tbuckley/cabot-search huggingface dataset:
The Prevalence of Anemia among Healthy Women in Japan.
Authors: Eiji Kusumi, Masahiro Kami, Midori Shoji, Shigeyuki Endou, Yukiko Kishi, Taro Shibata, Naoko Murashige, Tamae Hamaki, Tomoko Matsumura, Koichiro Yuji, Akiko Yoneyama
Journal: Blood (2005)
S-Phase Progression of North American ATLL Cells Is Critically Regulated By the Proto-Oncogene BCL6 and Targetable By PARP Inhibition
Authors: B. Hilda Ye, Elaine Chung, Kith Pradhan, Ana Acuna-Villaorduna, Yanhua Wang, Aditi Shastri, Advaitha Madireddy, Amit Verma, R.Alejandro Sica, Murali Janakiram
Journal: Blood (2019)
Daily Pulsed Electromagnetic Field (PEMF) therapy inhibits tumor angiogenesis via the hypoxia driven pathway: therapeutic implications
Authors: Ivan L. Cameron, L. Z. Sun, N. Short, W. E. Hardman, C. D. Williams
Journal: Cancer Research (2005)

1236  Ten minute daily PEMF inhibits hypoxia driven tumor angiogenesis and tumor growth (Williams et al. ’01 and Cameron et al. ’04) but does not inhibit non-hypoxia driven angiogenesis that normally occurs during embryogenesis and tail fin regeneration in Zebrafish (Short et al. ’05). Daily PEMF was found to retard angiogenesis and growth of a human breast cancer xenograph causing the tumor to develop proportionately larger areas of necrosis and hypoxia and smaller areas of proliferatively active cancer cells. It was also demonstrated that the daily PEMF therapy continued to inhibit tumor angiogenesis and tumor regrowth for two weeks following a standard course of ionizing radiation (IR) therapy (Cameron et al. ’04) however this PEMF therapy renders larger areas of the tumor hypoxic therefore is expected to lessen susceptibility to oxidative damage caused by further IR treatments or by oxidative dependent chemotherapy. This leads to the conclusion that PEMF is an effective adjunct therapy following IR therapy but that the continued daily PEMF therapy should be stopped sometime (perhaps 2-4 days) prior to a second round of IR therapy. The temporary cessation of PEMF prior to the second round of IR is necessary for resumption of angiogenesis, decrease of hypoxic areas and increase in proliferative active and well oxygenated areas within the tumor.
Local Manufacture of CD19 CAR-T Cells Using an Automated Closed-System: Robust Manufacturing and High Clinical Efficacy with Low Toxicities
Authors: Olga Molostova, Larisa Shelikhova, Dina Schneider, Rimma Khismatullina, Yakov Muzalevsky, Alexey Kazachenok, Liane Preussner, Georg Rauser, Julia Abugova, Elena Kurnikova, Dmitriy Pershin, Viktoria Zubachenko, Alexander Popov, Olga Illarionova, Natalia Miakova, Dmitry Litvinov, Galina Novichkova, Alexey A. Maschan, Rimas Orentas, Boro Dropulic, Michael Maschan
Journal: Blood (2019)
DRES-13. DUAL KINASE INHIBITION TO COMBAT EGFR-INHIBITOR RESISTANCE IN GLIOBLASTOMA
Authors: Erin Smithberger, Abigail Shelton, Madison Butler, Alex Flores, Ryan Bash, Steven Angus, Michael East, Noah Sciaky, Harshil Dhruv, Gary Johnson, Michael Berens, Frank Furnari, C Ryan Miller
Journal: Neuro-Oncology (2019)

Abstract Glioblastoma (GBM) is an aggressive primary brain tumor with a poor survival rate. One of the most common molecular alterations seen in GBM is amplification and/or mutation of the Epidermal Growth Factor Receptor (EGFR), which has made it an attractive therapeutic target. However, several EGFR tyrosine kinase inhibitors have been tested clinically in GBM with minimal success. One reason for this lack of efficacy could be due to acute, adaptive resistance via alternative pathway activation. To investigate this mechanism of tumor resistance, we used RNA-seq and multiplex inhibitor bead/mass spectrometry (MIB-MS) to analyze the transcriptomes and kinomes of genetically engineered murine astrocytes with common GBM genotypes. We have previously shown that 38% of the expressed kinome varied among a panel of diverse nGEM astrocytes harboring Cdkn2a deletion (C) plus Pten deletion (CP), wild-type human EGFR (CE) or EGFRvIII (CEv3) overexpression or both EGFRvIII overexpression and Pten deletion (CEv3P). Although CE have a similar transcriptional profile to C cells at baseline, when treated with the EGFR inhibitor afatinib, CE respond more similarly to CEv3 cells. When cells containing endogenous murine EGFR (C and CP) are treated with afatinib, fewer than 0.5% of kinases showed differential expression. In cells with EGFR overexpression alone, more than 6% of kinases were differentially expressed upon afatinib treatment, including Ntrk3, Fgfr2 and 3, Lyn, Bmx, Epha2 and 5, Fn3k, a kinase involved in fructosamine processing, and Nrbp2, a kinase involved in regulation of apoptosis. This effect was blunted in cells lacking Pten in addition to having EGFRvIII (CEv3P), resulting in less than 2% of kinases being differentially expressed. The only kinase upregulated in all three EGFR-overexpressing cell types was Coq8a, which is involved in electron transport and response to DNA damage. Given this overlap in response, Coq8a could be a potential dual treatment target for GBM.
