tbuckley/cabot-search huggingface dataset:
The Shifting Sands of Coronary Microvascular Dysfunction
Authors: William F. Fearon, Bernard De Bruyne
Journal: Circulation (2019)

Diagnosing coronary microvascular dysfunction (CMD) in the cardiac catheterization laboratory remains a challenge, particularly in stable patients with angina and no obstructive epicardial coronary artery disease.CMD is typically defined as elevated microvascular resistance that manifests as abnormal coronary microvascular vasodilation, impaired hyperemic myocardial flow, or myocardial ischemia without evidence of epicardial coronary artery disease. 1 This generic definition has the merit of creating a conceptual framework but should not obscure the 2 persistent issues we face with the microcirculation: (1) microvascular resistance is difficult to quantify; and (2) the structure of the microcirculation is largely unknown and is certainly more complicated than that of the classical model of a macrocirculation in miniature.The absence of an appropriate animal model further complicates the study of the microcirculation.In the catheterization laboratory, CMD can be diagnosed using angiographic techniques such as myocardial blush grade, but these are qualitative and applicable to acute CMD only.Traditionally, coronary flow reserve (CFR) defined as the ratio of hyperemic to resting flow measured with a Doppler wire has been the standard technique.However, CFR measurement is reliant on resting flow, a condition never really met in the catheterization laboratory, and its value is affected by changes in hemodynamics.In addition, CFR is not specific for the microcirculation because it interrogates both the epicardial artery and the microvasculature, so it may be skewed in the setting of occult epicardial coronary disease.In 2003, the index of microcirculatory resistance (IMR) was introduced as a metric to specifically assess minimal microvascular resistance. 2 IMR is calculated as distal coronary pressure divided by a thermodilution-derived flow index measured during maximal hyperemia with a coronary pressure/thermistor-tipped wire.IMR was subsequently shown to be more specific for the microvasculature, to be independent of hemodynamic changes, and to be more reproducible than CFR. 3 Most recently, it was shown that absolute microvascular resistance (expressed in Woods Units) can be derived from continuous coronary thermodilution. 4This method is now readily applicable in humans, precise and reproducible, and may offer better understanding of microvascular (dys)function and spur further development of treatment options. 5n unstable patients with CMD secondary to ST-segment-elevation myocardial infarction (STEMI), measurement of IMR has been shown to correlate with biomarker elevation, infarct size, and microvascular obstruction on noninvasive imaging and with clinical outcomes. 3In a large registry, IMR was an independent predictor of mortality when measured in patients with STEMI immediately after primary percutaneous coronary intervention, whereas CFR was not. 6Another study found that the addition of CFR did not improve the prognostic value of IMR alone. 7In
Quiescence/Mobilization of Hematopoietic Immature Cells Induced By Polyphenols through Modulation of APC/EPCR/PAR-1 Axis
Authors: Cristiane Okuda Torello, Erich V De Paula, Rodrigo Naoto Shiraishi, Santos Irene, Fernanda I Della Via, Mariana Pissarra, Marisa Claudia Alvarez De Prax, Mary L. S. Queiroz, Sara T Olalla Saad
Journal: Blood (2019)
Analysis of Factors Predictive of Risk of Transformation and Time to Transformation in Patients (pts) with Mantle Cell Lymphoma - Cohort Study of 369 Patients
Authors: Preetesh Jain, Rashmi Kanagal-Shamanna, Chi Young Ok, Gonzalez-Pagan Omarya, Lucy Navsaria, Graciela M. Nogueras González, Shaojun Zhang, Guangchun Han, Ahmad Ghorab, Prajwal Boddu, F. B. Hagemeister, Hun Ju Lee, Krystle Nomie, Changying Jiang, Luis Fayad, Jason R. Westin, Loretta J. Nastoupil, Sairah Ahmed, Swaminathan P. Iyer, Richard E. Champlin, Sattva S Neelapu, Jorge Enrique Romaguera, Nathan H. Fowler, Guilin Tang, Shaoying Li, Keyur Patel, Selvi Thirumurthi, Pan Tinsu, Guofang Xu, Linghua Wang, Michael L. Wang
