tbuckley/cabot-search huggingface dataset:
Donor Stem Cell Source Does Not Impact Outcome of High Risk (HR) Acute Myeloblastic Leukaemia (AML) Patients After Reduced Intensity Conditioning Allogeneic Hematopoietic Stem Cell Transplantation (RIC-ALLO).
Authors: Sabine Furst, Luca Castagna, Thomas Prébet, Claude Lemarie, Jean El Cheikh, Catherine Faucher, Norbert Vey, Aude Charbonnier, Patrick Ladaique, Christian Chabannon, Didier Blaise
Journal: Blood (2009)
Therapeutic strategies of drug repositioning targeting autophagy to induce cancer cell death: from pathophysiology to treatment
Authors: Go J. Yoshida
Journal: Journal of Hematology & Oncology (2017)

The 2016 Nobel Prize in Physiology or Medicine was awarded to the researcher that discovered autophagy, which is an evolutionally conserved catabolic process which degrades cytoplasmic constituents and organelles in the lysosome. Autophagy plays a crucial role in both normal tissue homeostasis and tumor development and is necessary for cancer cells to adapt efficiently to an unfavorable tumor microenvironment characterized by hypo-nutrient conditions. This protein degradation process leads to amino acid recycling, which provides sufficient amino acid substrates for cellular survival and proliferation. Autophagy is constitutively activated in cancer cells due to the deregulation of PI3K/Akt/mTOR signaling pathway, which enables them to adapt to hypo-nutrient microenvironment and exhibit the robust proliferation at the pre-metastatic niche. That is why just the activation of autophagy with mTOR inhibitor often fails in vain. In contrast, disturbance of autophagy–lysosome flux leads to endoplasmic reticulum (ER) stress and an unfolded protein response (UPR), which finally leads to increased apoptotic cell death in the tumor tissue. Accumulating evidence suggests that autophagy has a close relationship with programmed cell death, while uncontrolled autophagy itself often induces autophagic cell death in tumor cells. Autophagic cell death was originally defined as cell death accompanied by large-scale autophagic vacuolization of the cytoplasm. However, autophagy is a "double-edged sword" for cancer cells as it can either promote or suppress the survival and proliferation in the tumor microenvironment. Furthermore, several studies of drug re-positioning suggest that "conventional" agents used to treat diseases other than cancer can have antitumor therapeutic effects by activating/suppressing autophagy. Because of ever increasing failure rates and high cost associated with anticancer drug development, this therapeutic development strategy has attracted increasing attention because the safety profiles of these medicines are well known. Antimalarial agents such as artemisinin and disease-modifying antirheumatic drug (DMARD) are the typical examples of drug re-positioning which affect the autophagy regulation for the therapeutic use. This review article focuses on recent advances in some of the novel therapeutic strategies that target autophagy with a view to treating/preventing malignant neoplasms.
Impact of JAK2V617F Mutational Status on Clinical and Laboratory Phenotype at Diagnosis and during Follow-up in Patients with Essential Thrombocythemia
Authors: Elena Elli, Angelo Belotti, Matteo Parma, Federica Colnaghi, Arianna Colombo, Eraldo Lanzi, Pietro Pioltelli, Enrico Maria Pogliani
Journal: Blood (2008)
The Global Threat of Outdoor Ambient Air Pollution to Cardiovascular Health
Authors: Robert D. Brook, David E. Newby, Sanjay Rajagopalan
Journal: JAMA Cardiology (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 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
A Single Chronic Myeloid Leukemia (CML) Stem Cell Harboring Both BCR-ABL and JAK2-V617F Mutation Modeled by Induced Pluripotency
Authors: Ivan Sloma, Maria Teresa Mitjavila-Garcia, Olivier Feraud, Lucie Tosca, Sanaa El Marsafy, Emilie Gobbo, Dominique Divers, Alexis Proust, Marie Laure Bonnet, Frank Griscelli, Gerard Tachdjian, Annelise Bennaceur-Griscelli, Ali G Turhan
Journal: Blood (2012)
Elevated hematocrit enhances platelet accumulation following vascular injury
Authors: Bethany L. Walton, Marcus Lehmann, Tyler Skorczewski, Lori A. Holle, Joan D. Beckman, Jeremy A. Cribb, Micah J. Mooberry, Adam R. Wufsus, Brian C. Cooley, Jonathan W. Homeister, Rafal Pawlinski, Michael R. Falvo, Nigel S. Key, Aaron L. Fogelson, Keith B. Neeves, Alisa S. Wolberg
Journal: Blood (2017)
Cytomegalovirus Infections Following Reduced-Intensity Allogeneic Stem Cell Transplantation.
Authors: Ryotaro Nakamura, Sandra Cohen, Joycelynne Palmer, Ghislaine Hawkins, Bernard Tegtmeier, Ricardo Spielberger, Eileen Smith, James Ito, Margaret R. O’Donnell, David Smith, John A. Zaia, Stephen J. Forman
Journal: Blood (2004)
Thrombospondin-1 Polymorphisms Are Associated with Chronic Kidney Disease in Sickle Cell Anemia
Authors: Seethal A. Jacob, Enrico M. Novelli, Jeffrey S. Isenberg, Melanie E. