tbuckley/cabot-search huggingface dataset:
Abstract 192: Persistence of First Generation Adenovirus in the Myocardium: Refuting Old Dogma
Authors: Jacqueline K Olive, Megumi Mathison, Jaya Pratap Pinnamaneni, Vivek P Singh, Deepthi Sanagasetti, Jianchang Yang, Todd K Rosengart
Journal: Circulation Research (2017)

Introduction: Adenovirus (Ad) vectors do not integrate into host genomes and thus offer clinical benefits as non-mutagenic, acute-term gene delivery vehicles. One limitation to Ad vector use is the transient duration of transgene expression, supposedly resulting from immune-mediated cytolysis of Ad-infected cells. Our recent observation of Ad-induced transdifferentiation of infected cardiac fibroblasts into induced cardiomyocytes over 28 days in vivo called this premise into question. Therefore, we hypothesized that Ad remains in the myocardium for over 28 days and, to our knowledge, are the first to suggest alternate mechanisms for this persistence. Methods and Results: Ad encoding green fluorescent protein (AdGFP) or mock was administered via intramyocardial injection into Sprague-Dawley rats, and Ad genome and GFP expression were analyzed 3 or 28 days later (n=6 per group, 3 euthanized at each time point). Polymerase chain reaction typing and amplicon sequencing confirmed the presence of Ad DNA in all 6 treated animals. Quantitative real time polymerase chain reaction assays further demonstrated more than a three-fold increase in Ad DNA levels at both days 3 and 28 compared to untreated control animals (3.41±1.40 and 3.37±1.23, respectively). Thus, at 28 days Ad DNA persisted at a high level comparable to that which was present at 3 days. Next, AdGFP expression and host immune response were characterized by fluorescence microscopy and histology. We found that GFP-expressing cells decreased five-fold by 28 days (49±9 v. 3±0 cells). In addition, hematoxylin and eosin staining showed minimal infiltrating mononuclear inflammatory cells in AdGFP and mock-treated animals at both time points. Conclusions: Ad DNA and infected host cell persistence suggests that host-mediated cytolysis may not be responsible for the downregulation of transgene expression, indicating that Ad vectors may consequently be useful for therapies like cellular reprogramming wherein host cell persistence is required.
Mental Health of Transgender Adolescents Around the Globe—A Call for Comprehensive Assessment of Gender Identity
Authors: Brian C. Thoma, Sophia Choukas-Bradley
Journal: JAMA Network Open (2020)

