tbuckley/cabot-search huggingface dataset:
Abstract MP031: Prospective Association of Obstructive Sleep Apnea Risk Factors with Heart Failure with Preserved Ejection Fraction and Not Heart Failure with Reduced Ejection Fraction in Postmenopausal Women
Authors: Patrick Koo, Umama Gorsi, Mary Roberts, Charles Eaton
Journal: Circulation (2017)

Background: The relationship between obstructive sleep apnea (OSA) and heart failure (HF) has been under-researched especially in postmenopausal women. We therefore evaluated relationship between OSA risk factors and HFpEF and HFrEF in post-menopausal women. Methods: We performed a prospective analysis of a subset of participants who had adjudicated heart failure outcomes (n=42,362) in the Women Health Initiative Observational, Clinical Trial, and Extension Studies (1998-Present). The cohort was followed over an average of 13.4 years. Inverse probability weighting was employed to account for potential selection bias. Cox proportional hazards regression was used to examine the association between OSA risk factors and time to first hospitalized HF. Type of heart failure was determined using the ejection fraction (EF) obtained from 2D echocardiography. EF of ≥45% was categorized as HFpEF, and EF of &lt; 45% was categorized as HFrEF. Models were adjusted for age, race/ethnicity, education, income, marital status, systolic blood pressure, waist-to-hip ratio, diabetes, coronary heart disease, atrial fibrillation, use of hormone replacement therapy, use of sleep medications, modified Charlson comorbidity index, smoking, alcohol consumption, physical activity, and hysterectomy. We also created an OSA summary score (obesity, snoring, poor sleep quality, sleep fragmentation, daytime sleepiness, and hypertension) based on the Berlin questionnaire, which reliably predicts OSA, to examine its relationship with HF. Results: Of the 42,362 women, 1,054 (2.49%) had preserved EF, and 631 (1.49%) had reduced EF. Four of the 6 risk factors (obesity (HR=1.51, 95% CI 1.29-1.76), snoring (HR=1.23, 95% CI 1.04-1.45), sleep fragmentation (HR=1.15, 95% CI 1.01-1.31), and hypertension (HR=1.46, 95% CI 1.31-1.62)) were associated HFpEF after adjusting for confounders. Each additional OSA risk factor in an OSA summary score compared to no risk factors significantly increased the risk of HFpEF in a dose-response fashion (HR=1.36, 1.61, 2.01, 1.97, 2.02, and 2.74 for scores of 1-6, respectively; P trend &lt;0.001) and not HFrEF (P trend =0.26). Only hypertension was associated with HFrEF (HR=1.39, 95% CI 1.22-1.60). Conclusion: Having more OSA risk factors increases the risk of HFpEF but not HFrEF in postmenopausal women. Early recognition and management of OSA risk factors may play an important role in reducing risk of HFpEF in this population.
Pre-Transplant Evaluation with Both CT and PET Following Second-Line Therapy Is Essential for Predicting Outcome in Patients with Transplant- Eligible Relapsed and Primary Refractory Hodgkin Lymphoma
Authors: Alison J. Moskowitz, Stephen D. Nimer, Andrew D. Zelenetz, Tarun Kewalramani, Jill M Vanak, Jocelyn c Maragulia, Joachim Yahalom, Craig Moskowitz
Journal: Blood (2008)
Retinoic Acid and Arsenic Trioxide with or without Chemotherapy for Acute Promyelocytie Leukemia with Different Risk Stratifications: A Interim Analysis of China APL 2012 Study
Authors: Junmin Li, Li Chen, Hongming Zhu, Jiong Hu, Bing Chen, Xiaoyang Li, Lining Wang, Yunxiang Zhang, Yuhong Ren, Huijin Zhao, Yu Chen, Huiping Sun, Qiusheng Chen, Yu Chen, Weili Zhao, Jianqing Mi, Zhixiang Shen, Zhenyi Wang, Zhu Chen, Saijuan Chen
Journal: Blood (2016)
Abstract P3-06-03: The short term effects of an AKT inhibitor (AZD5363) on biomarkers of the AKT pathway and anti-tumour activity in a breast cancer paired biopsy study (STAKT trial)
Authors: JFR Roberston, KL Cheung, S Ahmed, RE Coleman, A Evans, C Holcombe, D Rea, P Rauchhaus, A Skene, R Littleford, A Jahan, S Kelly, JPO Lindermann, K Horgan, A Foxley, P Rugman, M Pass
Journal: Cancer Research (2017)

Abstract This abstract was withdrawn by the authors.