Journal: Blood (2019)
Adding Indoximod to Hypofractionated Radiotherapy with Anti-PD-1 Checkpoint Blockade Enhances Early NK and CD8+ T-Cell–Dependent Tumor Activity
Authors: Tsubasa Watanabe, Simone Gaedicke, Elena Guffart, Elke Firat, Gabriele Niedermann
Journal: Clinical Cancer Research (2019)

Abstract Purpose: There is growing interest in combinations of immunogenic radiotherapy (RT) and immune checkpoint blockade, but clinical responses are still limited. Therefore, we tested the triple therapy with an inhibitor of the indoleamine 2,3-dioxygenase pathway, which like immune checkpoints, downregulates the antitumor immune response. Experimental Design: Triple treatment with hypofractionated RT (hRT) + anti-PD-1 antibody (αPD1) + indoximod was compared with the respective mono- and dual therapies in two syngeneic mouse models. Results: The tumors did not regress following treatment with hRT + αPD1. The αPD1/indoximod combination was not effective at all. In contrast, triple treatment induced rapid, marked tumor regression, even in mice with a large tumor. The effects strongly depended on CD8+ T cells and partly on natural killer (NK) cells. Numbers and functionality of tumor-specific CD8+ T cells and NK cells were increased, particularly early during treatment. However, after 2.5–3 weeks, all large tumors relapsed, which was accompanied by increased apoptosis of tumor-infiltrating lymphocytes associated with a non-reprogrammable state of exhaustion, terminal differentiation, and increased activation-induced cell death, which could not be prevented by indoximod in these aggressive tumor models. Some mice with a smaller tumor were cured. Reirradiation during late regression (day 12), but not after relapse, cured almost all mice with a large B16-CD133 tumor, and strongly delayed relapse in the less immunogenic 4T1 model, depending on CD8+ T cells. Conclusions: Our findings may serve as a rationale for the clinical evaluation of this triple-combination therapy in patients with solitary or oligometastatic tumors in the neoadjuvant or the definitive setting.
CSIG-01. NA-K-CL COTRANSPORTER PROTEIN IN THE PATHOGENESIS OF LOW-GRADE GLIOMAS
Authors: Lanxin Luo, Xiudong Guan, Gulnaz Begum, Dawei Ding, Gary Kohanbash, Baoshan Sun, Dandan Sun
Journal: Neuro-Oncology (2019)

Abstract Low-grade gliomas (LGGs) present a high incidence of epilepsy, infiltrative growth, resistance to therapy, and high risk of transforming into high-grade gliomas (HGGs). Temozolomide (TMZ) is a conventional chemotherapy drug for adjuvant treatment of patients with high-risk LGGs. Na+-K+-2Cl- co-transporter 1 (NKCC1) regulates cell volume and intracellular Cl- concentration which promotes glioma cell migration, resistance to TMZ, and tumor-associated epilepsy. Our new bioinformatic analysis of TCGA and CGGA datasets shows that LGGs expressed higher SLC12A2 gene mRNA (encoding NKCC1 protein) than HGGs, which was confirmed at NKCC1 protein levels. In syngeneic mouse glioma models with intracranial transplantation of two different mouse glioma cell lines (GL26 and SB28), we detected upregulated NKCC1 protein expression in glioma tumor cells as well as in peri-tumor reactive astrocytes in response to TMZ monotherapy. This provided a rationale for us to test the efficacy of combining NKCC1 pharmacological blockade with TMZ on improving therapeutic outcomes. 5-day combination therapy of TMZ with potent NKCC1 inhibitor bumetanide reduced tumor proliferation, potentiated TMZ-mediated apoptosis, and decreased peri-tumor reactive astrocyte formation, which collectively led to suppressed tumor growth and prolonged survival of tumor-bearing mice. Taken together, these results demonstrate that NKCC1 protein plays multifaceted roles in regulating the pathogenesis of LGGs and its blockade presents therapeutic potentials for reducing TMZ-mediated resistance.