Yuanyuan Wang, PhD; Hui Yu, PhD; Yong Yang, MD; Jack Drescher, MD; Ronghua Li, MD; Weijia Yin, MSc; Renjie Yu, BSc; Shuilan Wang, MD; Wei Deng, MD; Qiufang Jia, MD; Kenneth J. Zucker, PhD; Runsen Chen, MBMS
Safety and efficacy of MD1003 (high-dose biotin) in patients with progressive multiple sclerosis (SPI2): a randomised, double-blind, placebo-controlled, phase 3 trial
Authors: Bruce A C Cree, Gary Cutter, Jerry S Wolinsky, Mark S Freedman, Giancarlo Comi, Gavin Giovannoni, Hans-Peter Hartung, Douglas Arnold, Jens Kuhle, Valerie Block, Frederick E Munschauer, Frédéric Sedel, Fred D Lublin, Stephen Reingold, Pierre Duquette, Tobias Derfuss, Franz Fazekas, Maria Pia Sormani, Robert P. Lisak, Jennifer Graves, Stephen Krieger, Rana K. Zabad, Scott Newsome, Joshua Barton, Richard MacDonell, Mark Marriott, Nina De Klippel, Guy Laureys, Barbara Willekens, Virginia Devonshire, Mark Freedman, J Marc Girard, Paul Giacomini, Roger McKelvey, Daniel Selchen, Galina Vorobeychik, Ludivine Witkowski, Radek Ampapa, Jana Lizrova Preiningerova, Eva Meluzinova, Radomir Talab, Marta Vachova, Orhan Aktas, Mathias Buttmann, Elias-Hamp Birte, Tania Kuempfel, Paul Friedemann, Daniela Rau, Gerd Reifschneider, Piotr Sokolowski, Hayrettin Tumani, Maria Satori, Carlo Pozzilli, Agata Klosek, Jozef Koscielniak, Fryze Waldemar, Malgorzata Zajda, Rafael Arroyo Gonzalez, Guillermo Izquierdo Ayuso, Victoria Fernandez Sanchez, Celia Oreja Guevara, Jose Enrique Martinez Rodriguez, Xavier Montalban, Lluis Ramio-Torrenta, Lou Brundin, Jan Lycke, Murat Terzi, Joe Guadagno, Don Mahad, Adrian Pace, Klaus Schmierer, Ahmed Toosy, Stewart Webb, Mark Agius, Lilyana Amezcua, Michelle Apperson, Bridget Bagert, Daniel Bandari, Evanthia Bernitsas, Jonathan Calkwood, Jonathan Carter, Bruce Cohen, Devon Conway, Joanna Cooper, John Corboy, Patricia Coyle, Bruce Cree, Mitchel Freedman, Corey Ford, Edward Fox, Myla Goldman, Benjamin Greenberg, Mariko Kita, Thomas Leist, Sharon Lynch, Aaron Miller, Harold Moses, Robert Naismith, Mary Ann Picone, Bhatia Perminder, Alexander Rae-Grant, Kottil Rammohan, Anthony Reder, Claire Riley, Derrick Robertson, Vernon Rowe, Shiv Saidha, Lawrence Samkoff, Christopher Severson, Kyle Smoot, Sharon Stoll, Randall Trudell, Bianca Weinstock-Guttman, Sanjay Yathiraj
Journal: The Lancet Neurology (2020)
TCT CONNECT-327 Conduction Abnormalities and Pacing Requirement After Transcatheter Mitral Valve Replacement
Authors: Georgios Christopoulos, Abhishek Deshmukh, Yong-Mei Cha, Paul Friedman, Samuel Asirvatham, Chet Rihal, Mackram Eleid, Mayra Guerrero
Journal: Journal of the American College of Cardiology (2020)
Hepatic inflammasome activation as origin of Interleukin-1α and Interleukin-1β in liver cirrhosis
Authors: Michael Praktiknjo, Robert Schierwagen, Sofia Monteiro, Cristina Ortiz, Frank Erhard Uschner, Christian Jansen, Joan Claria, Jonel Trebicka
Journal: Gut (2020)

We appreciate the interest of Stengel et al 1 in our recent multicenter study published in Gu t.1 2 The group suggests that peripheral blood mononuclear cells (PBMC) are a source of interleukin (IL)-1β in acute decompensation (AD) independent of the canonical inflammasome activation pathway.1

While we acknowledge this meticulous work performed, we still think that the source of IL-1 and, therefore, the site of inflammasome activation is rather the diseased liver than circulating PBMC. Especially since in our work, we found these pathways persistently increased even in compensated, recompensated and decompensated cirrhosis.

In order to prove the origin of IL-1α and IL-1β, we assessed gene expression in PBMC and liver from our animal model of compensated and recompensated (after recovery from AD) cirrhosis. In this model, bile duct ligation in rats was used to induce liver cirrhosis and lipopolysaccharide to induce AD as described previously.2 Gene expression of both IL-1α and IL-1β is significantly higher in liver tissue compared with PBMC in recompensated cirrhosis. In compensated cirrhosis, gene expression of IL-1α, but not IL-1β, is significantly increased in liver tissue compared with PBMC (figure 1A,B).



