tbuckley/cabot-search huggingface dataset:
Improvement of High‐Density Lipoprotein Function in Patients With Early Rheumatoid Arthritis Treated With Methotrexate Monotherapy or Combination Therapies in a Randomized Controlled Trial
Authors: Christina Charles‐Schoeman, Yuen Yin Lee, Ani Shahbazian, Xiaoyan Wang, David Elashoff, Jeffrey R. Curtis, Iris Navarro‐Millán, Shuo Yang, Lang Chen, Stacey S. Cofield, Larry W. Moreland, Harold Paulus, James O'Dell, Joan Bathon, S. L. Bridges, Srinivasa T. Reddy
Journal: Arthritis & Rheumatology (2016)

Abnormal function of high-density lipoprotein (HDL) has been implicated as a potential mechanism for the increased incidence of cardiovascular (CV) disease in patients with rheumatoid arthritis (RA). This study was undertaken to evaluate changes in HDL function and HDL-associated proteins over 2 years of follow-up in patients with early RA receiving either methotrexate (MTX) monotherapy, MTX + etanercept (ETN) combination therapy, or MTX + sulfasalazine (SSZ) + hydroxychloroquine (HCQ) triple therapy in the Treatment of Early Aggressive Rheumatoid Arthritis (TEAR) trial.The antioxidant capacity of HDL, paraoxonase 1 (PON-1) activity, and levels of HDL-associated haptoglobin (Hp), HDL-associated apolipoprotein A-I (Apo A-I), and myeloperoxidase (MPO) were measured in 550 TEAR participants at 4 time points (time 0 [pretreatment] and at 24, 48, and 102 weeks of treatment). Repeated-measures analysis using mixed-effects linear models with an autoregressive covariate structure was performed to model the within-subject covariance over time.Mixed-effects models, which were controlled for traditional CV risk factors, treatment regimen, prednisone use, and statin use, demonstrated significant associations between RA disease activity, measured using the Disease Activity Score in 28 joints, erythrocyte sedimentation rate, or C-reactive protein level, and the profile of HDL function over time. Specifically, decreases in RA disease activity over time were associated with increases in PON-1 activity and levels of HDL-associated Apo A-I, and decreases in the HDL inflammatory index and levels of MPO and HDL-associated Hp.Reduced disease activity in patients with early RA treated with MTX monotherapy, MTX + ETN combination therapy, or MTX + SSZ + HCQ triple therapy in the TEAR trial was associated with improvements in the HDL function profile. Additional studies are warranted to evaluate abnormal HDL function as a potential mechanism and therapeutic target for CV risk in patients with RA.
Giving Calcification Its Due: Recognition of a Diverse Disease
Authors: Joshua D. Hutcheson, Mark C. Blaser, Elena Aikawa
Journal: Circulation Research (2017)

C ardiovascular calcification is a growing burden and a leading predictor of and contributor to acute cardiovascular events.Arterial calcification associates with a 4-fold increase in cardiovascular events, and patients with aortic valve calcification have a 5-year event-free survival rate of only 26%, 1,2 worse than that of many cancers.Despite massive healthcare costs and extensive research efforts, effective therapeutic strategies remain elusive.Cardiovascular calcification, often generalized as one disease, is in reality a multifaceted disorder that occurs in diverse milieus as a result of multiple, interacting pathogenic processes.Herein, we explore these variables and propose a set of guidelines for studying cardiovascular calcification. Variability Between TissuesAlthough vascular and valvular calcification share several risk factors, only ≈25% to 50% of patients with aortic valve calcification also present with significant coronary artery disease, 3 suggesting that common risk factors initiate divergent disease processes.
Abstract B32: Feedback optimized gene electrotransfer for immunotherapy
Authors: Douglas W. Brown, Arya J. Bahrami, David A. Canton, Yi Xu, Gavin Y. Tse, Jean S. Campbell, Robert H. Pierce, Richard J. Connolly
Journal: Cancer Research (2017)