Impact of Somatic Mutations and Pretransplant Strategies on the Outcome of Patients Allografted for MDS or Secondary AML
Authors: Christina Rautenberg, Stefanie Stepanow, Michael Lauseker, Ulrich Germing, Paul Jäger, Stefanie Geyh, Esther Schuler, Karl Köhrer, Norbert Gattermann, Rainer Haas, Guido Kobbe, Thomas Schroeder
Journal: Blood (2019)
Both the rituximab dose and maintenance immunosuppression in steroid-dependent/frequently-relapsing nephrotic syndrome have important effects on outcomes
Authors: Eugene Yu-hin Chan, Hazel Webb, Ellen Yu, Gian Marco Ghiggeri, Markus J. Kemper, Alison Lap-tak Ma, Tomohiko Yamamura, Aditi Sinha, Arvind Bagga, Julien Hogan, Claire Dossier, Marina Vivarelli, Isaac Desheng Liu, Koichi Kamei, Kenji Ishikura, Priya Saini, Kjell Tullus
Journal: Kidney International (2019)
Patient-Specific Risk Factors Independently Influence Survival in Myelodysplastic Syndromes in an Unbiased Review of EHR Records
Authors: Travis Spaulding, Nicholas Strayer, Andrew Sochacki, Shannon Stockton, Alexander Silver, Rodney Dixon Dorand, Siwei Zhang, Ya-Chen Lin, Yaomin Xu, Michael R. Savona
Journal: Blood (2019)
Lower gut microbiome diversity and higher abundance of proinflammatory genus <i>Collinsella</i> are associated with biopsy-proven nonalcoholic steatohepatitis
Authors: Stuart Astbury, Edmond Atallah, Amrita Vijay, Guruprasad P Aithal, Jane I Grove, Ana M Valdes
Journal: Gut Microbes (2019)

There is increasing evidence for the role of gut microbial composition in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Nonalcoholic steatohepatitis (NASH) is the most serious form of NAFLD where inflammation causes liver damage that can progress to cirrhosis. We have characterized the gut microbiome composition in UK patients with biopsy-proven NASH (n = 65) and compared it to that in healthy controls (n = 76). We report a 7% lower Shannon alpha diversity in NASH patients without cirrhosis (n = 40) compared to controls (p = 2.7x 10−4) and a 14% drop in NASH patients with cirrhosis (n = 25, p = 5.0x 10−4). Beta diversity (Unweighted UniFrac distance) was also significantly reduced in both NASH (p = 5.6x 10−25) and NASH-cirrhosis (p = 8.1x 10−7) groups. The genus most strongly associated with NASH in this study was Collinsella (0.29% abundance in controls, 3.45% in NASH without cirrhosis (False Discovery Rate (FDR) p = .008), and 4.38% in NASH with cirrhosis (FDR p = .02)). This genus, which has been linked previously to obesity and atherosclerosis, was also positively correlated with fasting levels of triglycerides (p = .01) and total cholesterol (p = 1.2x 10−4) and negatively correlated with high-density lipoprotein cholesterol (p = 2.8x 10−6) suggesting that some of the pathways present in this microbial genus may influence lipid metabolism in the host. In patients, we also found decreased abundance of some of the Ruminococcaceae which are known to produce high levels of short-chain fatty acids which can lower inflammation. This may thus contribute to pathology associated with NASH.