Neutrophil Counts and Initial Presentation of 12 Cardiovascular Diseases
Authors: Anoop Dinesh Shah, Spiros Denaxas, Owen Nicholas, Aroon D. Hingorani, Harry Hemingway
Journal: Journal of the American College of Cardiology (2017)

Neutrophil counts are a ubiquitous measure of inflammation, but previous studies on their association with cardiovascular disease (CVD) were limited by small numbers of patients or a narrow range of endpoints.This study investigated associations of clinically recorded neutrophil counts with initial presentation for a range of CVDs.We used linked primary care, hospitalization, disease registry, and mortality data in England. We included people 30 years or older with complete blood counts performed in usual clinical care and no history of CVD. We used Cox models to estimate cause-specific hazard ratios (HRs) for 12 CVDs, adjusted for cardiovascular risk factors and acute conditions affecting neutrophil counts (such as infections and cancer).Among 775,231 individuals in the cohort, 154,179 had complete blood counts performed under acute conditions and 621,052 when they were stable. Over a median 3.8 years of follow-up, 55,004 individuals developed CVD. Adjusted HRs comparing neutrophil counts 6 to 7 versus 2 to 3 × 109/l (both within the 'normal' range) showed strong associations with heart failure (HR: 2.04; 95% confidence interval [CI]: 1.82 to 2.29), peripheral arterial disease (HR: 1.95; 95% CI: 1.72 to 2.21), unheralded coronary death (HR: 1.78; 95% CI: 1.51 to 2.10), abdominal aortic aneurysm (HR: 1.72; 95% CI: 1.34 to 2.21), and nonfatal myocardial infarction (HR: 1.58; 95% CI: 1.42 to 1.76). These associations were linear, with greater risk even among individuals with neutrophil counts of 3 to 4 versus 2 to 3 × 109/l. There was a weak association with ischemic stroke (HR: 1.36; 95% CI: 1.17 to 1.57), but no association with stable angina or intracerebral hemorrhage.Neutrophil counts were strongly associated with the incidence of some CVDs, but not others, even within the normal range, consistent with underlying disease mechanisms differing across CVDs. (White Blood Cell Counts and Onset of Cardiovascular Diseases: a CALIBER Study [CALIBER]; NCT02014610).
Rituximab exposure is influenced by baseline metabolic tumor volume and predicts outcome of DLBCL patients: a Lymphoma Study Association report
Authors: Mira Tout, Olivier Casasnovas, Michel Meignan, Thierry Lamy, Franck Morschhauser, Gilles Salles, Emmanuel Gyan, Corinne Haioun, Mélanie Mercier, Pierre Feugier, Sami Boussetta, Gilles Paintaud, David Ternant, Guillaume Cartron
Journal: Blood (2017)
Restoration of the CD4+CD25bright Regulatory Cell Subset in Patients with Crohn’s Disease Following Autologous Non-Myeloablative Stem Cell Transplantation (NST).
Authors: Larissa Verda, Yu Oyama, Robert Craig, Laisvyde Statkute, Nela Krosnjar, Kathleen Quigley, Richard K. Burt
Journal: Blood (2005)
Palifermin in Patients with Hematological Malignancies Undergoing Autologous Hematopoietic Stem Cell Transplantation (HSCT): The Italian Early Access Program (EAP).