Abstract Intratumoral electroporation of proinflammatory cytokine-encoding plasmid DNA promotes innate and adaptive immune responses that correlate with abscopal effects. The conditions selected to electroporate tumors are typically fixed parameters optimized in preclinical tumor models. These conditions have little translatability to clinically relevant tumors, as idealized models fail to capture the variability encountered in clinical tumors. Variables that affect treatment outcome include tumor size, degree of vascularization, fibrosis, and necrosis. These variables can result in sub-optimal gene transfer and variable therapeutic outcomes. To address the need to advance the practice of electroporation, a feedback controlled electroporation generator has been developed, which is capable of assessing the electrophysiological properties of tissue in real-time. Determination of these properties is accomplished by electrochemical impedance spectroscopy and model parameter estimation. Model parameters that estimate membrane integrity are used to adjust electroporation parameters for each applied pulse and stop the process when optimum gene transfer conditions are identified. Studies performed in syngeneic colon carcinoma tumors (MC38) and spontaneous mammary tumors (MMTV-PyVT) have demonstrated feedback-based electroporation is capable of achieving maximum expression of reporter genes with minimal collateral cell death. These findings represent an unprecedented advancement to the practice of gene electro-transfer, as retaining the viability of transfected cells is paramount to treatment success. Citation Format: Douglas W. Brown, Arya J. Bahrami, David A. Canton, Yi Xu, Gavin Y. Tse, Jean S. Campbell, Robert H. Pierce, Richard J. Connolly. Feedback optimized gene electrotransfer for immunotherapy. [abstract]. In: Proceedings of the AACR Special Conference on Engineering and Physical Sciences in Oncology; 2016 Jun 25-28; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2017;77(2 Suppl):Abstract nr B32.
Epithelial expression and function of trypsin-3 in irritable bowel syndrome
Authors: Claire Rolland-Fourcade, Alexandre Denadai-Souza, Carla Cirillo, Cintya Lopez, Josue Obed Jaramillo, Cleo Desormeaux, Nicolas Cenac, Jean-Paul Motta, Muriel Larauche, Yvette Taché, Pieter Vanden Berghe, Michel Neunlist, Emmanuel Coron, Sylvain Kirzin, Guillaume Portier, Delphine Bonnet, Laurent Alric, Stephen Vanner, Celine Deraison, Nathalie Vergnolle
Journal: Gut (2017)