Policy Recommendations for Pharmacy Benefit Managers to Stem the Escalating Costs of Prescription Drugs: A Position Paper From the American College of Physicians
Authors: Hilary Daniel, Sue S. Bornstein
Journal: Annals of Internal Medicine (2019)

Recent discussions about the increasing prices of prescription drugs have focused on pharmacy benefit managers (PBMs), third-party intermediaries for various types of employers and government purchasers who negotiate drug prices in health plans and thus play a crucial role in determining the amount millions of Americans pay for medications. In this position paper, the American College of Physicians expands on its position paper from 2016 by offering additional recommendations to improve transparency in the PBM industry and highlighting the need for reliable, timely, and relevant information on prescription drug pricing for physicians and patients.
Hematological Response to Eculizumab in Paroxysmal Nocturnal Hemoglobinuria: Application of a Novel Classification to Identify Unmet Clinical Needs and Future Clinical Goals
Authors: Pierre-Edouard Debureaux, Fabiana Cacace, Bruno G.P. Silva, Federica Barone, Rodrigo T Calado, Flore Sicre de Fontbrune, Juliette Soret-Dulphy, Patrizia Ricci, Michela Sica, Rosario Notaro, Phillip Scheinberg, Austin Kulasekararaj, Antonio M. Risitano, Régis Peffault de Latour, Camilla Frieri
Journal: Blood (2019)
Hospital Junior Staff
Authors: T. H. Sellors, H. H. Langston
Journal: BMJ (1965)

Sir,?The very real problems and grievances of junior hospital doctors were fully examined in  An Appraisal of the Hos pital   published by the B.M.A. in July {Supplement, 17 July, p. 70). The memorandum made far-reaching proposals about their pay, hours of work, residence charges and other expenses, residential accom modation, and study leave. Some of these proposals are about to be included in the profession's evidence to the Review Body, and others are under negouation with the Health Departments. The pay proposals in  An Appraisal of the Hospital Service were made in terms of the rates prevailing in 1963-6, and it was clearly indicated (in para graph 4 of the memorandum) that higher figures would be proposed to the Review Body for the period 1966-9. The Joint Consultants Committee's evidence to the Review Body is almost ready for submission. Expert economic and statisti cal advice on the betterment factor has been obtained ?nd substantially higher figures than those mentioned in  An Appraisal of the Hospital   will be proposed to the Review Body. A substantially higher mini mum figure than ?1,000 will be proposed for house-officers. The B M.A. has an active and representa tive Hospital Junior Staffs Group, whose considered views on the terms and condiuons of service of junior hospital doctors were published in the B.M.J. (Supplement, 21 August, p. 119) Full attention to these views ha> been paid by the Joint Consultants Com mittee in preparing its evidence for the Review Body, and there is very little of substance berween the desires of the Hospital Junior Staffs Group and the evidence being prepared by the Joint Evidence Qmimittee.?We are, etc., T. Holmes Sellors, Chairman, Joint Consultants Committee.