Authors: Laura M. Cavagna, Gaetano Bonifacio, Emanuele Angelucci, Alessandro Fanni, Giuseppe Milone, Eugenio Gallo, Elena Benincasa
Journal: Blood (2006)
Molecular Subtype Classification of Diffuse Large B-Cell Lymphoma By Immunohistochemical Algorithms and Automatic Supervised Classifiers
Authors: Yocanxóchitl Perfecto-Avalos, Luis Villela, Alejandro Garcia-Gonzalez, Ana G. Hernández-Reynoso, Gildardo Sánchez-Ante, Rita Q. Fuentes-Aguilar, Sean Scott, Carlos Ortiz-Hidalgo, Jose Borbolla Escoboza
Journal: Blood (2016)
Results of a Phase II Study of Guadecitabine (SGI-110) in Higher Risk MDS, CMML or Low Blast Count AML Patients Refractory to or Relapsing after Azacitidine (AZA) Treatment
Authors: Marie Sebert, Cecile Bally, Pierre Peterlin, Odile Beyne-Rauzy, Laurence Legros, marie Pierre Gourin, Laurence Sanhes, Eric Wattel, Emmanuel Gyan, Sophie Park, Aspasia Stamatoullas, Anne Banos, Kamel Laribi, Simone Jueliger, Luke Bevan, Cendrine Chaffaut, Rosa Sapena, Benedicte Samey, Fatiha Chermat, Sylvie Chevret, Lionel Ades, Pierre Fenaux
Journal: Blood (2016)
Transition of Pediatric Liver Transplanted Recipients to Adult Healthcare Service: A Single Center Cohort
Authors: A. Ferrarese, G. Germani, M. Cananzi, A. Zanetto, C. Bergamo, S. Shalaby, E. Nadal, I. Bortoluzzi, M. Senzolo, F.P. Russo, U. Cillo, P. Burra
Journal: Journal of Hepatology (2016)
Anti-Angiogenic in-Vivo Effect of Lenalidomide and Its Impact On Neoplastic and Non-Neoplastic Hematopoiesis in MDS with Del(5q) Chromosome Abnormality.
Authors: Guntram Buesche, Stephanie Dieck, Aristoteles Giagounidis, Gudrun Göhring, Brigitte Schlegelberger, Robert Knight, Carlo Aul, Hans Kreipe
Journal: Blood (2009)
CBL Mutations In Therapy-Related Leukemia and Infant Leukemia
Authors: Norio Shiba, Tomohiko Taki, Myoung-ja Park, Masayuki Nagasawa, Jyunko Takita, Motohiro Kato, Takashi Kanazawa, Manabu Sotomatsu, Hirokazu Arakawa, Yasuhide Hayashi
Journal: Blood (2010)
Poster Session III (Abstracts 1195 – 1637)
Authors: Vikash Reebye, Kai-Wen Huang, Katherine Czysz, Simona Ciriello, Stehpanie Dorman, Isabella Reccia, H. S. Lai, Ling Peng, Nikos Kostomitsopoulos, Joanna Nicholls, Robert Habib, Donald Tomalia, Pal Saetrom, Edmund Wilkes, Pedro Cutillas, John Rossi, Nagy Habib
Journal: Hepatology (2016)

AASLD Publications Hepatology Liver Transplantation Clinical Liver Disease Hepatology Communications AASLD Publications Hepatology Liver Transplantation Clinical Liver Disease Hepatology Communications
Abstract P1-04-07: Environmental influence on epigenetic markers in the development of breast cancer
Authors: C He, W Wu, H Gao, K Nephew, L Li, B Schneider, J Han, Y Liu
Journal: Cancer Research (2017)

Abstract Aberrant DNA methylation plays an important role in breast cancer initiation and progression. We hypothesize that environmental risk factors contribute to causal alterations in DNA methylation and that such causal changes have already occurred prospectively in normal breast tissue before tumor occurrence. In order to test this hypothesis, normal breast tissue from healthy women must be used. We therefore conducted an integrative molecular epidemiological study that combined the environmental regulation of DNA methylation in normal breast tissue and the differential DNA methylation profiling in tumor and normal breast tissue. We examined for the first time the environmental impact on DNA methylation in normal breast tissue from healthy women and determine the association of these epigenetic changes with breast cancer development. Potentially causal DNA methylation markers identified from our study has the potential to make a major scientific and clinical impact in understanding breast cancer etiology as well as developing novel, more effective prevention and treatment strategies. Citation Format: He C, Wu W, Gao H, Nephew K, Li L, Schneider B, Han J, Liu Y. Environmental influence on epigenetic markers in the development of 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 P1-04-07.