<h3>Objectives</h3> Proteases are key mediators of pain and altered enteric neuronal signalling, although the types and sources of these important intestinal mediators are unknown. We hypothesised that intestinal epithelium is a major source of trypsin-like activity in patients with IBS and this activity signals to primary afferent and enteric nerves and induces visceral hypersensitivity. <h3>Design</h3> Trypsin-like activity was determined in tissues from patients with IBS and in supernatants of Caco-2 cells stimulated or not. These supernatants were also applied to cultures of primary afferents. mRNA isoforms of trypsin (<i>PRSS1</i>, <i>2</i> and <i>3</i>) were detected by reverse transcription-PCR, and trypsin-3 protein expression was studied by western blot analysis and immunohistochemistry. Electrophysiological recordings and Ca<sup>2+</sup> imaging in response to trypsin-3 were performed in mouse primary afferent and in human submucosal neurons, respectively. Visceromotor response to colorectal distension was recorded in mice administered intracolonically with trypsin-3. <h3>Results</h3> We showed that stimulated intestinal epithelial cells released trypsin-like activity specifically from the basolateral side. This activity was able to activate sensory neurons. In colons of patients with IBS, increased trypsin-like activity was associated with the epithelium. We identified that trypsin-3 was the only form of trypsin upregulated in stimulated intestinal epithelial cells and in tissues from patients with IBS. Trypsin-3 was able to signal to human submucosal enteric neurons and mouse sensory neurons, and to induce visceral hypersensitivity in vivo, all by a protease-activated receptor-2-dependent mechanism. <h3>Conclusions</h3> In IBS, the intestinal epithelium produces and releases the active protease trypsin-3, which is able to signal to enteric neurons and to induce visceral hypersensitivity.
The Grey Zone between Burkitt and Diffuse Large B Cell Lymphomas: Impact of Chromosomal Breakponts at Myc and Other Loci.
Authors: Eugenia Haralambieva, Evert-jan Boerma, Gustaaf van Imhoff, Stefano Rosati, Ed Schuuring, Hans-Konrad Mueller-Hermelink, Philip M. Kluin, German Ott
Journal: Blood (2004)
Donor C3435T Polymorphism in the Multidrug Resistance 1 (MDR1) Gene Is Associated with the Incidence of Acute and Chronic Graft-Versus-Host Disease after Allogeneic Hematopoietic Stem Cell Transplantation.
Authors: Avichai Shimoni, Olga Ostrovsky, Hanan Galski, Izhar Hardan, Noga Shem-Tov, Ronit Yerushalmi, Antonis Papatryphonos, Arnon Nagler
Journal: Blood (2006)
A Whole Genome Analysis Identifies SLCO1B1 as a Determinant of Methotrexate Pharmacokinetics and Adverse Effects
Authors: Lisa R Trevino, Noriko Shimasaki, Wenjian Yang, John C. Panetta, Cheng Cheng, Deqing Pei, Diana Chan, Alex Sparreboom, Kathleen M Giacomini, Ching-Hon Pui, William E. Evans, Mary V. Relling
Journal: Blood (2008)
Improved Outcome of Combination Therapy with ATRA, Anthracyclines and Cytarabine, AML99-M3 Protocol, for Childhood Acute Promyelocytic Leukemia.
Authors: Masue Imaizumi, Akio Tawa, Ryoji Hanada, Masahiro Tsuchida, Ken Taguchi, Ryoji Kobayashi, Akira Morimoto, Hideki Nakayama, Kazuko Hamamoto, Kazuko Kudo, Hiromasa Yabe, Hisato Kigasawa, Keizo Horibe, Shigeru Tsuchiya, Ichiro Tsukimoto
Journal: Blood (2005)
Azacitidine Prolongs Overall Survival (OS) and Reduces Infections and Hospitalizations in Patients (Pts) with WHO-Defined Acute Myeloid Leukemia (AML) Compared with Conventional Care Regimens (CCR)
Authors: Pierre Fenaux, Ghulam J Mufti, Eva Hellström-Lindberg, Valeria Santini, Norbert Gattermann, Guillermo Sanz, Alan F. List, Steven D. Gore, John F Seymour, Jay Backstrom, Linda Zimmerman, David McKenzie, C. L. Beach, Lewis B. Silverman
Journal: Blood (2008)
<i>Notes from the Field</i>: Pan-Resistant New Delhi Metallo-Beta-Lactamase-Producing <i>Klebsiella pneumoniae</i> — Washoe County, Nevada, 2016
Authors: Lei Chen, Randall Todd, Julia Kiehlbauch, Maroya Walters, Alexander Kallen
Journal: MMWR Morbidity and Mortality Weekly Report (2017)
A Detailed Analysis of Myelodysplastic Syndrome Complicated By Autoimmune or Inflammatory Disorders: A Possible Efficacy of Low-Dose Lenalidomide
Authors: Yasunobu Takeoka, Akiko Miura, Koji Nakamura, Junko Nakamura, Ryosuke Yamamura, Taku Araki, Hirohisa Nakamae, Masayuki Hino, Kensuke Ohta
Journal: Blood (2014)
Prostate-specific IL-6 transgene autonomously induce prostate neoplasm through amplifying inflammation in the prostate and peri-prostatic adipose tissue
Authors: Gang Liu, Jinyu Zhang, Lewis Frey, Xiao Gang, Kongming Wu, Qian Liu, Michael Lilly, Jennifer Wu
Journal: Journal of Hematology & Oncology (2017)

