tbuckley/cabot-search huggingface dataset:
Papillary Thyroid Carcinoma in Ectopic Thyroid Tissue Within a Suspected Cervical Paraganglioma
Authors: Marcel Ernesto Sambo Salas, Diego Muñoz Moreno, Laura Gonzalez Fernandez, Patricia Nuñez Ramos, Maria Cebollero Presmanes
Journal: Clinical Nuclear Medicine (2021)

Abstract Ectopic differentiated thyroid carcinoma represents less than 1% of all thyroid carcinoma cases, which usually arises along the cervical midline, and (delving into literature) there are scarce reports of such entity in nuclear medicine imaging studies. We present a rare case of a confirmed synchronous, orthotopic, and heterotopic (in lateral ectopic thyroid tissue) differentiated thyroid carcinoma in a patient who was previously misdiagnosed as having a cervical paraganglioma, based on compatible clinical, analytical, and imagenological (both structural and functional) findings.
LIN28B alters ribosomal dynamics to promote metastasis in MYCN-driven malignancy
Authors: Pavlos Missios, Edroaldo Lummertz da Rocha, Daniel S. Pearson, Julia Philipp, Maria M. Aleman, Mehdi Pirouz, Dorian Farache, Joseph W. Franses, Caroline Kubaczka, Kaloyan M. Tsanov, Deepak K. Jha, Brian Pepe-Mooney, John T. Powers, Richard I. Gregory, Amy S.Y. Lee, Daniel Dominguez, David T. Ting, George Q. Daley
Journal: Journal of Clinical Investigation (2021)

High expression of LIN28B is associated with aggressive malignancy and poor survival. Here, probing MYCN-amplified neuroblastoma as a model system, we showed that LIN28B expression was associated with enhanced cell migration in vitro and invasive and metastatic behavior in murine xenografts. Sequence analysis of the polyribosome fraction of LIN28B-expressing neuroblastoma cells revealed let-7–independent enrichment of transcripts encoding components of the translational and ribosomal apparatus and depletion of transcripts of neuronal developmental programs. We further observed that LIN28B utilizes both its cold shock and zinc finger RNA binding domains to preferentially interact with MYCN-induced transcripts of the ribosomal complex, enhancing their translation. These data demonstrated that LIN28B couples the MYCN-driven transcriptional program to enhanced ribosomal translation, thereby implicating LIN28B as a posttranscriptional driver of the metastatic phenotype.
Hepatic Cavernous Hemangioma Mimicking Metastasis of Midgut Neuroendocrine Neoplasia on 18F-Fluorodihydroxyphenylalanine PET/CT
Authors: Lucia Noskovicova, Martina Kovacova, Jan Janik, Juraj Marcinek, Sona Balogova
Journal: Clinical Nuclear Medicine (2021)

Abstract A 61-year-old man after resection of well-differentiated midgut neuroendocrine neoplasia (NEN) was referred to 18 F-fluorodihydroxyphenylalanine PET/CT for localization of recurrent midgut NEN in the context of clinical symptoms and mild elevation of serum CgA (chromogranin A) levels. Isolated hepatic focus of increased 18 F-Fluorodihydroxyphenylalanine uptake was detected. The biopsy of this focus, followed by radiofrequency ablation, revealed a hepatic cavernous hemangioma. Complete remission of midgut NEN was confirmed during 4-year clinical and imaging follow-up. The persistent mild elevation of serum CgA was retrospectively attributed to treatment with proton-pump inhibitors.
Abstract 10826: Lineage Specific Integrin Alpha V Augmentation Promotes Tgf-β Induced Integrin-FAK-Akt <sup>thr308</sup> Signaling Pathway
Authors: Ken Nakamura, Nobu Yokoyama, Albert J Pedroza, Alex R Dalal, Tetsuro Uchida, Michael P Fischbein
Journal: Circulation (2021)