Veneto-STOP Study: Sequential Assessment of Minimal Residual Disease By Next Generation Sequencing to Optimize Outcomes and Minimize Exposure in Venetoclax-Treated CLL Patients
Authors: Chaitra S. Ujjani, Lindsey E. Roeker, Mazyar Shadman, Kate J Whitaker, Allison P. Jacob, Mark B. Geyer, Colleen Dorsey, Andrew D. Zelenetz, Anthony R. Mato
Journal: Blood (2019)
Mild and severe beta-thalassemia among homozygotes from Turkey: identification of the types by hybridization of amplified DNA with synthetic probes
Authors: JC Diaz-Chico, KG Yang, TA Stoming, DG Efremov, A Kutlar, F Kutlar, M Aksoy, C Altay, A Gurgey, Y Kilinc
Journal: Blood (1988)
Comprehensive Clonal Mapping of Hematopoiesis in Vivo in Humans By Retroviral Vector Insertional Barcoding
Authors: Luca Biasco, Serena Scala, Francesca Dionisio, Andrea Calabria, Luca Basso Ricci, Samantha Scaramuzza, Cristina Baricordi, Stefania Giannelli, Victor X Neduva, David J Dow, Danilo Pellin, Paola Vicard, Clelia Di Serio, Eugenio Montini, Luigi Naldini, Alessandro Aiuti
Journal: Blood (2014)
The Pro-Adhesive and Reduced Angiogenic Properties of Endothelial Colony Forming Cells (ECFC) from JAK2V617F MPN Patients Are Not Related to the Expression of the JAK2 mutation in These Cells: A Potential Role of ADAM17
Authors: Bruno Kosa Lino Duarte, Stephanie Ospina-Prieto, Lucia Helena Siqueira, Jessica O F Guanaes, Fernando Ferreira Costa, Margareth C Ozelo
Journal: Blood (2019)
T-Cell Mediated Cytopenias in Patients with Myelodysplastic Syndromes Respond to Intravenous Immunoglobulin
Authors: Jonathan Feld, Francesca Schieppati, Rosalie Odchimar-Reissig, Erin P. Demakos, Shyamala C. Navada, Lewis R. Silverman
Journal: Blood (2019)
Anaerobic Antibiotics and the Risk of Graft-Versus-Host Disease after Allogeneic Hematopoietic Stem Cell Transplantation
Authors: John Tanaka, Rebecca Young, Lisa Spees, Kirsten Jenkins, Anthony D. Sung, Paul L. Martin, Sarah Heston, Jillian C. Thompson, Patrick Seed, Mehreen Arshad, Matthew Kelly
Journal: Blood (2019)
The CCND1 870G Risk Allele Is Enriched in African Individuals with Plasma Cell Dyscrasias
Authors: Linda B Baughn, Zhou Li, Kathryn E. Pearce, Celine M. Vachon, Mei-Yin Polley, Jonathan J Keats, Eran Elhaik, Michael L. Baird, Terry Therneau, James R. Cerhan, P. Leif Bergsagel, Angela Dispenzieri, S.Vincent Rajkumar, Yan Asmann, Shaji K. Kumar
Journal: Blood (2019)
Surgery in Octogenarians
Authors: R. W. Raven
Journal: BMJ (1955)

rectum and died of another cause at the age of 87.In some aged patients the application of coagulation diathermy to an obstructing carcinoma of the rectum is a useful method of treatment; one patient lived 2 1/12 years.TABLE I.-Octogenarians with Malignant Lesions Treated Surgically Age of Disease Patient!I Dses 85 Carcinoma rectum 88 83 90 83 Carcinoma colon, perforated Enlarged prostate; retention of urine 83 Carcinoma colon -complete in- testinal occlu- sion 82 Carcinoma pelvic colon 81 Carcinoma pelvic colon with pel- vic abscess 86
Transcatheter Aortic Valve Replacement for Patients at Low Surgical Risk—Selective or Ubiquitous?
Authors: Michael J. Reardon, Patrick T. O’Gara, Martin B. Leon
Journal: JAMA Cardiology (2019)

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 Cardiology 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 Cardiology journal
Long-Term Safety and Efficacy of Hyper-CVAD Plus Ponatinib As Frontline Therapy for Adults with Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia
Authors: Nicholas J. Short, Hagop M. Kantarjian, Farhad Ravandi, Xuelin Huang, Naval G. Daver, Courtney D. DiNardo, Marina Y Konopleva, Naveen Pemmaraju, William G. Wierda, Guillermo Garcia-Manero, Koji Sasaki, Jorge E. Cortes, Rebecca Garris, Marygrace Ward, Binru Huang, Corabelle Encarnacion, Christopher Loiselle, Joseph D. Khoury, Jeffrey L. Jorgensen, Nitin Jain, Joie Alvarez, Nicole Tippett, Susan M. O'Brien, Elias Jabbour
