tbuckley/cabot-search huggingface dataset:
Treatment until progression: Data of the “on-treatment” population of the FIRE-3 (AIO KRK-0306) study.
Authors: Sebastian Stintzing, Ludwig Fischer von Weikersthal, Thomas Decker, Alexander Kiani, Ursula Vehling-Kaiser, Salah-Eddin Al-Batran, Tobias Heintges, Christian Lerchenmueller, Christoph Kahl, Gernot Seipelt, Frank Kullmann, Martina Stauch, Carsten Hielscher, Swantje Held, Dominik Paul Modest, Markus H. Moehler, Werner Scheithauer, Andreas Jung, Thomas Kirchner, Volker Heinemann
Journal: Journal of Clinical Oncology (2015)

3589 Background: The FIRE-3 study (AIO KRK-0306) was designed as a randomized multicenter trial to compare the efficacy of FOLFIRI plus cetuximab (cet) to FOLFIRI plus bevacizumab (bev) as first-line treatment in KRAS WT mCRC patients. FOLFIRI plus cet as first-line treatment of KRAS WT mCRC patients resulted in comparable overall response rates (ORR) and progression free survival (PFS) when compared to FOLFIRI plus bev. Overall survival (OS) was significantly longer in the FOLFIRI plus cet arm. Methods: In this exploratory analysis outcome parameters were calculated in dependence of progression during antibody treatment. As reported before by Saltz et al. (ASCO GI 2007) an “on study treatment” population was defined using all RAS wild-type pts that were treated until progression or death occurred. To exclude early progressing patients the analysis was also performed in patients with a PFS >6 months. Results: See Table. Conclusions: In general, patients progressing during 1st-line treatment had a shorter PFS and OS than patients that had progressed after stop of treatment for any cause. Patients that discontinued treatment for other reasons than progression had a significantly longer median OS when treated with FOLFIRI plus cetuximab in first-line when compared to FOLFIRI plus bevacizumab. This effect was also seen after exclusion of early progressors (PFS <6 mo). All patients Median PFS (95% CI) p Median OS (95% CI) p PFS event during treatment FOLFIRI + Cet (n= 72 ) 7.6 (6.1-9.7) 0.94 22.6 (17.3-27.9) 0.50 FOLFIRI + Bev (n= 74 ) 7.4 (6.0-9.0) 20.8 (15.5-23.7) PFS event after treatment FOLFIRI + Cet (n= 106 ) 10.8 (10.0-13.3) 0.59 38.3 (27.1-45.0) 0.01 FOLFIRI + Bev (n= 111) 11.7 (10.3-13.1) 28.2 (24.8-33.3) Patients PFS >6months Median PFS (95% CI) p Median OS (95% CI) p PFS event during treatment FOLFIRI + Cet (n= 46 ) 11.0 (8.8-12.2) 0.85 27.9 (23.6-33.8) 0.85 FOLFIRI + Bev (n= 46) 9.9 (9.0-11.7) 26.1 (23.1-31.5) PFS event after treatment FOLFIRI + Cet (n= 91 ) 12.4 (10.5-14.1) 0.35 38.7 (36.4-49.8) 0.002 FOLFIRI + Bev (n= 100) 12.4 (11.1-13.4) 28.8 (25.6-35.0)
A Myeloablative Conditioning Regimen Is Required to Produce Durable Engraftment and Immune Reconsitution in Related and Unrelated Multi-Antigen HLA Mismatched Pan-T-Cell Depleted Limited T-Cell Add-Back Transplants.
Authors: Jack W. Hsu, Scott D. Rowley, Stuart L. Goldberg, David S. Siegel, Robert A. Preti, Andrew L. Pecora
Journal: Blood (2004)
Using Design Thinking to Differentiate Useful From Misleading Evidence in Observational Research
Authors: Steven N. Goodman, Sebastian Schneeweiss, Michael Baiocchi
Journal: JAMA (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
NR1D1 Recruitment to Sites of DNA Damage Inhibits Repair and Is Associated with Chemosensitivity of Breast Cancer
Authors: Na-Lee Ka, Tae-Young Na, Hyelin Na, Min-Ho Lee, Han-Su Park, Sewon Hwang, Il Yong Kim, Je Kyung Seong, Mi-Ock Lee
Journal: Cancer Research (2017)