Introduction: Marfan syndrome (MFS) patients classically develop focal aortic root aneurysms. Aortic root smooth muscle cells (SMCs) develop predominately from second heart field (SHF), whereas ascending aorta/arch SMCs originate from cardiac neural crest (CNC). We previously demonstrated induced pluripotent stem cell (iPSC)-derived SHF SMCs overexpress integrin αV (ITGAV). Therefore, we hypothesize that ITGAV promotes SHF SMC proliferation, contributing to thoracic aortic root aneurysm development. Methods: iPSCs from MFS patients (n=2) and healthy control (n=1) were differentiated into SHF and CNC SMCs. ITGAV-pFAK-pAkt Thr308 levels were detected with western blot and ELISA at baseline and following recombinant TGF-β (2ng/ml) and/or an ITGAV antagonist (GLPG0187, 10nM) for 24 hours. Cell proliferation was measured with quantitative BrdU assay. Results: Baseline ITGAV-pFAK-pAkt Thr308 activation were significantly elevated in MFS SHF lines (n=5 experimental replicates) compared to MFS CNC (n=5) or control SHF (n=4, p&lt;0.05). Addition of recombinant TGF-β to SMC differentiation media further enhanced pFAK-pAkt Thr308 levels in MFS SHF. Treatment with GLPG0187 reduced pFAK-pAkt Thr308 in MFS SHF and CNC, confirming ITGAV-mediated signaling promotes pathologic FAK- Akt Thr308 activation. SMCs from MFS SHF (n=6) had increased proliferation compared to other SMCs (p&lt;0.01 vs MFS CNC and control SHF) which was reversed to the same level as control SHF (p=0.132) with GLPG0187 treatment. Conclusions: The integrin-FAK-Akt Thr308 signaling pathway is activated in iPSC SMCs from MFS patients specifically from the SHF lineage, which is further exacerbated by TGF-β. Mechanistically, this pathway promotes SMC proliferation in vitro . ITGAV blockade via GLPG0187 may be a promising therapeutic approach for MFS aneurysmal growth.
13P Durvalumab + chemotherapy in patients (pts) with advanced EGFR mutation-positive (EGFRm) NSCLC whose disease progressed on first-line (1L) osimertinib: An ORCHARD study interim analysis
Authors: B.C. Cho, M-J. Ahn, C. Baik, R. García, J.W. Goldman, S-W. Kim, J.S. Lee, M. Nishio, S. Ponce, R. Salgia, S. Teraoka, T. Yoshida, H.A. Yu, H. Ambrose, J. Cosaert, R. Hartmaier, J. Maidment, M. Pluta, I. Okamoto
Journal: Annals of Oncology (2022)
Abstract P150: Blood Pressure Trajectories For 16 Years And The Development Of Left Ventricular Hypertrophy And Increased Left Atrial Size: The Korean Genome And Epidemiology Study
Authors: Ju-mi Lee, Seong Hwan Kim, Seung Ku Lee, Chol Shin, Jae-Hyeong Park
Journal: Circulation (2022)