Abstract PD2-06: Mismatch repair deficiency induces endocrine therapy resistance in breast cancer
Authors: S Haricharan, J Schmelz, C Schmidt, P Singh, K Holloway, M Anurag, V Suman, JA Olson, K Hunt, MN Bainbridge, MJ Ellis
Journal: Cancer Research (2017)

Abstract Estrogen receptor positive (ER+) breast cancer accounts for the majority of breast cancers diagnosed worldwide but fortunately, outcomes are markedly improved by pharmacological interventions that interrupt ER function. Unfortunately, suppression of relapse risk from early stage disease with endocrine therapy (anti-estrogens or aromatase inhibitors) is only ∼50%, and for advanced disease, pan endocrine therapy resistance is almost inevitable. While many mechanisms for intrinsic and acquired endocrine resistance have been explored, links between defects in DNA repair, the fundamental drivers of cancer pathogenesis, and endocrine therapy resistance have been understudied. Here we link mismatch repair (MMR) deficiency to poor clinical outcomes in ER+ breast cancer using whole exome DNA sequencing data and mRNA expression analysis. We subsequently demonstrate that MMR deficiency bypasses ER dependent cell cycle regulation through disruption of Chk2/p21-mediated feedback inhibition of CDK4 in breast cancer cell lines and tumor samples, as well as through correlations with human clinical data. We also show that pharmacological targeting of CDK4 significantly inhibits growth of MMR-deficient ER+ breast cancer cells in vitro and in vivo. This mechanism provides a new explanation for why endocrine therapy resistant ER+ breast cancers can respond to CDK inhibition and suggests that primary tumors exhibiting MMR deficiency are good candidates for adjuvant CDK4 inhibitor treatment. Citation Format: Haricharan S, Schmelz J, Schmidt C, Singh P, Holloway K, Anurag M, Suman V, Olson JA, Hunt K, Bainbridge MN, Ellis MJ. Mismatch repair deficiency induces endocrine therapy resistance 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 PD2-06.
24 Months Update of the TOPS Study: a Phase III, Randomized, Open-Label Study of 400mg/d (SD-IM) Versus 800mg/d (HD-IM) of Imatinib Mesylate (IM) in Patients (Pts) with Newly Diagnosed, Previously Untreated Chronic Myeloid Leukemia in Chronic Phase (CML-CP).
Authors: Michele Baccarani, Brian J. Druker, Jorge Cortes-Franco, Timothy P. Hughes, Dong-Wook Kim, Fabrizio Pane, Susan Branford, Yu Jin, Tillmann Krahnke, Marc Rudoltz, Jerald P. Radich, François Guilhot
Journal: Blood (2009)
Contents Vol. 68, 1999
Authors: Irena Heszen-Niejodek, Louis A. Gottschalk, Maciej Januszek, G. Majella de Jong, Eric van Sonderen, Paul M.G. Emmelkamp, Miranda A.L. van Tilburg, Elisabeth H.M. Eurelings-Bontekoe, Ad J.J.M. Vingerhoets, Guus L. van Heck, Barbara Mangweth, Georg Kemmler, Christoph Ebner, Christine De Col, Johannes Kinzl, Wilfried Biebl, Ad Vingerhoets, J. López-Castillo, M. Gurpegui, J.L. Ayuso-Mateos, J.D. Luna, J. Catalan, Carol S. Stilley, David J. Miller, Jan D. Manzetti, Ignazio R. Marino, Robert J. Keenan, Barbara Buddeberg-Fischer, Richard Klaghofer, Victoria Reed, Giovanni A. Fava, Lara Mangelli, Brunna Tuschen-Caffier, Claus Vögele, Mutsuhiro Nakao, Shinobu Nomura, Tatsuo Shimosawa, Toshiro Fujita, Tomifusa Kuboki
Journal: Psychotherapy and Psychosomatics (1999)
Adhesion of Hairy Cells Leukemia (HCL) Cells to Stromal Cells Can Be Inhibited by Blocking VLA-4 Integrins and CXCR4 Chemokine Receptors
Authors: Mariela Sivina, Robert J. Kreitman, Amnon Peled, Farhad Ravandi, Jan A. Burger
Journal: Blood (2011)
Assessing the potential pandemic risk of recent avian influenza viruses
Authors: Ian G. Barr
Journal: European Respiratory Journal (2017)