Figure 1 
(A) Gene expression of interleukin (IL)-1α and (B) IL-1β in liver tissue and peripheral …
FRI0200 Electrocardiographic alterations in systemic sclerosis and in rheumatoid arthritis
Authors: BN Stamenkovic, AM Stankovic, BK Lovic, SA Ilic, DB Djordjevic, JM Nedovic, SK Stojanovic
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> Myocardial involvement is a common finding in patients with systemic sclerosis. It is also present in rheumatoid arthritis, but very rarely. Different alterations can be revealed by an electrocardiographic examination. <h3>Objectives</h3> Aim of this study was to evaluate and to compare the frequency and type of electrocardiographic alteration in patients with systemic sclerosis and rheumatoid arthritis. <h3>Methods</h3> In the study group of 40 pts with SSc (38 female, 2 male mean age 52,85 ± 12,44) and 22 pts with RA (20 female,2 male; mean age 51,45 ± 11,41) clinical, laboratory and ECG examination were done. All the patients with SSc were divided into two subgroup: with diffuse (dSSc) and localised (lSSc) SSc. The electrocardiographic data of each of these subgroup were compared. The existance of the next ECG abnormalities we were investigated: ventricular premature beats (VPB), supraventricular premature beats (SVPB), arrhythmia absoluta, left bundle branch block (LBBB), left anterior fascicular block (LAFB), complete right bundle branch block (CRBBB), atrioventricular block (AV block), infarct or pseudounfarct, ST depression. <h3>Results</h3> Electrocardiographic alterations were found in 65% of SSc patients, but only in 18,19% of RA patients. The difference was significant (p &lt; 0,001) Table 1. In the dSSc group, ECG alterations were found in 6 pts (15%)- not significant compared to the lSSc group (5 pts, 12,5%). p = o,220. ST depression was found in 2 pts (5%) with dSSc, but only in 1 pts (4,5%) with RA. Infarct or pseudoinfarct were found in 9 pts (22,5%) with SSc (6 in dSSc, 3 in lSSc). <h3>Conclusion</h3> The results of our study showed a significant prevalence of ECG alterations in SSc, but low prevalence in RA. Differences between a presence of alterations in two subgroup (dSSc, lSSc) of SSc is not significant (p = 0,220).
Neoadjuvant Chemotherapy Increases Cytotoxic T Cell, Tissue Resident Memory T Cell, and B Cell Infiltration in Resectable NSCLC
Authors: Pierre-Olivier Gaudreau, Marcelo V. Negrao, Kyle G. Mitchell, Alexandre Reuben, Erin M. Corsini, Jun Li, Tatiana V. Karpinets, Qi Wang, Lixia Diao, Jing Wang, Lorenzo Federico, Edwin R. Parra-Cuentas, Roohussaba Khairullah, Carmen Behrens, Arlene M. Correa, Daniel Gomez, Latasha Little, Curtis Gumbs, Humam N. Kadara, Junya Fujimoto, Daniel J. McGrail, Ara A. Vaporciyan, Stephen G. Swisher, Garrett Walsh, Mara B. Antonoff, Annikka Weissferdt, Hai Tran, Emily Roarty, Cara Haymaker, Chantale Bernatchez, Jianhua Zhang, P. Andrew Futreal, Ignacio I. Wistuba, Tina Cascone, John V. Heymach, Boris Sepesi, Jianjun Zhang, Don L. Gibbons
Journal: Journal of Thoracic Oncology (2020)

IntroductionThe combination of programmed cell death protein-1 or programmed death-ligand 1 immune checkpoint blockade and chemotherapy has revolutionized the treatment of advanced NSCLC, but the mechanisms underlying this synergy remain incompletely understood. In this study, we explored the relationships between neoadjuvant chemotherapy and the immune microenvironment (IME) of resectable NSCLC to identify novel mechanisms by which chemotherapy may enhance the effect of immune checkpoint blockade.MethodsGenomic, transcriptomic, and immune profiling data of 511 patients treated with neoadjuvant chemotherapy followed by surgery (NCT) versus upfront surgery (US) were compared with determined differential characteristics of the IMEs derived from whole-exome sequencing (NCT = 18; US = 73), RNA microarray (NCT = 45; US = 202), flow cytometry (NCT = 17; US = 39), multiplex immunofluorescence (NCT = 10; US = 72), T-cell receptor sequencing (NCT = 16 and US = 63), and circulating cytokines (NCT = 18; US = 73).ResultsNCT was associated with increased infiltration of cytotoxic CD8+ T cells and CD20+ B cells. Moreover, NCT was associated with increases in CD8+CD103+ and CD4+CD103+PD-1+TIM3− tissue resident memory T cells. Gene expression profiling supported memory function of CD8+ and CD4+ T cells. However, NCT did not affect T-cell receptor clonality, richness, or tumor mutational burden. Finally, NCT was associated with decreased plasma BDNF (TrkB) at baseline and week 4 after surgery.ConclusionsOur study supports that, in the context of resectable NSCLC, neoadjuvant chemotherapy promotes antitumor immunity through T and B cell recruitment in the IME and through a phenotypic change toward cytotoxic and memory CD8+ and CD4+ memory helper T cells.
Engineering Tolerance toward Allogeneic CAR-T Cells by Regulation of MHC Surface Expression with Human Herpes Virus-8 Proteins
Authors: Xiaomei Wang, Fabricio G. Cabrera, Kelly L. Sharp, David M. Spencer, Aaron E. Foster, J. Henri Bayle
Journal: Molecular Therapy (2020)