Background: Single blood pressure (BP) measurement is associated with the development of target organ damage including left ventricular hypertrophy (LVH) and left atrial (LA) enlargement (LAE). However, long-term patterns of BP and their effects on LVH and LAE are poorly understood. We evaluated the association between BP trajectories and the presence of LVH and LAE. Methods: This analysis enrolled participants who attended a health examination from 2001 to 2016 (visit 1 to 8) in Ansan cohort study. Among the initial total of 10030 participants, we excluded 1787 participants because their BP measurements were less than three times. An additional 5678 participants were excluded because they had no echocardiographic examinations to evaluate LVH at visit 8. Thus, we enrolled 2,565 participants (1267 males, 47.8 ± 6.7 years old) in this study. The previous studies selected mid-BP for identifying trajectories because Mid-BP showed the greatest predictive utility for cardiovascular diseases. Based on the previous study, we also used mid-BP to identify trajectories. The current sample has more than three times times of BP measurements over 16 years. Latent mixture modeling was used to identify trajectories in mid-BP over time. Linear logistic regression was used for assessing BP trajectories with the outcomes. Results: We identified 4 distinct mid-BP trajectories: group 1 (lowest, 20.9%, n = 536), group 2 (36.2%, n = 928), group 3 (32.3%, n = 828), and group 4 (highest, 10.6%, n = 273). Compared with the lowest group, trajectories with elevated mid BP had greater odds ratios having LVH and LAE by multivariable-adjusted regression models. Adjusted odd ratios for LVH were 1.432 (95% CI = 1.138 -1.802, P = 0.002) for group 2, 2.718 (95% CI = 2.103 - 3.513, P &lt; 0.001) for group 3, and 2.480 (95% CI = 1.742 - 3.530, P &lt; 0.001) for group 4. Adjusted odd ratios for LAE were 1.200 (95% CI = 0.814 - 1.769, P = 0.358) for group 2, 1.599 (95% CI = 1.084 - 2.360, P = 0.018) for group 3, and 1.944 (95% CI = 1.212 - 3.118, P = 0.006) for group 4. Conclusions: Our study suggests that long-term higher mid-BP were an independent risk factor for having LVH among middle-aged males and females. Also, higher mid-BP was an independent risk factor for having future LAE in middle-aged females. Higher long-term mid-BP was an independent risk factor of cardiac structural changes such as LVH and LAE among middle-aged population.
Gene replacement therapy with onasemnogene abeparvovec in children with spinal muscular atrophy aged 24 months or younger and bodyweight up to 15 kg: an observational cohort study
Authors: Claudia Weiß, Andreas Ziegler, Lena-Luise Becker, Jessika Johannsen, Heiko Brennenstuhl, Gudrun Schreiber, Marina Flotats-Bastardas, Corinna Stoltenburg, Hans Hartmann, Sabine Illsinger, Jonas Denecke, Astrid Pechmann, Wolfgang Müller-Felber, Katharina Vill, Astrid Blaschek, Martin Smitka, Lieske van der Stam, Katja Weiss, Benedikt Winter, Klaus Goldhahn, Barbara Plecko, Veronka Horber, Günther Bernert, Ralf A Husain, Christian Rauscher, Regina Trollmann, Sven F Garbade, Andreas Hahn, Maja von der Hagen, Angela M Kaindl
Journal: The Lancet Child & Adolescent Health (2021)
52P ROS1 aberrations in non-small cell lung cancer patients without rearrangements: Clinical and molecular characteristics
Authors: M. Glaser, C. von Levetzow, S. Michels, L. Nogova, M. Katzenmeier, C. Wömpner, J. Schmitz, E. Bitter, I. Terjung, E. Passmann, D. Schaufler, A. Eisert, R. Fischer, R. Riedel, J-P. Weber, S. Hahne, S. Merkelbach-Bruse, R. Büttner, J. Wolf, M. Scheffler
Journal: Annals of Oncology (2022)
Stem cell-laden hydrogel bioink for generation of high resolution and fidelity engineered tissues with complex geometries
Authors: Oju Jeon, Yu Bin Lee, Sang Jin Lee, Nazilya Guliyeva, Joanna Lee, Eben Alsberg
Journal: Bioactive Materials (2021)