A commentary on “Cost-effectiveness of a national quality improvement programme to improve survival after emergency abdominal surgery, Health Economic Evaluation” (Int J Surg 2019; Oct 8. pii: S1743-9191(19)30264-X [Epub ahead of print]). What is the real impact of a quality improvement (QI) Programme for emergency abdominal surgery in quality of life?
Authors: Leandro Ryuchi Iuamoto, Alberto Meyer
Journal: International Journal of Surgery (2019)
Blockade of IL-15 Utilizing Bnz-1, a Selective γ-Chain Inhibiting Peptide, Is Safe and Has Clinical Activity in Patients with T-Cell Large Granular Lymphocytic Leukemia (T-LGLL): Results of a Phase I/II Multi-Center Clinical Trial
Authors: Jonathan E. Brammer, Lubomir Sokol, Yutaka Tagaya, Kerry Rogers, Anjali Mishra, Thomas A. Waldmann, Nazli Azimi, Paul Frohna, Anoshie Ratnayake, Thomas P Loughran, Karen Ballen
Journal: Blood (2019)
The Role of Proteasome Activator PA28α in Multiple Myeloma
Authors: Yanyan Gu, Benjamin G Barwick, Mala Shanmugam, Craig C Hofmeister, Jonathan L. Kaufman, Ajay K Nooka, Vikas A. Gupta, Madhav V Dhodapkar, Lawrence H. Boise, Sagar Lonial
Journal: Blood (2019)
CD20 Is an Unstable Target in Primary-Refractory High-Grade Lymphomas
Authors: Ryan N Rys, Dominique Geoffrion, Christopher Rushton, Miguel Alcaide, Raoul Santiago, Koren Kathleen Mann, Svetlana Dmitrienko, Tina Petrogiannis-Haliotis, Sarit Assouline, Ryan D. Morin, Nathalie Johnson
Journal: Blood (2019)
Genomic Resources for Darters (Percidae: Etheostominae) Provide Insight into Postzygotic Barriers Implicated in Speciation
Authors: Rachel L Moran, Julian M Catchen, Rebecca C Fuller
Journal: Molecular Biology and Evolution (2019)

Abstract Comparative genomic approaches are increasingly being used to study the evolution of reproductive barriers in nonmodel species. Although numerous studies have examined prezygotic isolation in darters (Percidae), investigations into postzygotic barriers have remained rare due to long generation times and a lack of genomic resources. Orangethroat and rainbow darters naturally hybridize and provide a remarkable example of male-driven speciation via character displacement. Backcross hybrids suffer from high mortality, which appears to promote behavioral isolation in sympatry. To investigate the genomic architecture of postzygotic isolation, we used Illumina and PacBio sequencing to generate a chromosome-level, annotated assembly of the orangethroat darter genome and high-density linkage maps for orangethroat and rainbow darters. We also analyzed genome-wide RADseq data from wild-caught adults of both species and laboratory-generated backcrosses to identify genomic regions associated with hybrid incompatibles. Several putative chromosomal translocations and inversions were observed between orangethroat and rainbow darters, suggesting structural rearrangements may underlie postzygotic isolation. We also found evidence of selection against recombinant haplotypes and transmission ratio distortion in backcross hybrid genomes, providing further insight into the genomic architecture of genetic incompatibilities. Notably, regions with high levels of genetic divergence between species were enriched for genes associated with developmental and meiotic processes, providing strong candidates for postzygotic isolating barriers. These findings mark significant contributions to our understanding of the genetic basis of reproductive isolation between species undergoing character displacement. Furthermore, the genomic resources presented here will be instrumental for studying speciation in darters, the most diverse vertebrate group in North America.