Allogeneic, off-the-shelf (OTS) chimeric antigen receptor (CAR) cell therapies have the potential to reduce manufacturing costs and variability while providing broader accessibility to cancer patients and those with other diseases. However, host-versus-graft reactivity can limit the durability and efficacy of OTS cell therapies requiring new strategies to evade adaptive and innate-immune responses. Human herpes virus-8 (HHV8) maintains infection, in part, by evading host T and natural killer (NK) cell attack. The viral K3 gene encodes a membrane-tethered E3 ubiquitin ligase that discretely targets major histocompatibility complex (MHC) class I components, whereas K5 encodes a similar E3 ligase with broader specificity, including MHC-II and the MHC-like MHC class I polypeptide-related sequence A (MIC-A)- and sequence B (MIC-B)-activating ligands of NK cells. We created γ-retroviruses encoding K3 and/or K5 transgenes that efficiently transduce primary human T cells. Expression of K3 or K5 resulted in dramatic downregulation of MHC-IA (human leukocyte antigen [HLA]-A, -B, and -C) and MHC class II (HLA-DR) cell-surface expression. K3 expression was sufficient for T cells to resist exogenously loaded peptide-MHC-specific cytotoxicity, as well as recognition in one-way allogeneic mixed lymphocyte reactions. Further, in immunodeficient mice engrafted with allogeneic T cells, K3-transduced T cells selectively expanded in vivo. Ectopic K5 expression in MHC class I-, MIC-A+/B+ K562 cells also reduced targeting by primary NK cells. Coexpression of K3 in prostate stem cell antigen (PSCA)-directed, inducible MyD88/CD40 (iMC)-enhanced CAR-T cells did not impact cytotoxicity, T cell growth, or cytokine production against HPAC pancreatic tumor target cells, whereas K5-expressing cells showed a modest reduction in interleukin (IL)-2 production without effect on cytotoxicity. Together, these results support application of these E3 ligases to advance development of OTS CAR-T cell products.
Динамика внешнесекреторной функции поджелудочной железы у больных хроническим панкреатитом в сочетании с хроническим бронхитом под влиянием терапии препаратом магния
Authors: N.B. Gubergrits, L.A. Yaroshenko
Journal: GASTROENTEROLOGY (2013)

Обследовано 64 больных хроническим панкреатитом в сочетании с хроническим бронхитом. По результатам фекального эластазного теста показано, что включение препарата магния в комплексную терапию способствует улучшению внешнесекреторной функции поджелудочной железы.
Liver disease in cystic fibrosis: A prospective study on incidence, risk factors, and outcome
Authors: Carla Colombo, Pier Maria Battezzati, Andrea Crosignani, Alberto Morabito, Diana Costantini, Rita Padoan, Annamaria Giunta
Journal: Hepatology (2002)

Incidence of liver disease (LD) associated with cystic fibrosis (CF) and its clinical characterization still is unsettled. We have assessed prospectively the incidence and risk factors of this complication, and its impact on the clinical course of CF. Between 1980 and 1990, we enrolled 177 CF patients without LD in a systematic clinical, laboratory, ultrasonography screening program of at least a 10-year duration. During a 14-year median follow-up (2,432 patient-years), 48 patients developed LD, with cirrhosis already present in 5. Incidence rate (number of cases per 100 patient-years) was 1.8% (95% confidence interval: 1.3-2.4), with sharp decline after the age of 10 years and higher risk in patients with a history of meconium ileus (incidence rate ratio, 5.5; 2.7-11), male sex (2.5; 1.3-4.9), or severe mutations (2.4; 1.2-4.8) at multivariate analysis. Incidence of cirrhosis was 4.5% (2.3-7.8) during a median period of 5 years from diagnosis of liver disease. Among the 17 cirrhotic patients, 13 developed portal hypertension, 4 developed esophageal varices, 1 developed liver decompensation requiring liver transplantation. Development of LD did not condition different mortality (death rate ratio, 0.4; 0.1-1.5) or higher incidence of other clinically relevant outcomes. In conclusion, LD is a relatively frequent and early complication of CF, whose detection should be focused at the first life decade in patients with history of meconium ileus, male sex, or severe genotype. Although LD does not condition a different clinical course of CF, in some patients it may progress rapidly and require liver transplantation. (Hepatology2002;36:1374-1382).
TCT CONNECT-154 Cardiovascular Mortality After Functionally Guided Treatment of Coronary Bifurcation Lesions: Insights From FIESTA Registry
Authors: Dobrin Vassilev, Niya Mileva, Carlos Collet, Pavel Nikolov, Georgi Dimitrov, Kiril Karamfiloff, Vladimir Naunov, Gianluca Rigatelli, Robert Gil, Patrick Serruys
Journal: Journal of the American College of Cardiology (2020)
Turbocharging NIV: how to increase oxygen delivery in home mechanical ventilators
Authors: Georgios Kaltsakas, Nicholas Hart
Journal: Thorax (2020)