Abstract DNA repair capacity is critical for survival of cancer cells upon therapeutic DNA damage and thus is an important determinant of susceptibility to chemotherapy in cancer patients. In this study, we identified a novel function of nuclear receptor NR1D1 in DNA repair, which enhanced chemosensitivity in breast cancer cells. NR1D1 inhibited both nonhomologous end joining and homologous recombination double-strand breaks repair, and delayed the clearance of γH2AX DNA repair foci that formed after treatment of doxorubicin. PARylation of NR1D1 by PARP1 drove its recruitment to damaged DNA lesions. Deletion of the ligand binding domain of NR1D1 that interacted with PARP1, or treatment of 6-(5H)-phenanthridinone, an inhibitor of PARP1, suppressed the recruitment of NR1D1 to DNA damaged sites, indicating PARylation as a critical step for the NR1D1 recruitment. NR1D1 inhibited recruitment of the components of DNA damage response complex such as SIRT6, pNBS1, and BRCA1 to DNA lesions. Downregulation of NR1D1 in MCF7 cells resulted in resistance to doxorubicin, both in vitro and in vivo. Analysis of four public patient data sets indicated that NR1D1 expression correlates positively with clinical outcome in breast cancer patients who received chemotherapy. Our findings suggest that NR1D1 and its ligands provide therapeutic options that could enhance the outcomes of chemotherapy in breast cancer patients. Cancer Res; 77(9); 2453–63. ©2017 AACR.
Subject Index Vol. 63, 1995
Authors: Ross J. Baldessarini, G. Nordby, Ø. Ekeberg, S. Knardahl, I. Os, Jan K. Bleeker, Leida M. Lamers, Ineke M. Leenders, Dick C. Kruyssen, Maarten L. Simoons, Rutger W. Trijsburg, Ruud A. Erdman, Isao Fukunishi, Takashi Moroji, Shohei Okabe, M.Z. Azhar, S.L. Varma, Marcin Ziółkowski, Tomasz Gruss, Janusz K. Rybakowski, P. Cathébras, L. Jacquin, M. le Gal, C. Fayol, K. Bouchou, H. Rousset, Galina Velikova, Peter J. Selby, Philip R. Snaith, Paul G. Kirby, C.L. Mulder, M.H. Antoni, P.M.G. Emmelkamp, P.J. Veugelers, T.G.M. Sandfort, F.A.J.R. van de Vijver, M.J. de Vries, G.W.B. Näring, C.P.F. van der Staak, Mark A. Lumley, Kevin J. Roby, Jonathan E. Alpert, Lisa A. Uebelacker, Nancy E. McLean, Melissa Abraham, Jerrold F. Rosenbaum, Maurizio Fava, E.M. Friedman
Journal: Psychotherapy and Psychosomatics (1995)
Characterization of Early Human B Cell Development by Gene Expression Profiling.
Authors: Marit E. Hystad, Trond H. Bo, Edith Rian, June H. Myklebust, Einar Sivertsen, Lise Forfang, Michael Chiorazzi, Andreas Rosenwald, Inge Jonassen, Louis M. Staudt, Erlend B. Smeland
Journal: Blood (2006)
Praise for an Obituary
Authors: Donald A. B. Lindberg
Journal: JAMA (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Abstract P4-03-07: Inhibition of cancer-associated fibroblast function by farnesoid X receptor activation: Experimental basis for a novel therapeutic strategy in breast cancer
Authors: I Barone, V Vircillo, C Giordano, R Tarallo, A Rinaldi, G Bruno, D Bonofiglio, S Catalano, S Ando'
Journal: Cancer Research (2017)