The causative role of the pro-inflammatory cytokine IL-6 in prostate cancer progression has been well established at molecular level. However, whether and how IL-6 may play a role in prostate cancer risk and development is not well defined. One limitation factor to acquiring this knowledge is the lack of appropriate animal models. We generated a novel line of prostate-specific IL-6 transgenic mouse model. We compared the prostate pathology, tumorigenic signaling components, and prostate tumor microenvironment of the IL-6 transgenic mice with wild type littermates. With this model, we demonstrate that IL-6 induces prostate neoplasm autonomously. We further demonstrate that transgenic expression of IL-6 in the prostate activates oncogenic pathways, induces autocrine IL-6 secretion and steadily-state of STAT3 activation in the prostate tissue, upregulates paracrine insulin-like growth factor (IGF) signaling axis, reprograms prostate oncogenic gene expression, and more intriguingly, amplifies inflammation in the prostate and peri-prostatic adipose tissue. The pro-inflammatory IL-6 is autonomous oncogene for the prostate. IL-6 induces prostate oncogenesis through amplifying local inflammation. We also presented a valuable animal model to study inflammation and prostate cancer development.
A Phase 1 Study of the Anti-CD37 Antibody-Drug Conjugate AGS67E in Advanced Lymphoid Malignancies. Interim Results
Authors: Ahmed Sawas, Kerry J. Savage, Raymond Perez, Ranjana H Advani, Anna Butturini, Jacqueline Lackey, Fabio Trave, Banmeet Anand, Yao Huang, Leonard Reyno, Owen A. O'Connor
Journal: Blood (2015)
Incidence of Febrile Episode During Stem Cell Mobilization (SCM) After High Dose Ciclophosphamide Chemotherapy (HD-CTX) and G-CSF (filgrastim or lenograstim) Administration in Multiple Myeloma (MM) Patients: II Interim Evaluation
Authors: Enrico Orciuolo, Gabriele Buda, E. Mauro, E. Marturano, Domenico Pastore, Paola Della Cioppa, Giuseppe Pietrantuono, Letizia Lombardini, Nicola Di Renzo, Giuseppe Irrera, Clotilde Cangialosi, Marino Brunori, Mario Petrini
Journal: Blood (2008)
CNS-targeted autoimmunity leads to increased influenza mortality in mice
Authors: Justin D. Glenn, Matthew D. Smith, Pei Xue, Yee Chan-Li, Samuel Collins, Peter A. Calabresi, Maureen R. Horton, Katharine A. Whartenby
Journal: The Journal of Experimental Medicine (2017)

The discovery that central nervous system (CNS)–targeted autoreactive T cells required a process of licensing in the lung revealed an unexpected relationship between these organs. The clinical and immunological significance of this finding is bidirectional in that it showed not only a mechanism by which T cells become pathogenic before entering the CNS, but also the potential for this process to influence lung immunity as well. Epidemiological studies have shown that people with multiple sclerosis (MS) suffer from increased morbidity and mortality from infectious diseases, independent of immunosuppressive therapies. Respiratory infections account for a large percentage of deaths of people with MS. In this study, to investigate the mechanisms responsible for this enhanced susceptibility, we established a comorbid model system in which mice with experimental autoimmune encephalomyelitis (EAE) were administered a sublethal dose of influenza. Whereas mice with either EAE alone or influenza alone survived, 70% of comorbid mice died as a result of uncontrolled viral replication. Immunological analyses revealed that the induction of EAE led to a surprising alteration of the lung milieu, converting an effective stimulatory influenza-reactive environment into a suppressive one. These results provide mechanistic information that may help to explain the unexpected immunological interactions.
Flavopiridol Can Be Safely Administered Using a Pharmacologically Derived Schedule and Demonstrates Activity In Relapsed and Refractory Non-Hodgkin's Lymphoma.
Authors: Jeffrey A. Jones, Leslie Andritsos, Robert Baiocchi, Don M Benson, Kristie A. Blum, Beth Christian, Deidre Deam, Joseph M. Flynn, Amy J. Johnson, Mitch A. Phelps, Pierluigi Porcu, John C. Byrd, Michael R. Grever
Journal: Blood (2010)
Promising Efficacy with the New Anti-CD20 Antibody GA101 In Heavily Pre-Treated NHL Patients – First Results From a Phase II Study In Patients with Relapsed/Refractory DLBCL and MCL
Authors: Guillaume Cartron, Catherine Thieblemont, Philippe Solal-Celigny, Franck Morschhhauser, Corinne Haioun, Reda Bouabdallah, Thierry Lamy, Noel Milpied, Steven Le Gouill, Pierre Feugier, Joe Birkett, Michael K. Wenger, Elina Asikanius, Gilles Salles
Journal: Blood (2010)
Impaired SUMOylation of nuclear receptor LRH-1 promotes nonalcoholic fatty liver disease
Authors: Sokrates Stein, Vera Lemos, Pan Xu, Hadrien Demagny, Xu Wang, Dongryeol Ryu, Veronica Jimenez, Fatima Bosch, Thomas F. Lüscher, Maaike H. Oosterveer, Kristina Schoonjans
Journal: Journal of Clinical Investigation (2017)