Recently, 3D bioprinting has been explored as a promising technology for biomedical applications with the potential to create complex structures with precise features. Cell encapsulated hydrogels composed of materials such as gelatin, collagen, hyaluronic acid, alginate and polyethylene glycol have been widely used as bioinks for 3D bioprinting. However, since most hydrogel-based bioinks may not allow rapid stabilization immediately after 3D bioprinting, achieving high resolution and fidelity to the intended architecture is a common challenge in 3D bioprinting of hydrogels. In this study, we have utilized shear-thinning and self-healing ionically crosslinked oxidized and methacrylated alginates (OMAs) as a bioink, which can be rapidly gelled by its self-healing property after bioprinting and further stabilized via secondary crosslinking. It was successfully demonstrated that stem cell-laden calcium-crosslinked OMA hydrogels can be bioprinted into complicated 3D tissue structures with both high resolution and fidelity. Additional photocrosslinking enables long-term culture of 3D bioprinted constructs for formation of functional tissue by differentiation of encapsulated human mesenchymal stem cells.
SMC-Derived Hyaluronan Modulates Vascular SMC Phenotype in Murine Atherosclerosis
Authors: Felicia Hartmann, Daniel J. Gorski, Alexandra A.C. Newman, Susanne Homann, Anne Petz, Katherine M. Owsiany, Vlad Serbulea, Yu-Qing Zhou, Rebecca A. Deaton, Michelle Bendeck, Gary K. Owens, Jens W. Fischer
Journal: Circulation Research (2021)

Rationale: Plaque instability remains poorly understood and new therapeutic approaches to reduce plaque rupture and subsequent clinical events are of great interest. Recent studies revealed an important role of phenotypic switching of smooth muscle cells (SMC) in controlling plaque stability, including ECM (extracellular matrix) deposition. Objective: The aim of this study was to elucidate the role of hyaluronan derived from SMC–hyaluronan synthase 3 ( Has3 ), in phenotypic switching and plaque stability in an animal model of atherosclerosis. Methods and Results: A mouse line with SMC-specific deletion of Has3 and simultaneous SMC-lineage tracing ( e YFP [enhanced yellow fluorescent protein]) on an Apoe −/− background was used. Lineage tracing of SMC with e YFP revealed that SMC-specific deletion of Has3 significantly increased the number of LGALS3 + (galectin-3) transition state SMC and decreased ACTA2 + (alpha-smooth muscle actin) SMC. Notably, SMC- Has3 deletion led to significantly increased collagen deposition and maturation within the fibrous cap and the whole lesion, as evidenced by picrosirius red staining and LC-PolScope analysis. Single-cell RNA sequencing of brachiocephalic artery lesions demonstrated that the loss of SMC- Has3 enhanced the transition of SMC to a Lgals3 + , ECM-producing phenotype with elevated acute-phase response gene expression. Experiments using cultured murine aortic SMC revealed that blocking CD44 (cluster of differentiation-44), an important hyaluronan binding receptor, recapitulated the enhanced acute-phase response, and synthesis of fibrous ECM. Conclusions: These studies provide evidence that the deletion of SMC- Has3 results in an ECM-producing transition state SMC phenotype (characterized by LGALS3 + expression), likely via reduced CD44 signaling, resulting in increased collagen formation and maturation, an index consistent with increased plaque stability.
Micropeptide ASAP encoded by LINC00467 promotes colorectal cancer progression by directly modulating ATP synthase activity
Authors: Qiwei Ge, Dingjiacheng Jia, Dong Cen, Yadong Qi, Chengyu Shi, Junhong Li, Lingjie Sang, Luo-jia Yang, Jiamin He, Aifu Lin, Shujie Chen, Liangjing Wang
Journal: Journal of Clinical Investigation (2021)

Emerging evidence has shown that open reading frames inside long noncoding RNAs (lncRNAs) could encode micropeptides. However, their roles in cellular energy metabolism and tumor progression remain largely unknown. Here, we identified a 94 amino acid–length micropeptide encoded by lncRNA LINC00467 in colorectal cancer. We also characterized its conservation across higher mammals, localization to mitochondria, and the concerted local functions. This peptide enhanced the ATP synthase construction by interacting with the subunits α and γ (ATP5A and ATP5C), increased ATP synthase activity and mitochondrial oxygen consumption rate, and thereby promoted colorectal cancer cell proliferation. Hence, this micropeptide was termed ATP synthase–associated peptide (ASAP). Furthermore, loss of ASAP suppressed patient-derived xenograft growth with attenuated ATP synthase activity and mitochondrial ATP production. Clinically, high expression of ASAP and LINC00467 predicted poor prognosis of colorectal cancer patients. Taken together, our findings revealed a colorectal cancer–associated micropeptide as a vital player in mitochondrial metabolism and provided a therapeutic target for colorectal cancer.
Abstract EP08: Cardiometabolic Diseases, Quality Of Life And Sleep In Adults With Hiv In The Deep South
Authors: Ene M Enogela, Raymond Jones, Thomas W Buford, Pariya L Wheeler
Journal: Circulation (2022)