Abstract This abstract was withdrawn by the authors.
Surgical Training to Proficiency
Authors: Pamela A. Lipsett
Journal: JAMA Surgery (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Surgery HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Surgery journal
Erratum: Hepatic expansion of a virus-specific regulatory CD8+ T cell population in chronic hepatitis C virus infection (Journal of Clinical Investigation (2004) 113 (963-972) DOI:10.1172/JCI200420515)
Authors: Daniele Accapezzato, Vittorio Francavilla, Marino Paroli, Marco Casciaro, Lucia Valeria Chircu, Agostino Cividini, Sergio Abrignani, Mario U. Mondelli, Vincenzo Barnaba
Journal: Journal of Clinical Investigation (2004)
A Novel Observation That Heme Oxygenase-1 (HO-1) Deficient Mice Are Easy Mobilizers and That HO-1 Plays An Important Role in Maintaining Expression of SDF-1 in Bone Marrow (BM) Stroma and Promotes Retention of Hematopoietic Stem/Progenitor Cells (HSPCs) in the Bone Marrow Microenvironment
Authors: Marcin Wysoczynski, Janina Ratajczak, Gregg Rokosh, Roberto Bolli, Mariusz Z Ratajczak
Journal: Blood (2011)
Novel Mutations of the JAK2 Gene and Erythropoietin Receptor Gene in Japanese Chronic Myeloproliferative Diseases.
Authors: Mitsuharu Inami, Hiroki Yamaguchi, Setsuo Hasegawa, Seiji Gomi, Ayako Watanabe, Fumiko Kosaka, Yoshio Mitamura, Ai Kobayashi, Sayaka Kimura, Kazuo Dan, Koiti Inokuchi
Journal: Blood (2007)
Preclinical Characterization of TTI-281, a Novel, Orally Bioavailable BET Inhibitor: Predictive Biomarker Identification and Combination Treatment Analysis
Authors: Jaehyun Choi, Chunlei Wang, Zezhou Wang, Aaron D. Schimmer, Penka S. Petrova, Malik Slassi, Robert A. Uger
Journal: Blood (2016)
Distinct Clinical and Biological Implications of Various DNTMT3A Mutations in Myeloid Neoplasms
Authors: Suresh Kumar Balasubramanian, Mai Ali, Taha Bat, Bhumika Patel, Bartlomiej P Przychodzen, Cassandra M. Hirsch, Aziz Nazha, Hetty E. Carraway, Mikkael A. Sekeres, Jaroslaw P Maciejewski
Journal: Blood (2016)
Fecal microbiota transplantation in metabolic syndrome: History, present and future
Authors: P. F. de Groot, M. N. Frissen, N. C. de Clercq, M. Nieuwdorp
Journal: Gut Microbes (2017)

The history of fecal microbiota transplantation (FMT) dates back even to ancient China. Recently, scientific studies have been looking into FMT as a promising treatment of various diseases, while in the process teaching us about the interaction between the human host and its resident microbial communities. Current research focuses mainly on Clostridium difficile infections, however interest is rising in other areas such as inflammatory bowel disease (IBD) and the metabolic syndrome.With regard to the latter, the intestinal microbiota might be causally related to the progression of insulin resistance and diabetes. FMT in metabolic syndrome has proven to be an intriguing method to study the role of the gut microbiota and open the way to new therapies by dissecting in whom insulin resistance is driven by microbiota. In this article we review the history of FMT, the present evidence on its role in the pathophysiology of metabolic syndrome and its efficacy, limitations and future prospects.
Optimizing a Drone Network to Deliver Automated External Defibrillators
Authors: Justin J. Boutilier, Steven C. Brooks, Alyf Janmohamed, Adam Byers, Jason E. Buick, Cathy Zhan, Angela P. Schoellig, Sheldon Cheskes, Laurie J. Morrison, Timothy C. Y. Chan
Journal: Circulation (2017)

Public access defibrillation programs can improve survival after out-of-hospital cardiac arrest, but automated external defibrillators (AEDs) are rarely available for bystander use at the scene. Drones are an emerging technology that can deliver an AED to the scene of an out-of-hospital cardiac arrest for bystander use. We hypothesize that a drone network designed with the aid of a mathematical model combining both optimization and queuing can reduce the time to AED arrival.
Identification of CCND2 As a RUNX1/ETO Target Required for Leukaemic Propagation
Authors: Lynsey McKenzie, Natalia Martinez-Soria, Julia Draper, Sirintra Nakjang, Helen J Blair, Christian Wichmann, Josef Vormoor, Constanze Bonifer, Georges Lacaud, Olaf Heidenreich
Journal: Blood (2016)
Replacement Therapy for Surgery in FVII Deficiency: The Ster Experience Concerning 63 Interventions.
Authors: Guglielmo Mariani, Angelika Batorova, Alberto Dolce, Sergio Siragusa, Mario Lapecorella, Jens Bierre Knudsen, Giovanni Di Minno, Elvira Grandone, Giuseppe Tagariello, AnnaRita Tagliaferri, Guenter K.H. K.H. Auerswald, Jørgen Ingerslev
Journal: Blood (2009)
Abstract P3-08-08: Preferences for breast cancer risk reduction among <i>BRCA1</i> and <i>BRCA2</i> mutation carriers: A discrete choice experiment
Authors: A Liede, G Evans, KA Metcalfe, M Price, C Snyder, HT Lynch, S Friedman, J Amelio, J Posner, G Lindeman, CA Mansfield
Journal: Cancer Research (2017)