Highly pathogenic avian influenza viruses (HPAI) of the influenza A, H5N1 subtype (the H refers to the type of haemagglutinin and the N refers to the type of neuraminidase) have circulated in various parts of Asia since 1996, infecting millions of birds and, occasionally, humans [1, 2]. Since 2014, a subclade of these viruses has further reassorted into what have been referred to as H5Nx viruses, owing to the variety of N genes that have successfully reassorted with this H5 haemagglutinin. These reassortants have spread in an unprecedented fashion over 60 countries [3], with H5N8 and H5N2 outbreaks in Europe and North America [4, 5] having caused major economic losses in the poultry industry. The H5N6 has replaced H5N1 as the dominant HPAI in Southern China, especially in ducks and geese [6]. The H5N6 virus appears to have low mortality in ducks and geese even though it was still 100% lethal in chickens [7] and has also occasionally infected humans in China, where 16 cases have been detected in the last 2 years, with 11 deaths (ages, 11–65 years; median age, 40 years) [8]. It is essential to carefully monitor avian H5Nx influenza viruses as they continue to evolve <http://ow.ly/B0QF308Zoqv>
Post Thaw Colony Forming Units (CFU) Is a Strong Independent Predictor of Engraftment after Unrelated Donor Umbilical Cord Blood Transplantation (UCBT).
Authors: Kristin M. Page, Adam Mendizabal, Barbara Waters-Pick, Sophia Avrutsky, Melissa Reese, Vinod Prasad, Joanne Kurtzberg
Journal: Blood (2007)
Payer Coverage for Hereditary Cancer Panels: Barriers, Opportunities, and Implications for the Precision Medicine Initiative
Authors: Julia R. Trosman, Christine B. Weldon, Michael P. Douglas, Allison W. Kurian, R. Kate Kelley, Patricia A. Deverka, Kathryn A. Phillips
Journal: Journal of the National Comprehensive Cancer Network (2017)

Background: Hereditary cancer panels (HCPs), testing for multiple genes and syndromes, are rapidly transforming cancer risk assessment but are controversial and lack formal insurance coverage. We aimed to identify payers' perspectives on barriers to HCP coverage and opportunities to address them. Comprehensive cancer risk assessment is highly relevant to the Precision Medicine Initiative (PMI), and payers' considerations could inform PMI's efforts. We describe our findings and discuss them in the context of PMI priorities. Methods: We conducted semi-structured interviews with 11 major US payers, covering >160 million lives. We used the framework approach of qualitative research to design, conduct, and analyze interviews, and used simple frequencies to further describe findings. Results: Barriers to HCP coverage included poor fit with coverage frameworks (100%); insufficient evidence (100%); departure from pedigree/family history–based testing toward genetic screening (91%); lacking rigor in the HCP hybrid research/clinical setting (82%); and patient transparency and involvement concerns (82%). Addressing barriers requires refining HCP-indicated populations (82%); developing evidence of actionability (82%) and pathogenicity/penetrance (64%); creating infrastructure and standards for informing and recontacting patients (45%); separating research from clinical use in the hybrid clinical-research setting (44%); and adjusting coverage frameworks (18%). Conclusions: Leveraging opportunities suggested by payers to address HCP coverage barriers is essential to ensure patients' access to evolving HCPs. Our findings inform 3 areas of the PMI: addressing insurance coverage to secure access to future PMI discoveries; incorporating payers' evidentiary requirements into PMI's research agenda; and leveraging payers' recommendations and experience to keep patients informed and involved.