Journal: Blood (2019)
Cistrome Partitioning Reveals Convergence of Somatic Mutations and Risk Variants on Master Transcription Regulators in Primary Prostate Tumors
Authors: Parisa Mazrooei, Ken J. Kron, Yanyun Zhu, Stanley Zhou, Giacomo Grillo, Tahmid Mehdi, Musaddeque Ahmed, Tesa M. Severson, Paul Guilhamon, Nicholas Sinnott Armstrong, Vincent Huang, Takafumi N. Yamaguchi, Michael Fraser, Theodorus van der Kwast, Paul C. Boutros, Housheng Hansen He, Andries M. Bergman, Robert G. Bristow, Wilbert Zwart, Mathieu Lupien
Journal: Cancer Cell (2019)
Phase 1 Trial of Cladribine, High-Dose Cytarabine, G-CSF, and Dose-Escalated Mitoxantrone (CLAG-M) Plus Gemtuzumab Ozogamicin in Adults with Newly-Diagnosed Acute Myeloid Leukemia (AML) or Other High-Grade Myeloid Neoplasm
Authors: Colin D. Godwin, Megan Othus, Mary-Elizabeth M. Percival, Bart L. Scott, Pamela S. Becker, Kelda M. Gardner, Sioban B. Keel, Tejaswini M. Dhawale, Vivian G. Oehler, Janis L. Abkowitz, Anna B. Halpern, Paul C. Hendrie, Kaysey F. Orlowski, Alice Woo, Elihu H. Estey, Roland B. Walter
Journal: Blood (2019)
MET Inhibition Elicits PGC1α-Dependent Metabolic Reprogramming in Glioblastoma
Authors: Yiru Zhang, Trang T.T. Nguyen, Enyuan Shang, Angeliki Mela, Nelson Humala, Aayushi Mahajan, Junfei Zhao, Chang Shu, Consuelo Torrini, Maria J. Sanchez-Quintero, Giulio Kleiner, Elena Bianchetti, Mike-Andrew Westhoff, Catarina M. Quinzii, Georg Karpel-Massler, Jeffrey N. Bruce, Peter Canoll, Markus D. Siegelin
Journal: Cancer Research (2019)

The receptor kinase c-MET has emerged as a target for glioblastoma therapy. However, treatment resistance emerges inevitably. Here, we performed global metabolite screening with metabolite set enrichment coupled with transcriptome and gene set enrichment analysis and proteomic screening, and identified substantial reprogramming of tumor metabolism involving oxidative phosphorylation and fatty acid oxidation (FAO) with substantial accumulation of acyl-carnitines accompanied by an increase of PGC1α in response to genetic (shRNA and CRISPR/Cas9) and pharmacologic (crizotinib) inhibition of c-MET. Extracellular flux and carbon tracing analyses (U-13C-glucose, U-13C-glutamine, and U-13C-palmitic acid) demonstrated enhanced oxidative metabolism, which was driven by FAO and supported by increased anaplerosis of glucose carbons. These findings were observed in concert with increased number and fusion of mitochondria and production of reactive oxygen species. Genetic interference with PGC1α rescued this oxidative phenotype driven by c-MET inhibition. Silencing and chromatin immunoprecipitation experiments demonstrated that cAMP response elements binding protein regulates the expression of PGC1α in the context of c-MET inhibition. Interference with both oxidative phosphorylation (metformin, oligomycin) and β-oxidation of fatty acids (etomoxir) enhanced the antitumor efficacy of c-MET inhibition. Synergistic cell death was observed with c-MET inhibition and gamitrinib treatment. In patient-derived xenograft models, combination treatments of crizotinib and etomoxir, and crizotinib and gamitrinib were significantly more efficacious than single treatments and did not induce toxicity. Collectively, we have unraveled the mechanistic underpinnings of c-MET inhibition and identified novel combination therapies that may enhance its therapeutic efficacy. SIGNIFICANCE: c-MET inhibition causes profound metabolic reprogramming that can be targeted by drug combination therapies.
