ettrich, Thomas J., primary, Azoitei, Ninel, primary, Hao, Li, primary, Fürstberger, Axel, primary, Kaminska, Ewa K., primary, Sparrer, Konstantin M.J., primary, Rasche, Volker, primary, Wiese, Sebastian, primary, Kestler, Hans A., primary, Möller, Peter, primary, Seufferlein, Thomas, primary, Frappart, Pierre-Olivier, primary, and Kleger, Alexander, primary

Published
2023
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376. Data from RINT1 Regulates SUMOylation and the DNA Damage Response to Preserve Cellular Homeostasis in Pancreatic Cancer

Author

Arnold, Frank, primary, Gout, Johann, primary, Wiese, Heike, primary, Weissinger, Stephanie E., primary, Roger, Elodie, primary, Perkhofer, Lukas, primary, Walter, Karolin, primary, Scheible, Jeanette, primary, Prelli Bozzo, Caterina, primary, Lechel, André, primary, Ettrich, Thomas J., primary, Azoitei, Ninel, primary, Hao, Li, primary, Fürstberger, Axel, primary, Kaminska, Ewa K., primary, Sparrer, Konstantin M.J., primary, Rasche, Volker, primary, Wiese, Sebastian, primary, Kestler, Hans A., primary, Möller, Peter, primary, Seufferlein, Thomas, primary, Frappart, Pierre-Olivier, primary, and Kleger, Alexander, primary

Published
2023
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377. Data from Heterochromatin Protein 1α Mediates Development and Aggressiveness of Neuroendocrine Prostate Cancer

Author

Ci, Xinpei, primary, Hao, Jun, primary, Dong, Xin, primary, Choi, Stephen Y., primary, Xue, Hui, primary, Wu, Rebecca, primary, Qu, Sifeng, primary, Gout, Peter W., primary, Zhang, Fang, primary, Haegert, Anne M., primary, Fazli, Ladan, primary, Crea, Francesco, primary, Ong, Christopher J., primary, Zoubeidi, Amina, primary, He, Housheng H., primary, Gleave, Martin E., primary, Collins, Colin C., primary, Lin, Dong, primary, and Wang, Yuzhuo, primary

Published
2023
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378. Supplementary Information from Heterochromatin Protein 1α Mediates Development and Aggressiveness of Neuroendocrine Prostate Cancer

Author

Ci, Xinpei, primary, Hao, Jun, primary, Dong, Xin, primary, Choi, Stephen Y., primary, Xue, Hui, primary, Wu, Rebecca, primary, Qu, Sifeng, primary, Gout, Peter W., primary, Zhang, Fang, primary, Haegert, Anne M., primary, Fazli, Ladan, primary, Crea, Francesco, primary, Ong, Christopher J., primary, Zoubeidi, Amina, primary, He, Housheng H., primary, Gleave, Martin E., primary, Collins, Colin C., primary, Lin, Dong, primary, and Wang, Yuzhuo, primary

Published
2023
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379. Supplementary figure legends from BIRC6 Targeting as Potential Therapy for Advanced, Enzalutamide-Resistant Prostate Cancer

Author

Luk, Iris Sze Ue, primary, Shrestha, Raunak, primary, Xue, Hui, primary, Wang, Yuwei, primary, Zhang, Fang, primary, Lin, Dong, primary, Haegert, Anne, primary, Wu, Rebecca, primary, Dong, Xin, primary, Collins, Colin C., primary, Zoubeidi, Amina, primary, Gleave, Martin E., primary, Gout, Peter W., primary, and Wang, Yuzhuo, primary

Published
2023
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380. Supplementary Table 3 from High Fidelity Patient-Derived Xenografts for Accelerating Prostate Cancer Discovery and Drug Development

Author

Lin, Dong, primary, Wyatt, Alexander W., primary, Xue, Hui, primary, Wang, Yuwei, primary, Dong, Xin, primary, Haegert, Anne, primary, Wu, Rebecca, primary, Brahmbhatt, Sonal, primary, Mo, Fan, primary, Jong, Lina, primary, Bell, Robert H., primary, Anderson, Shawn, primary, Hurtado-Coll, Antonio, primary, Fazli, Ladan, primary, Sharma, Manju, primary, Beltran, Himisha, primary, Rubin, Mark, primary, Cox, Michael, primary, Gout, Peter W., primary, Morris, James, primary, Goldenberg, Larry, primary, Volik, Stanislav V., primary, Gleave, Martin E., primary, Collins, Colin C., primary, and Wang, Yuzhuo, primary