In patients with hypoxaemic respiratory failure, supplement oxygen is added to a non-invasive ventilator to increase the fraction of inspired oxygen (FiO2). The FiO2 delivered through these domiciliary, non-critical care ventilators is limited and it is determined by a number of factors, including mode of ventilation, location of the oxygen connection point, intentional and unintentional leak, oxygen flow rate, length of circuit and type of interface.1 2 In this issue of the Journal , Mebrate et al 3 described a novel adaptation for two commercially available non-invasive ventilators, which increases FiO2 delivery. The process of increasing oxygen mass in a motor engine is called turbocharging and the approach by …
TCT CONNECT-200 Transthoracic Echocardiography–Guided Device Closure of Atrial Septal Defect (ASD) in Adult and Pediatric Population
Authors: Parag Barwad, Sanjeev Naganur, Pruthvi C. R, Krishna Prasad, Bhupendra Kumar Sihag
Journal: Journal of the American College of Cardiology (2020)
TCT CONNECT-387 Effect of Comorbidities on Mortality After Coronary Intervention in Patients Older Than 80 Years
Authors: David Martí, Damaris Carballeira, Ricardo Concepcion, Maria Jose Morales, Freddy Delgado, Alexander Marschall, Belén Biscotti, Juan Duarte, Carmen De Juan, Edurne Lopez-Soberon, Salvador Alvarez
Journal: Journal of the American College of Cardiology (2020)
TCT CONNECT-442 Association of Hospital Procedure Volume With Outcomes of Percutaneous Left Atrial Appendage Occlusion
Authors: Salik Nazir, Keerat Rai Ahuja, Dhaval Kolte, Toshiaki Isogai, Nobuaki Michihata, Anas Saad, P. Kasi Ramanathan, Walid Saliba, Oussama Wazni, Amar Krishnaswamy, Samir Kapadia
Journal: Journal of the American College of Cardiology (2020)
Improved Genome Editing through Inhibition of FANCM and Members of the BTR Dissolvase Complex
Authors: Gustavo de Alencastro, Francesco Puzzo, Mara Pavel-Dinu, Feijie Zhang, Sirika Pillay, Karim Majzoub, Matthew Tiffany, Hagoon Jang, Adam Sheikali, M. Kyle Cromer, Ruhikanta Meetei, Jan E. Carette, Matthew H. Porteus, Katja Pekrun, Mark A. Kay
Journal: Molecular Therapy (2020)