Congenital Dyserythropoietic Anemia Type I Due to Biallelic CDAN1 mutations: Report from the Congenital Dyserythropoietic Anemia Registry (CDAR)
Authors: Omar Niss, Robert B. Lorsbach, David K. Buchbinder, Satheesh Chonat, Morgan L. McLemore, Timothy McCavit, Jeffrey H Schwartz, Jessica Meznarich, Katie Seu, Wenying Zhang, Theodosia A. Kalfa
Journal: Blood (2019)
Lesion-Level Response Dynamics to Programmed Cell Death Protein (PD-1) Blockade
Authors: Juan C. Osorio, Kathryn C. Arbour, Dung T. Le, Jennifer N. Durham, Andrew J. Plodkowski, Darragh F. Halpenny, Michelle S. Ginsberg, Peter Sawan, Joseph G. Crompton, Helena A. Yu, Azadeh Namakydoust, Barzin Y. Nabet, Jamie E. Chaft, Gregory J. Riely, Hira Rizvi, Luis A. Diaz, Matthew D. Hellmann
Journal: Journal of Clinical Oncology (2019)

Response to programmed cell death protein 1 (PD-1) blockade is often conceptualized as resulting from reinvigoration of tumor-infiltrating lymphocytes. However, recruited antitumor immunity from the periphery may also be an important contributor to response. A detailed assessment of the response dynamics of individual metastasis could provide insight to the systemic and local features that mediate response and resistance to immunotherapy.Patients with metastatic non-small-cell lung cancer (NSCLC) or mismatch repair deficiency (MMRD) carcinoma treated with PD-1 monotherapy were evaluated independently. Absolute and percent change of each target lesion were quantified at each computed tomography scan using RECIST. Patterns of progression were predefined as systemic or mixed and were correlated with clinical outcomes.A total of 761 individual lesions from 214 patients with NSCLC and 290 lesions from 78 patients with MMRD carcinoma were examined. Individual target lesion responses aligned with best overall response of each patient (85% NSCLC and 93% MMRD lesions responded in patients with partial response/complete response). In responding patients, timing of response was uniform (73% NSCLC and 76% MMRD lesions responded synchronously), and deeper responses were associated with prolonged progression-free survival and overall survival. By contrast, at progression, mixed progression was common (45% of NSCLC and 53% of MMRD) and associated with improved survival compared with those who experienced systemic progression (NSCLC hazard ratio [HR], 0.58; P = .001; MMRD HR, 0.40; P = .07). Organ sites had differential responses, with lymph node and liver metastasis among the most and least responsive, respectively.Temporal-spatial patterns of response across individual metastases tend to be uniform, favoring the role of peripheral, clonally directed antitumor immunity as a key mediator of response to PD-1 blockade. In contrast, progression is more heterogeneous, potentially revealing the clinical importance of local features and intertumoral heterogeneity.
“Screening for lung cancer: time for large-scale screening by chest computed tomography.” Dekel Shlomi, Ronny Ben-Avi, Gingy Ronen Balmor, Amir Onn and Nir Peled. <i>Eur Respir J</i> 2014; 44: 217–238
Journal: European Respiratory Journal (2019)

It has been brought to our attention that a sentence regarding lung cancer detection rates in this article was ambiguous in its originally published form, appearing on page 220, section entitled "Low-dose CT screening detection rates", second sentence:"Detection rate of lung cancer ranged between 1.1-2% in baseline screening and false-positive rates of 90-96%."The authors wish to clarify the matter and point out that the sentence should more correctly read:"Detection rate of lung cancer ranged between 1.1-2% in baseline screening and false-detection rates of 90-96%."
Efficacy and Safety of Azacitidine (AZA) in Combination with the Anti-PD-L1 Durvalumab (durva) for the Front-Line Treatment of Older Patients (pts) with Acute Myeloid Leukemia (AML) Who Are Unfit for Intensive Chemotherapy (IC) and Pts with Higher-Risk Myelodysplastic Syndromes (HR-MDS): Results from a Large, International, Randomized Phase 2 Study
Authors: Amer M. Zeidan, James Cavenagh, Maria Teresa Voso, David Taussig, Mar Tormo, Isaac Boss, Wilbert B. Copeland, Vanessa E. Gray, Alessandro Previtali, Tim O'Connor, Shelonitda Rose, CL Beach, Lewis R. Silverman
Journal: Blood (2019)
Phase 2 Study of Alemtuzumab Added to Dose-Adjusted EPOCH-R in Relapsed and Refractory Aggressive B-Cell Lymphomas
Authors: Sanjal Desai, Christopher Melani, Kieron Dunleavy, Stefania Pittaluga, Mark A. Ahlman, Andrea Nicole Lucas, Seth M. Steinberg, Elaine S. Jaffe, Mark Roschewski, Wyndham Wilson
Journal: Blood (2019)