Abstract This abstract was withdrawn by the authors.
Abstract P6-01-15: Novel regulation of breast cancer cell aggressiveness by cancer testis antigen
Authors: A Kannan, RM Wells, M Ikebe, S Dasgupta
Journal: Cancer Research (2017)

Abstract We recently demonstrated that a vesicular endocytosis associated protein SH3GL2, attenuates spontaneous metastases of breast cancer cells by inducing a mesenchymal to epithelial differentiation and the onset of the intrinsic apoptotic pathway. The present study aims to understand the molecular mechanism behind the SH3Gl2 mediated reduction of spontaneous metastasis of the breast cancer cells. We employed a cDNA microarray analysis of the SH3GL2-overexpressing breast cancer cells exhibiting reduced pulmonary metastasis and identified a 12.1 fold downregulation of SPANXB1, a cancer-testis antigen that regulates sperm motility. A limited number of studies reported an association between increased SPANXB1 expression and progression of melanoma and hepatocellular carcinoma. Augmented SPANXB1 mRNA and protein expression was evident in primary breast tumors and its upregulation was associated with pulmonary metastasis of breast cancer cells. However, the expression pattern of SPANXB1 and its role in BCa development and progression is unknown. By immunohistochemical analysis, we detected high expression (p=0.002) of SPANXB1 in 78% (18/23) of the primary breast cancer tissues and corresponding lymph node metastases compared to the matched normal breast tissues. A couple of non-tumorigenic human breast epithelial cell lines were stably transformed with SPANXB1 to understand its effect on cellular growth and progression. The SPANXB1-transformed cells exhibited increased invasion (p=0.0001) and epithelial to mesenchymal transition accompanied by an augmented expression ratio of Vimentin/E-Cadherin, molecules regulating differentiation and metastasis. The SPANXB1-transformed cells also exhibited a markedly reduced expression of SH3GL2, implicating a SPANXB1:SH3GL2 crosstalk accompanied by an enhanced production of lactate (p=0.004). Our investigation identifies new breast cancer promoting role of a cancer testis antigen, which bears potential for biomarker and targeted therapeutic development. Citation Format: Kannan A, Wells RM, Ikebe M, Dasgupta S. Novel regulation of breast cancer cell aggressiveness by cancer testis antigen [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P6-01-15.
Abstract BS1-2: Epigenetic targets in breast cancer
Authors: K Polyak
Journal: Cancer Research (2017)