Published
2023
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381. Supplementary Figures 1 - 9 from High Fidelity Patient-Derived Xenografts for Accelerating Prostate Cancer Discovery and Drug Development

Author

Lin, Dong, primary, Wyatt, Alexander W., primary, Xue, Hui, primary, Wang, Yuwei, primary, Dong, Xin, primary, Haegert, Anne, primary, Wu, Rebecca, primary, Brahmbhatt, Sonal, primary, Mo, Fan, primary, Jong, Lina, primary, Bell, Robert H., primary, Anderson, Shawn, primary, Hurtado-Coll, Antonio, primary, Fazli, Ladan, primary, Sharma, Manju, primary, Beltran, Himisha, primary, Rubin, Mark, primary, Cox, Michael, primary, Gout, Peter W., primary, Morris, James, primary, Goldenberg, Larry, primary, Volik, Stanislav V., primary, Gleave, Martin E., primary, Collins, Colin C., primary, and Wang, Yuzhuo, primary

Published
2023
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382. Data from High Fidelity Patient-Derived Xenografts for Accelerating Prostate Cancer Discovery and Drug Development

Author

Lin, Dong, primary, Wyatt, Alexander W., primary, Xue, Hui, primary, Wang, Yuwei, primary, Dong, Xin, primary, Haegert, Anne, primary, Wu, Rebecca, primary, Brahmbhatt, Sonal, primary, Mo, Fan, primary, Jong, Lina, primary, Bell, Robert H., primary, Anderson, Shawn, primary, Hurtado-Coll, Antonio, primary, Fazli, Ladan, primary, Sharma, Manju, primary, Beltran, Himisha, primary, Rubin, Mark, primary, Cox, Michael, primary, Gout, Peter W., primary, Morris, James, primary, Goldenberg, Larry, primary, Volik, Stanislav V., primary, Gleave, Martin E., primary, Collins, Colin C., primary, and Wang, Yuzhuo, primary

Published
2023
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383. Supplementary Table 1 from High Fidelity Patient-Derived Xenografts for Accelerating Prostate Cancer Discovery and Drug Development

Author

Lin, Dong, primary, Wyatt, Alexander W., primary, Xue, Hui, primary, Wang, Yuwei, primary, Dong, Xin, primary, Haegert, Anne, primary, Wu, Rebecca, primary, Brahmbhatt, Sonal, primary, Mo, Fan, primary, Jong, Lina, primary, Bell, Robert H., primary, Anderson, Shawn, primary, Hurtado-Coll, Antonio, primary, Fazli, Ladan, primary, Sharma, Manju, primary, Beltran, Himisha, primary, Rubin, Mark, primary, Cox, Michael, primary, Gout, Peter W., primary, Morris, James, primary, Goldenberg, Larry, primary, Volik, Stanislav V., primary, Gleave, Martin E., primary, Collins, Colin C., primary, and Wang, Yuzhuo, primary

Published
2023
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384. Supplementary Table 2 from High Fidelity Patient-Derived Xenografts for Accelerating Prostate Cancer Discovery and Drug Development

Author

Lin, Dong, primary, Wyatt, Alexander W., primary, Xue, Hui, primary, Wang, Yuwei, primary, Dong, Xin, primary, Haegert, Anne, primary, Wu, Rebecca, primary, Brahmbhatt, Sonal, primary, Mo, Fan, primary, Jong, Lina, primary, Bell, Robert H., primary, Anderson, Shawn, primary, Hurtado-Coll, Antonio, primary, Fazli, Ladan, primary, Sharma, Manju, primary, Beltran, Himisha, primary, Rubin, Mark, primary, Cox, Michael, primary, Gout, Peter W., primary, Morris, James, primary, Goldenberg, Larry, primary, Volik, Stanislav V., primary, Gleave, Martin E., primary, Collins, Colin C., primary, and Wang, Yuzhuo, primary

Published
2023
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386. Data from TIF1γ Suppresses Tumor Progression by Regulating Mitotic Checkpoints and Chromosomal Stability

Author

Pommier, Roxane M., primary, Gout, Johann, primary, Vincent, David F., primary, Alcaraz, Lindsay B., primary, Chuvin, Nicolas, primary, Arfi, Vanessa, primary, Martel, Sylvie, primary, Kaniewski, Bastien, primary, Devailly, Guillaume, primary, Fourel, Geneviève, primary, Bernard, Pascal, primary, Moyret-Lalle, Caroline, primary, Ansieau, Stéphane, primary, Puisieux, Alain, primary, Valcourt, Ulrich, primary, Sentis, Stéphanie, primary, and Bartholin, Laurent, primary