Computed Tomography Total Airway Count Is Associated with the Number of Micro–Computed Tomography Terminal Bronchioles
Authors: Miranda Kirby, Naoya Tanabe, Dragoş M. Vasilescu, Joel D. Cooper, John E. McDonough, Stijn E. Verleden, Bart M. Vanaudenaerde, Don D. Sin, Wan C. Tan, Harvey O. Coxson, James C. Hogg
Journal: American Journal of Respiratory and Critical Care Medicine (2019)
Results from Treatment of a Large Cohort of ATL Patients from a Country with High HTLV1 Prevalence
Authors: Horia Bumbea, Ambroise Marçais, Daniel Coriu, Alina Daniela Tanase, Andrei Colita, Alexandru Bardas, Anca Roxana Lupu, Ana-Maria Vladareanu, Minodora Cezarina Onisai, Viola Maria Popov, Iuliana Iordan, Magda Diana Cisleanu, Daniela Stefania Vasile, Cristina Maria Ciufu, Zsofia Varady, Oana Gabriela Craciun, Daniela Georgeta Georgescu, Mihaela Andreescu, Cristina Mambet, Carmen C. Diaconu, Laura Necula, Monica Bunaciu, Adriana Necula, Stefan N Constantinescu, Olivier Hermine
Journal: Blood (2019)
Novel Evidence That the Pannexin 1 Channel Is Involved in Adenosine Triphosphate (ATP) Release from Cells for Optimal Mobilization of Hematopoietic Stem Progenitor Cells, and the Pannexin 1 SNP 5 (Rs3020015) T/C Polymorphism Characterizes Poor Mobilizer Status in Patients
Authors: Monika Cymer, Mateusz Adamiak, Marta Skoda, Marta Antonina Libura, Elzbieta Urbanowska, Magdalena Kucia, Mariusz Z Ratajczak
Journal: Blood (2019)
Investigation of New Therapeutic Compounds for Juvenile Myelomonocytic Leukemia Using Induced Pluripotent Stem Cells with Stably Activated Ras Pathway
Authors: Lisa Maria Kuhn, Cyrill Schipp, Daniel Hein, Bianca Killing, Nan Qin, Vera H Jepsen, Heinz Ahlert, Jasmin Bartl, Viktoria Marquardt, David Pauck, Kai Völtzke, Jonathan Lim, Gabriel Leprivier, Marc Remke, Sanil Bhatia, Thorsten Rosenbaum, Arndt Borkhardt, Ute Fischer
Journal: Blood (2019)
Serum Creatine Kinase and Exercise
Authors: B. P. Hughes
Journal: BMJ (1965)

Natural Hepatotoxins SIR,-The juxtaposition of your recent leading article (15 May, p. 1261) on natural hepatotoxins with that on communication difficulties inherent in the increasing proliferation of specialist journals (" Too Many Words," p. 1264) was timely.For the ques- tion, " Are these toxins in any part responsible for the chronic liver disease which is so wide-
Characteristics and Outcomes of Therapy-Related Versus De Novo Acute Myeloid Leukemia with Normal Karyotype
Authors: Bachar Samra, Guillaume Richard-Carpentier, Farhad Ravandi, Tapan M. Kadia, Veronica A Guerra, Naval G. Daver, Courtney D. DiNardo, Ghayas C. Issa, Prithviraj Bose, Musa Yilmaz, Maro Ohanian, Gautam M. Borthakur, Guillermo Garcia-Manero, Sherry A. Pierce, Jorge E. Cortes, Hagop M. Kantarjian, Nicholas J. Short
Journal: Blood (2019)
PDTM-27. THE CRISPR-Cas9 SYSTEM-MEDIATED ENDOGENOUS GENE-REARRANGEMENT INDUCED C11orf95-RELA FUSION IN VITRO AND IN VIVO THAT LED TO DEVELOPMENT OF BRAIN TUMORS
Authors: Mutsumi Takadera, Tatsuya Ozawa, Tetsuya Yamamoto, Koichi Ichimura
Journal: Neuro-Oncology (2019)

Abstract Recent large-scale genomic studies of ependymal tumors have identified recurrent RELA and YAP1 fusion genes in supratentorial ependymomas. We have so far shown that C11orf95-RELA fusion was a potent oncogene capable of inducing human ependymoma-like tumors in the RCAS/tv-a retroviral gene transfer system. However, molecular mechanism underlying the tumor formation has not been fully investigated. Given that C11orf95-RELA fusion genes are caused by gene rearrangement between C11orf95 and RELA gene due to chromothripsis involving 11q, it has been suggested that expression of these fusion genes is regulated under the C11orf95 promoter. In this study, we developed a system to reproduce the oncogenic gene rearrangement using the CRISPR-Cas9 system and examined if consequent endogenous ependymoma fusion genes are competent to form brain tumor in mice. Initially, we designed guide RNAs on the human and mouse genomic loci corresponding to breakpoints observed in human RELA fusion positive ependymomas and introduced them into HEK293T or NIH3T3 cells. RT-PCR and immunoblot analyses revealed that a combination of multiple guide RNAs efficiently induced gene rearrangement between C11orf95 and RELA gene, resulting in C11orf95-RELA fusion protein. Subsequently, we introduced the same guide RNAs using a lentiviral gene transfer system into mouse brain. Brain tumor formation was observed around 2 months after the guide RNA delivery, indicating successful gene rearrangement followed by C11orf95-RELA fusion expression in vivo. These results thus firmly establish that a gene rearrangement is the mechanism to form the C11orf95-RELA fusion which is the direct driver of tumorigenesis. Furthermore, we found that endogenous YAP1-FAM118B fusion gene can be also induced with a similar experimental strategy to that of C11orf95-RELA fusion. Our system to simulate genomic event will provide insights into the tumorigenic mechanism of ependymomas that harbor various fusion genes.