Introduction: Cardiometabolic diseases (CMDs) are prevalent among middle-aged and older people living with HIV (OPLWH), particularly in the Deep South. However, the role CMDs play on quality-of-life outcomes among OPLWH remain understudied. Purpose: The purpose of this observational study was to examine the association between CMDs and physical health-related quality of life (P-HRQOL) and quality of sleep among PLWH in the Deep South. Methods: This cross-sectional study included N=261 HIV-infected participants aged 40+ recruited from a University HIV/AIDS clinic located in the Southeastern United States. CMDs were self-reported and consisted of hypertension, heart failure, stroke, diabetes mellitus, Angina due to heart disease, and high cholesterol. P-HRQOL and sleep quality scores were obtained using the Medical Outcome Study HIV Health Survey (MOS-HIV) and Pittsburgh sleep quality index (PSQI). We performed regression analyses (adjusting for demographic confounders and depression) for each outcome to assess the association between CMDs and P-HRQOL and sleep quality among OPLWH. Results: The average age of participants was 51.10 ± 6.78, with 82.8% being non-white and 35.6% being males. The overall prevalence of having ≥ 1CMD was 64.4% (High cholesterol: 52.8%; Diabetes Mellitus: 22.8%; Stroke: 5.68%; Angina/chest pain: 4.5%; Heart Failure: 6.8%; Hypertension 84%). P-HRQOL scores were significantly lower in PLWH with ≥1 CMD compared to the non-CMD group (45.53 ± 11.54 Vs. 49.67 ± 10.77, p&lt;0.01). PSQI sleep disturbance scores were significantly higher among participants with ≥1CMD compared to the non-CMD group (9.28 ± 4.42 vs. 7.26 ± 4.17, p&lt;0.01). In the covariate adjusted regression analysis, each additional CMD resulted in a 1.83 decrease in P-HRQOL while PSQI sleep disturbance increased by 0.74. Conclusion: In a sample of PLWH in the Deep South, the presence of CMDs increased the risk for poor P-HRQOL and greater sleep disturbances. Interventions that focus on targeting P-HRQOL and sleep quality in OPLWH with CMDs are necessary to improve long-term outcomes.
Robust Response to Futibatinib in a Patient With Metastatic FGFR-Addicted Cholangiocarcinoma Previously Treated Using Pemigatinib
Authors: Anil K. Rengan, Crystal S. Denlinger
Journal: Journal of the National Comprehensive Cancer Network (2022)