Published
2023
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387. Evolutionary conservation of the fidelity of transcription

Author

Chung, Claire, primary, Verheijen, Bert M., additional, Navapanich, Zoe, additional, McGann, Eric G., additional, Shemtov, Sarah, additional, Lai, Guan-Ju, additional, Arora, Payal, additional, Towheed, Atif, additional, Haroon, Suraiya, additional, Holczbauer, Agnes, additional, Chang, Sharon, additional, Manojlovic, Zarko, additional, Simpson, Stephen, additional, Thomas, Kelley W., additional, Kaplan, Craig, additional, van Hasselt, Peter, additional, Timmers, Marc, additional, Erie, Dorothy, additional, Chen, Lin, additional, Gout, Jean-Franćois, additional, and Vermulst, Marc, additional

Published
2023
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388. A cross-over, randomised feasibility study of digitally printed versus hand-painted artificial eyes in adults: PERSONAL-EYE-S - a study protocol

Author

Gout, Taras, primary, Zoltie, Tim, additional, Woodward, Amie, additional, Coleman, Elizabeth, additional, Boele, Florien, additional, Chang, Bernard, additional, Bartlett, Paul, additional, Ronaldson, Sarah, additional, Kalantzis, George, additional, Theaker, Mike, additional, El-Hindy, Nabil, additional, Walshaw, Emma, additional, and Watson, Judith, additional

Published
2023
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390. Publisher Correction: IFNγ binding to extracellular matrix prevents fatal systemic toxicity

Author

Kemna, Josephine, primary, Gout, Evelyne, additional, Daniau, Leon, additional, Lao, Jessica, additional, Weißert, Kristoffer, additional, Ammann, Sandra, additional, Kühn, Ralf, additional, Richter, Matthias, additional, Molenda, Christine, additional, Sporbert, Anje, additional, Zocholl, Dario, additional, Klopfleisch, Robert, additional, Lortat-Jacob, Hugues, additional, Aichele, Peter, additional, Kammertoens, Thomas, additional, and Blankenstein, Thomas, additional

Published
2023
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392. IFNγ binding to extracellular matrix prevents fatal systemic toxicity

Author

Kemna, Josephine, primary, Gout, Evelyne, additional, Daniau, Leon, additional, Lao, Jessica, additional, Weißert, Kristoffer, additional, Ammann, Sandra, additional, Kühn, Ralf, additional, Richter, Matthias, additional, Molenda, Christine, additional, Sporbert, Anje, additional, Zocholl, Dario, additional, Klopfleisch, Robert, additional, Lortat-Jacob, Hugues, additional, Aichele, Peter, additional, Kammertoens, Thomas, additional, and Blankenstein, Thomas, additional

Published
2023
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395. The fidelity of transcription in human cells

Author

Chung, Claire, primary, Verheijen, Bert M., additional, Zhang, Xinmin, additional, Huang, Biao, additional, Coakley, Aeowynn, additional, McGann, Eric, additional, Wade, Emily, additional, Dinep-Schneider, Olivia, additional, LaGosh, Jessica, additional, Anagnostou, Maria-Eleni, additional, Simpson, Stephen, additional, Thomas, Kelly, additional, Ernst, Mimi, additional, Rattray, Allison, additional, Lynch, Michael, additional, Kashlev, Mikhail, additional, Benayoun, Berenice A., additional, Li, Zhongwei, additional, Strathern, Jeffrey, additional, Gout, Jean-Francois, additional, and Vermulst, Marc, additional

Published
2023
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396. Malignant Progression of an Ancestral Bone Marrow Clone Harboring a CIC-NUTM2A Fusion in Isolated Myeloid Sarcoma

Author

Kamens, Jennifer L., primary, Dang, Jinjun, additional, Shaw, Timothy I., additional, Gout, Alexander M., additional, Newman, Scott, additional, Hagiwara, Kohei, additional, Smith, Amelia M.R., additional, Obermayer, Alyssa N., additional, Aldridge, Sarah, additional, Ma, Jing, additional, Zhang, Yang, additional, Wu, Gang, additional, Leventaki, Vasiliki, additional, Santiago, Teresa, additional, Raimondi, Susana, additional, Nakitandwe, Joy, additional, Pappo, Alberto, additional, Li, Chunliang, additional, Zhang, Jinghui, additional, and Gruber, Tanja A., additional

Published
2023
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