Recombinant adeno-associated virus (rAAV) vectors have the unique property of being able to perform genomic targeted integration (TI) without inducing a double-strand break (DSB). In order to improve our understanding of the mechanism behind TI mediated by AAV and improve its efficiency, we performed an unbiased genetic screen in human cells using a promoterless AAV-homologous recombination (AAV-HR) vector system. We identified that the inhibition of the Fanconi anemia complementation group M (FANCM) protein enhanced AAV-HR-mediated TI efficiencies in different cultured human cells by ∼6- to 9-fold. The combined knockdown of the FANCM and two proteins also associated with the FANCM complex, RecQ-mediated genome instability 1 (RMI1) and Bloom DNA helicase (BLM) from the BLM-topoisomerase IIIα (TOP3A)-RMI (BTR) dissolvase complex (RMI1, having also been identified in our screen), led to the enhancement of AAV-HR-mediated TI up to ∼17 times. AAV-HR-mediated TI in the presence of a nuclease (CRISPR-Cas9) was also increased by ∼1.5- to 2-fold in FANCM and RMI1 knockout cells, respectively. Furthermore, knockdown of FANCM in human CD34+ hematopoietic stem and progenitor cells (HSPCs) increased AAV-HR-mediated TI by ∼3.5-fold. This study expands our knowledge on the mechanisms related to AAV-mediated TI, and it highlights new pathways that might be manipulated for future improvements in AAV-HR-mediated TI.
FRI0152 Criyoglobulinemia in hepatitis c infective hemodialysis and renal transplantation patients
Authors: E Dalkilic, M Gullulu, G Karadogan, M Yavuz, K Dilek, A Ersoy, M Yurtkuran
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> Hepatitis C infection (HCV) is an important problem among hemodialysis and renal transplantation patients. It has been showed that HCV infection is closely associated with mixed type criyoglobulinemia, despite this close relationship, the correlation of HCV and essential mixed criyoglobulinemia has been analysed in a very limited number of studies in hemodialysed and renal transplant patients. <h3>Objectives</h3> In this study, we aimed to investigate the prevalence of criyoglobulinemia in HCV positive hemodialysis patients, renal transplant patients and in patients with chronic liver disease in Turkey which type I HCV is the dominant form. <h3>Methods</h3> Criyoglobulinemia was studied in 41 hemodialysis, 10 renal transplant and 17 chronic liver disease patients with HCV infection. Anti-HCV antibodies were detected by second and third generation ELISA and for criyoglobulins centrifugation and cold incubation techniques were used. <h3>Results</h3> None of the HCV positive hemodialysis and renal transplant patients were found to have criyoglobulinemia, on the other hand criyoglobulinemia was present in only one patient with HCV positive chronic liver disease. <h3>Conclusion</h3> Type I HCV is the most common hepatitis C virus type in our hemodialysis unit and in Turkey, so this low prevalence of criyoglobulinemia may be associated with the genotype of HCV and the differences of the geographic areas.
TCT CONNECT-359 In-Hospital Outcomes After Transcatheter Mitral Valve Repair With MitraClip in Patients With Chronic Kidney Disease: An Analysis From the 2010–2016 National Inpatient Sample
Authors: Hemang Panchal, Gregg Stone, Anshul Saxena, Arun Nagabandi, Charles Davidson, Martin Leon, Nirat Beohar
Journal: Journal of the American College of Cardiology (2020)
Long-term metabolic evolution of brain metastases with suspected radiation necrosis following stereotactic radiosurgery: longitudinal assessment by F-DOPA PET
Authors: Francesco Cicone, Luciano Carideo, Claudia Scaringi, Andrea Romano, Marcelo Mamede, Annalisa Papa, Anna Tofani, Giuseppe Lucio Cascini, Alessandro Bozzao, Francesco Scopinaro, Giuseppe Minniti
Journal: Neuro-Oncology (2020)

The evolution of radiation necrosis (RN) varies depending on the combination of radionecrotic tissue and active tumor cells. In this study, we characterized the long-term metabolic evolution of RN by sequential PET/CT imaging with 3,4-dihydroxy-6-[18F]-fluoro-l-phenylalanine (F-DOPA) in patients with brain metastases following stereotactic radiosurgery (SRS).Thirty consecutive patients with 34 suspected radionecrotic brain metastases following SRS repeated F-DOPA PET/CT every 6 months or yearly in addition to standard MRI monitoring. Diagnoses of local progression (LP) or RN were confirmed histologically or by clinical follow-up. Semi-quantitative parameters of F-DOPA uptake were extracted at different time points, and their diagnostic performances were compared with those of corresponding contrast-enhanced MRI.Ninety-nine F-DOPA PET scans were acquired over a median period of 18 (range: 12-66) months. Median follow-up from the baseline F-DOPA PET/CT was 48 (range 21-95) months. Overall, 24 (70.6%) and 10 (29.4%) lesions were classified as RN and LP, respectively. LP occurred after a median of 18 (range: 12-30) months from baseline PET. F-DOPA tumor-to-brain ratio (TBR) and relative standardized uptake value (rSUV) increased significantly over time in LP lesions, while remaining stable in RN lesions. The parameter showing the best diagnostic performance was rSUV (accuracy = 94.1% for the optimal threshold of 1.92). In contrast, variations of the longest tumor dimension measured on contrast-enhancing MRI did not distinguish between RN and LP.F-DOPA PET has a high diagnostic accuracy for assessing the long-term evolution of brain metastases following SRS.