Treatment of High Risk Diffuse Large B-Cell Lymphomas (DLBCL) with Ntensive Induction Chemotherapy, Rituximab and Autologous Stem Cell Transplant.
Authors: Robert Pytlik, Marek Trneny, David Belada, Jan Pirnos, Katerina Kubackova, Milada Jankovska, Ingrid Vasova, Tomas Kozak, Jana Pukyova, Jana Pribylova, Hana Siffnerova, Pavel Zak, Michaela Hamouzova, Pavel Klener
Journal: Blood (2005)
Fractionated Dosing of CLR 131 in Patients with Relapsed or Refractory Multiple Myeloma (RRMM)
Authors: Sikander Ailawadhi, Patrick J. Stiff, Emad Ibrahim, Anusha Vallurupalli, Elizabeth H. Cull, Damian J. Green, Kate Oliver, Jarrod Longcor
Journal: Blood (2019)
Public Health Insurance Expansion for Immigrant Children and Interstate Migration of Low-Income Immigrants
Authors: Vasil I. Yasenov, Duncan Lawrence, Fernando S. Mendoza, Jens Hainmueller
Journal: JAMA Pediatrics (2019)

Federal policy changes in 2002 and 2009 led some states to expand public health insurance coverage to non-US-born children and pregnant women who are lawful permanent residents during their first 5 years of residency in the United States. In other states, there were concerns that insurance expansion could attract immigrants to relocate to gain free health insurance coverage.To examine whether expansion of public health insurance to non-US-born, lawful permanent resident children and pregnant women during their first 5 years of residency is associated with increased interstate migration among these groups.This difference-in-differences analysis included data on 208 060 immigrants from the American Community Survey from 2000 through 2016, with analysis including all 50 states and the District of Columbia. The study sample included 2 treatment groups that became eligible under the expanded coverage: lawful permanent resident adults with at least 1 non-US-born child younger than 18 years (n = 36 438) and lawful permanent resident women of reproductive age (n = 87 418). Control groups that remained ineligible under the expanded coverage included lawful permanent resident adults without non-US-born children (n = 171 622), lawful permanent resident single men (n = 56 142), and lawful permanent resident postreproductive women (n = 15 129). A difference-in-differences design compared migration rates between eligible and ineligible immigrant groups before and after insurance coverage expansions. Data analysis was performed from November 3, 2018, to May 31, 2019.Public health insurance coverage for immigrant women and children who were lawful permanent residents within 5 years of residency.Migration to a health expansion state from any other state and from a neighboring state.Of 208 060 immigrants (47% women in the weighted sample; mean [SD] age, 32.97 [12.94] years; 63% Hispanic), the mean (SD) annual move rate across the entire sample was 3% (17%). Expansion of public health insurance to non-US-born children or pregnant women within their first 5 years of residency was not associated with interstate movement for health care benefits. Coverage expansion for non-US-born children of lawful permanent residents was not associated with a change in the rate of in-migration higher than 1.78 percentage points or lower than -1.28 percentage points. The corresponding estimate for coverage expansion of lawful permanent resident pregnant women was a change higher than 1.38 percentage points and lower than -1.20 percentage points.The results suggest that states considering expanding health care benefits coverage to recently arrived immigrant children and pregnant women may be unlikely to experience in-migration of these persons from other states, which has important implications for understanding short- and long-term program costs.