Abstract Epigenetic regulators are emerging therapeutic targets in various human cancer types including breast cancer. Histone modification (e.g., methylation and acetylation) regulates chromatin structure and transcription, and abnormalities in this process lead to perturbed development and differentiation. Similarly, DNA methylation patterns are commonly perturbed in tumors and this can increase genetic instability and also cellular heterogeneity within tumors. The demonstration of frequent somatic mutations in histones and epigenetic regulators factors in a wide range of human cancer types underscores the importance of epigenetic regulation in tumorigenesis. In breast cancer, genes encoding transcriptional regulators (e.g., FOXA1, GATA3) are among the most frequently mutated genes, suggesting a key role for perturbed epigenetic programs in tumorigenesis. Epigenetic regulators are broadly categorized into writers – enzymes that catalyze the placement of modifications in histones or DNA such as histone and DNA methyltransferases, erasers – enzymes that remove histone or DNA modifications including histone and DNA demethylases, and readers – proteins that recognize a specific histone or DNA modification to help concentrate an enzymatic or structural protein complex. BET bromodomain family of chromatin regulators (e.g., BRD4) recognize acetylated histones and play a key role in the assembly of active transcription complexes. Targeting of these proteins by BET bromodomain inhibitors (BBDIs) have been shown to inhibit the growth of several cancer types and they appear promising novel therapeutic agents in breast cancer as well. However, a significant fraction of breast cancer cells is not sensitive to BBDIs and even some of the initial responsive ones relatively quickly acquire resistance due to activation of anti-apoptotic pathways and bromodomain-independent recruitment of BRD4 to the chromatin. Thus, inhibitors of BET bromodomain proteins alone or in combination with other compounds provide a promising novel therapeutic strategy for the treatment of breast tumors. Citation Format: Polyak K. Epigenetic targets in breast cancer [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr BS1-2.
Contents Vol. 70, 2001
Authors: Jean Cottraux, Ivan Note, Sai Nan Yao, Sylviane Lafont, Brigitte Note, Evelyne Mollard, Martine Bouvard, Alain Sauteraud, Marc Bourgeois, Jean-François Dartigues, Gieta van der Pompe, Michael H. Antoni, Hugo J. Duivenvoorden, Alexander de Graeff, R.F.A. Simonis, Sytze G.L. van der Vegt, Cobi J. Heijnen, Eamonn Ferguson, Giovanni A. Fava, Fedra Ottolini, Nicoletta Sonino, Valdo Ricca, Edoardo Mannucci, Barbara Mezzani, Sandra Moretti, Milena Di Bernardo, Marco Bertelli, Carlo M. Rotella, Carlo Faravelli, Ludwig Teusch, Hildegard Böhme, Jobst Finke, Markus Gastpar
Journal: Psychotherapy and Psychosomatics (2001)
Lenalidomide Plus Bortezomib and Dexamethasone (RVD) Followed by Lenalidomide Plus Dexamethasone As Salvage Treatment for Myeloma Patients in First Relapse After Autologous Stem Cell Transplantation. Single Institution Experience
Authors: Karim Belhadj, Kamel Amraoui, Violaine Safar, Isabelle Gaillard, Taoufik El Gnaoui, Jehan Dupuis, Alain Luciani, Valérie Molinier-Frenkel, Alain Rahmouni, Corinne Haioun
Journal: Blood (2011)
Tissue Expression and Pharmacological In Vitro Analyses of mTOR and SSTR Pathways in Adrenocortical Carcinoma
Authors: Antonina Germano, Ida Rapa, Eleonora Duregon, Arianna Votta, Jessica Giorcelli, Consuelo Buttigliero, Giorgio V Scagliotti, Marco Volante, Massimo Terzolo, Mauro Papotti
Journal: Endocrine Pathology (2017)
Evaluation of hepatitis B reactivation among 62,920 veterans treated with oral hepatitis C antivirals
Authors: Pamela S. Belperio, Troy A. Shahoumian, Larry A. Mole, Lisa I. Backus
Journal: Hepatology (2017)

Reactivation of hepatitis B virus (HBV) has been reported in hepatitis C virus–infected individuals receiving direct‐acting antiviral (DAA) therapy. The overall risk among patients with current or prior HBV infection in the context of DAA treatment is unknown. The aim of this evaluation was to identify and characterize HBV reactivation among veterans treated with oral DAA therapy. This retrospective evaluation included 62,290 hepatitis C virus–infected veterans completing oral DAA treatment. Baseline HBV infection status for each veteran was identified from HBV laboratory data performed prior to DAA initiation. To assess for HBV reactivation and hepatitis we identified all hepatitis B surface antigen (HBsAg), HBV DNA, and alanine aminotransferase results obtained while on DAA treatment or 7 days after. HBV reactivation was defined as a &gt;1000 IU/mL increase in HBV DNA or HBsAg detection in a person who was previously negative. Prior to DAA treatment 85.5% (53,784/62,920) had HBsAg testing and 0.70% (377/53,784) were positive; 84.6% (53,237/62,920) had a hepatitis B surface antibody test, of which 42.2% (22,479/53,237) were positive. In all, 9 of 62,290 patients treated with DAAs had evidence of HBV reactivation occurring while on DAA treatment. Eight occurred in patients known to be HBsAg‐positive, and 1 occurred in a patient known to be isolated hepatitis B core antibody–positive. Seventeen other patients had small increases in HBV DNA levels that did not qualify as HBV reactivation. Only 3 of the 9 patients identified with HBV reactivation in this cohort exhibited peak alanine aminotransferase elevations &gt;2 times the upper limit of normal. Conclusion : HBV reactivation of varying severity, even in the setting of isolated hepatitis B core antibody, with or without accompanying hepatitis can occur—though the occurrence of accompanying severe hepatitis was rare. (H epatology 2017;66:27–36).