Hepatic steatosis is caused by metabolic imbalances that could be explained in part by an increase in de novo lipogenesis that results from increased sterol element binding protein 1 (SREBP-1) activity. The nuclear receptor liver receptor homolog 1 (LRH-1) is an important regulator of intermediary metabolism in the liver, but its role in regulating lipogenesis is not well understood. Here, we have assessed the contribution of LRH-1 SUMOylation to the development of nonalcoholic fatty liver disease (NAFLD). Mice expressing a SUMOylation-defective mutant of LRH-1 (LRH-1 K289R mice) developed NAFLD and early signs of nonalcoholic steatohepatitis (NASH) when challenged with a lipogenic, high-fat, high-sucrose diet. Moreover, we observed that the LRH-1 K289R mutation induced the expression of oxysterol binding protein-like 3 (OSBPL3), enhanced SREBP-1 processing, and promoted de novo lipogenesis. Mechanistically, we demonstrated that ectopic expression of OSBPL3 facilitates SREBP-1 processing in WT mice, while silencing hepatic Osbpl3 reverses the lipogenic phenotype of LRH-1 K289R mice. These findings suggest that compromised SUMOylation of LRH-1 promotes the development of NAFLD under lipogenic conditions through regulation of OSBPL3.
Simultaneous Analysis of Multiple Chromosomal Aberrations in Chronic Lymphocytic Leukemia (CLL) by Multiplex Ligation-Dependent Probe Amplification (MLPA).
Authors: Marian J.P.L. Stevens-Kroef, Annet Simons, Michael Egmont Petersen, Hanneke Gorissen, Yvonne Nanciu, Arjan Buijs, Reinier Raymakers, Ad Geurts van Kessel
Journal: Blood (2006)
Mechanisms, Pathophysiology, and Management of Obesity
Authors: Steven B. Heymsfield, Thomas A. Wadden
Journal: New England Journal of Medicine (2017)

Obesity is prevalent in the U.S. population and contributes significantly to morbidity and mortality. Treatments include behavioral therapy, pharmacotherapy, and bariatric surgery. Some sequelae of obesity are reversed with weight loss. Maintaining weight loss is a challenge.
A Combination of EVI1 and PRDM16 Expression Clarified the Clinical Features of Intermediate/High Risk Patients in Pediatric Acute Myeloid Leukemia
Authors: Genki Yamato, Norio Shiba, Yusuke Hara, Myoung-Ja Park, Manabu Sotomatsu, Kentaro Ohki, Hitoshi Ichikawa, Daisuke Tomizawa, Takashi Taga, Keizo Horibe, Akio Tawa, Hirokazu Arakawa, Souichi Adachi, Yasuhide Hayashi
Journal: Blood (2015)
Economic Value and Cost-Effectiveness of Cardiac Resynchronization Therapy Among Patients With Mild Heart Failure
Authors: Michael R. Gold, Amie Padhiar, Stuart Mealing, Manpreet K. Sidhu, Stelios I. Tsintzos, William T. Abraham
Journal: JACC Heart Failure (2017)

This study investigated the cost effectiveness of early cardiac resynchronization therapy (CRT) implantation among patients with mild heart failure (HF). The differential cost effectiveness between CRT using a defibrillator (CRT-Ds) and CRT using a pacemaker (CRT-P) was also assessed.Cardiac resynchronization has been shown to be cost effective in New York Heart Association (NYHA) functional classes III/IV but is less studied in class II HF. The incremental costs of early CRT implementation in mild HF compared with the costs potentially avoided because of delaying disease progression to advanced HF are also unknown. Finally, combined biventricular pacing and defibrillator (CRT-D) devices are more expensive than biventricular pacemakers (CRT-P), but the relative cost effectiveness is controversial.Data from the 5-year follow-up phase of REVERSE (REsynchronization reVErses Remodeling in Systolic Left vEntricular Dysfunction) were used. The economics were evaluated from the U.S. Medicare perspective based on published clinical projections.Probabilistic estimates yielded $8,840/quality-adjusted life year (QALY) gained (95% confidence interval [CI]: $6,705 to $10,804/QALY gained) for CRT-ON versus CRT-OFF (i.e., programmed "ON" or "OFF" at pre-specified post-implantation timings) and $43,678/QALY gained for CRT-D versus CRT-P (95% CI: $35,164 to $53,589/QALY gained) over the patient's lifetime. Results were robust to choice of patient subgroup and alterations of ±10% to key model parameters. An "early" CRT-D class II strategy totaled $95,292 compared with $91,511 for a "late" implantation. An "early" implant offered on average 1.00 year of additional survival for $3,781, resulting in an ICER of $3,795/LY gained.This study demonstrates CRT cost effectiveness in mild HF. The incremental CRT-D costs are justified by the anticipated benefits, despite increased procurement costs and shorter generator longevities. "Early" CRT-D implants have essential cost parity with "late" implants while increasing the patient's survival. (REsynchronization reVErses Remodeling in Systolic Left vEntricular Dysfunction [REVERSE]; NCT00271154).
Correction: In vivo NCL targeting affects breast cancer aggressiveness through miRNA regulation
Authors: Flavia Pichiorri, Dario Palmieri, Luciana De Luca, Jessica Consiglio, Jia You, Alberto Rocci, Tiffany Talabere, Claudia Piovan, Alessandro Lagana, Luciano Cascione, Jingwen Guan, Pierluigi Gasparini, Veronica Balatti, Gerard Nuovo, Vincenzo Coppola, Craig C. Hofmeister, Guido Marcucci, John C. Byrd, Stefano Volinia, Charles L. Shapiro, Michael A. Freitas, Carlo M. Croce
Journal: The Journal of Experimental Medicine (2017)