Abstract Futibatinib is a novel FGFR inhibitor currently under investigation as a second-line treatment for locally advanced or metastatic cholangiocarcinoma harboring FGFR2 gene fusions and rearrangements. As FGFR -targeted therapies move into the frontline setting, sequencing of these drugs remains undetermined. To date, no study has investigated the use of futibatinib in the context of pemigatinib resistance. We describe a 50-year-old woman with metastatic FGFR -aberrant intrahepatic cholangiocarcinoma who showed a robust response to futibatinib for 23.6 months, having previously benefited from pemigatinib. Futibatinib was safely used despite her history of decompensated cirrhosis and significant cytopenias. We observed a reduction in CA 19-9 level and a partial radiographic response on futibatinib. Serial next-generation sequencing and cell-free DNA testing proved crucial to making appropriate treatment decisions.
SARS-CoV-2 infection and vaccination trigger long-lived B and CD4+ T lymphocytes with implications for booster strategies
Authors: Alessio Mazzoni, Anna Vanni, Michele Spinicci, Giulia Lamacchia, Seble Tekle Kiros, Arianna Rocca, Manuela Capone, Nicoletta Di Lauria, Lorenzo Salvati, Alberto Carnasciali, Elisabetta Mantengoli, Parham Farahvachi, Lorenzo Zammarchi, Filippo Lagi, Maria Grazia Colao, Francesco Liotta, Lorenzo Cosmi, Laura Maggi, Alessandro Bartoloni, Gian Maria Rossolini, Francesco Annunziato
Journal: Journal of Clinical Investigation (2022)

BACKGROUNDImmunization against SARS-CoV-2, the causative agent of COVID-19, occurs via natural infection or vaccination. However, it is currently unknown how long infection- or vaccination-induced immunological memory will last.METHODSWe performed a longitudinal evaluation of immunological memory to SARS-CoV-2 up to 1 year after infection and following mRNA vaccination in naive individuals and individuals recovered from COVID-19 infection.RESULTSWe found that memory cells are still detectable 8 months after vaccination, while antibody levels decline significantly, especially in naive individuals. We also found that a booster injection is efficacious in reactivating immunological memory to spike protein in naive individuals, whereas it was ineffective in previously SARS-CoV-2-infected individuals. Finally, we observed a similar kinetics of decay of humoral and cellular immunity to SARS-CoV-2 up to 1 year following natural infection in a cohort of unvaccinated individuals.CONCLUSIONShort-term persistence of humoral immunity, together with the reduced neutralization capacity versus the currently prevailing SARS-CoV-2 variants, may account for reinfections and breakthrough infections. Long-lived memory B and CD4+ T cells may protect from severe disease development. In naive individuals, a booster dose restored optimal anti-spike immunity, whereas the needs for vaccinated individuals who have recovered from COVID-19 have yet to be defined.FUNDINGThis study was supported by funds to the Department of Experimental and Clinical Medicine, University of Florence (Project Excellence Departments 2018-2022), the University of Florence (project RICTD2122), the Italian Ministry of Health (COVID-2020-12371849), and the region of Tuscany (TagSARS CoV 2).
HER2-Negative Schnitzler Metastasis to the Rectum Detected Using 18F-FDG PET/CT
Authors: Shu Wang, Shan Jing, Bulin Du, Yaming Li, Xuena Li
Journal: Clinical Nuclear Medicine (2022)

Gastric carcinoma metastasis occurs via hematogenous, lymphatic, or peritoneal seeding. We describe FDG PET/CT findings of Schnitzler metastasis to the rectum in a 39-year-old woman who had radical gastrectomy for signet ring gastric adenocarcinoma 2 years prior. FDG PET/CT demonstrated increased homogeneous round activity in the inner layer of rectal wall. Occult metastases of gastric carcinoma tend to be difficult to treat and have a poor prognosis. However, in some cases, FDG PET/CT might be beneficial for early detection and diagnosis of Schnitzler metastasis.
TREM2 interacts with TDP-43 and mediates microglial neuroprotection against TDP-43-related neurodegeneration
Authors: Manling Xie, Yong U. Liu, Shunyi Zhao, Lingxin Zhang, Dale B. Bosco, Yuan-Ping Pang, Jun Zhong, Udit Sheth, Yuka A. Martens, Na Zhao, Chia-Chen Liu, Yongxian Zhuang, Liewei Wang, Dennis W. Dickson, Mark P. Mattson, Guojun Bu, Long-Jun Wu
Journal: Nature Neuroscience (2021)
Cancer Screening—The Good, the Bad, and the Ugly
Authors: H. Gilbert Welch
Journal: JAMA Surgery (2022)

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