Successful Management of Transplant-Ineligible Patients with Refractory/Relapsed Multiple Myeloma By Using a Biweekly or Longer Modified Bortezomib Schedule As Interval Maintenance therapy
Authors: Michihide Tokuhira, Yuta Kimura, Tatsuki Tomikawa, Yasuyuki Takahashi, Morihiko Sagawa, Tomoe Nemoto, Takayuki Tabayashi, Reiko Watanabe, Masahiro Kizaki
Journal: Blood (2014)
Predicting Event-Free and Overall Survival after Treatment of Myeloma with the Proteasome Inhibitor Bortezomib with Pre-Treatment and 48-Hour Post-Therapy Gene Expression Patterns.
Authors: William Barlow, Zhan Fenghuang, Yongsheng Huang, Sisi Kapp, Erik Rasmussen, Bart Barlogie, John Crowley, John Shaughnessy
Journal: Blood (2004)
A Comprehensive TALEN-Based Knockout Library for Generating Human-Induced Pluripotent Stem Cell–Based Models for Cardiovascular Diseases
Authors: Ioannis Karakikes, Vittavat Termglinchan, Diana A. Cepeda, Jaecheol Lee, Sebastian Diecke, Ayal Hendel, Ilanit Itzhaki, Mohamed Ameen, Rajani Shrestha, Haodi Wu, Ning Ma, Ning-Yi Shao, Timon Seeger, Nicole Woo, Kitchener D. Wilson, Elena Matsa, Matthew H. Porteus, Vittorio Sebastiano, Joseph C. Wu
Journal: Circulation Research (2017)

Rationale: Targeted genetic engineering using programmable nucleases such as transcription activator–like effector nucleases (TALENs) is a valuable tool for precise, site-specific genetic modification in the human genome. Objective: The emergence of novel technologies such as human induced pluripotent stem cells (iPSCs) and nuclease-mediated genome editing represent a unique opportunity for studying cardiovascular diseases in vitro. Methods and Results: By incorporating extensive literature and database searches, we designed a collection of TALEN constructs to knockout 88 human genes that are associated with cardiomyopathies and congenital heart diseases. The TALEN pairs were designed to induce double-strand DNA break near the starting codon of each gene that either disrupted the start codon or introduced a frameshift mutation in the early coding region, ensuring faithful gene knockout. We observed that all the constructs were active and disrupted the target locus at high frequencies. To illustrate the utility of the TALEN–mediated knockout technique, 6 individual genes ( TNNT2, LMNA/C, TBX5, MYH7, ANKRD1 , and NKX2.5 ) were knocked out with high efficiency and specificity in human iPSCs. By selectively targeting a pathogenic mutation ( TNNT2 p.R173W ) in patient-specific iPSC-derived cardiac myocytes, we demonstrated that the knockout strategy ameliorates the dilated cardiomyopathy phenotype in vitro. In addition, we modeled the Holt–Oram syndrome in iPSC-cardiac myocytes in vitro and uncovered novel pathways regulated by TBX5 in human cardiac myocyte development. Conclusions: Collectively, our study illustrates the powerful combination of iPSCs and genome editing technologies for understanding the biological function of genes, and the pathological significance of genetic variants in human cardiovascular diseases. The methods, strategies, constructs, and iPSC lines developed in this study provide a validated, readily available resource for cardiovascular research.
Use of Ketamine in Clinical Practice
Authors: Charles F. Zorumski, Charles R. Conway
Journal: JAMA Psychiatry (2017)

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PI3K Inhibition with GDC-0941 Has Greater Efficacy Compared to p110δ-Selective Inhibition with CAL-101 in Mantle Cell Lymphoma and May Be Particularly Advantageous in Multiply Relapsed Patients
Authors: Sunil Iyengar, Andrew J. Clear, Andrew Owen, Lenushka Maharaj, Janet Matthews, Maria Calaminici, Rebecca Auer, Essam Ghazaly, Sameena Iqbal, John G. Gribben, Simon Joel
Journal: Blood (2011)