Vol. 210, No. 5, May 2013. Pages [951–968][1].

The authors regret that in their original paper, the RNU6 loading control panels shown in Fig. 1 (E and F) were incorrect as a result of an error in figure presentation during the final production process. The conclusions of the experiments shown in
Lower adenoma miss rate with FUSE vs. conventional colonoscopy with proximal retroflexion: a randomized back-to-back trial
Authors: Ioannis Papanikolaou, Periklis Apostolopoulos, Georgios Tziatzios, Erasmia Vlachou, Athanasios Sioulas, Dimitrios Polymeros, Andreas Karameris, Ioannis Panayiotides, Georgios Alexandrakis, George Dimitriadis, Konstantinos Triantafyllou
Journal: Endoscopy (2017)

<b>Background and study aims</b> Full-spectrum colonoscopy (FSC) promises to increase adenoma detection by providing a wider field of view. The aim of this study was to compare adenoma miss rates of FSC with those of conventional colonoscopy complemented by right-colon re-examination using scope retroflexion (CC/R). <b>Patients and methods</b> At two tertiary endoscopy facilities, patients who were scheduled for colonoscopy for the assessment of symptoms or for colorectal cancer screening/surveillance were randomized (1:1) to undergo same-day, back-to-back colonoscopies (FSC or CC/R first), performed by one of five endoscopists who had documented adenoma detection rates > 35 %. Per-protocol data were analyzed. <b>Results</b> We randomized 220 patients. There were five FSC technical failures (three air pump and two left screen); therefore, 107 and 108 cases were analyzed in the FSC and CC/R index procedure arms, respectively. Withdrawal times were similar for FSC and CC/R (7.7 minutes vs. 7.6 minutes). Overall, we detected 3 cancers and 153 adenomas (FSC = 92; CC/R = 61); 81 were detected in the proximal colon, 3 of which were detected by retroflexed examination. By per-lesion analysis, FSC showed a significantly lower adenoma miss rate compared with CC/R overall (10.9 % [95 % confidence interval (CI) 3.8 to 18.1] vs. 33.7 % [95 %CI 23.4 to 44.1]) and in the proximal colon (13.9 % [95 %CI 2.6 to 25.2] vs. 42.2 % [95 %CI 27.8 to 56.7]). The advanced adenoma miss rate was lower with FSC overall (4.3 % [95 %CI – 4.0 to 12.7] vs. 25.9 % [95 %CI 9.4 to 42.5]). There were no adverse events. <b>Conclusions</b> FSC outperformed conventional colonoscopy with right-colon scope retroflexion in the detection of missed adenomas, both overall and in the proximal colon, even when performed by experienced endoscopists. Trial registered at ClinicalTrials.gov (NCT02117674).
Immunoglobulin G4 (IgG4)-Related Hypophysitis
Authors: Fabio Rotondo, Amro Qaddoura, Luis V. Syro, Jason Karamchandani, David G. Munoz, Mariam J. Arroyave, William P. Ospina, Michael D. Cusimano, Kalman Kovacs
Journal: Endocrine Pathology (2017)