Debulking Eliminates Need for Hospitalization Prior to Initiating Frontline Venetoclax Therapy in Previously Untreated CLL Patients: A Phase 3b Study
Authors: Jeff P. Sharman, David Andorsky, Jason M. Melear, Sudhir Manda, Bertrand M. Anz, Kathryn S. Kolibaba, Habte A Yimer, John M Burke, Suzanne R. Fanning, Jay Courtright, Miguel Islas-Ohlmayer, Suman Kambhampati, Abdullah Al Masud, Todd Zimmerman, Jacqueline Nielsen, Tamas Vizkelety, Dingfeng Jiang, Ian W. Flinn
Journal: Blood (2019)
TMIC-40. YKL-40 AS MODULATOR OF CANCER STEM CELL PHENOTYPIC TRANSITIONS IN HUMAN GLIOBLASTOMAS
Authors: Charlotte Guetta-Terrier, Bedia Akosman, Suchitra Kamle, Eduardo Fajardo, Andras Fiser, Chun G Lee, Steven A Toms, Jack A Elias, Nikos Tapinos
Journal: Neuro-Oncology (2019)

Abstract Glioblastoma (GBM) is one of the most aggressive human tumors. Recent studies have shown that GBM “aggressiveness” is mainly due to populations of glioma stem cells (GSCs) within the tumor mass, which exhibit high migratory potential [3–5], form secondary tumors and can resist chemotherapy and radiation [6]. GSCs exhibit remarkable plasticity, are able to transition between immature and differentiated stages as well as reversibly express various phenotypic markers depending on the tumor microenvironment [7, 8]. Given such challenging features, GSCs have been subject of extensive research. YKL-40 (or Chitinase 3-like1) is a secreted glycoprotein normally expressed by numerous cell types including neutrophils and macrophages [11]. YKL-40 is highly expressed in numerous types of cancer such as breast, colon, lung, ovary, prostate, rectum and GBM [12–15]. RNA-seq on patient-derived GBMs and TCGA database analysis, showed that YKL-40 is one of the highest expressed genes in GBM. YKL-40 expression is associated with the invasiveness, therapy resistance and low survival rate of patients [16]. Here, we aim to elucidate the mechanistic function of YKL-40 in the microenvironment of human glioblastomas and determine its role as a new therapeutic target. We hypothesize that YKL-40 regulates transitions of GSCs phenotypes that underlie glioblastoma invasiveness and aggression. Our preliminary data show that incubation of patient-derived GSCs with YKL-40 induces a marked phenotypic change of GSCs from CD133+/Sox2+ to CD44+/YKL40+. We also performed RNA-seq and ATAC-seq to study the role of YKL-40 in gene expression and chromatin accessibility and identified the YKL-40-modulated transcriptional regulatory network that drives the phenotypic “switch” of GSCs. Finally, we used a novel humanized monoclonal antibody against YKL-40 to treat orthotopic glioblastoma xenografts and show significant reduction of tumor volume. Our work implicates YKL-40 as a microenvironment modulator of GSC phenotypic transitions and demonstrates pre-clinical efficacy of targeting YKL-40 to reduce tumor burden.
Disease Model of Atherosclerosis Using Werner Syndrome Patient-Derived Induced Pluripotent Stem Cells Reveals Excessive Inflammatory Response Against Ox-LDL
Authors: Sudip Kumar Paul, Masamitsu Sone, Hisaya Kato, Yoshiro Maezawa, Yasuo Ouchi, Koutaro Yokote, Koji Eto, Naoya Takayama
Journal: Blood (2019)
Multicenter, Open-Label, Single Arm, Phase II Exploratory Study to Evaluate the Effect of a One-Year Consolidation Treatment with Ponatinib 15 Mg on Treatment Free-Remission Rate in Patients with Philadelphia-Positive Chronic Myeloid Leukemia, Who Had Previously Achieved a Deep Molecular Response with Imatinib (PonaZero_study)
Authors: Valentin Garcia Gutierrez, Luis Felipe Casado, Rosa Ayala, Fermin Sanchez-Guijo, Juan Carlos Hernandez Boluda, María Teresa Gomez Casares, Blanca Xicoy, Begonya Maestro, Juan Luis Steegmann, Arturo Garcia de Diego
Journal: Blood (2019)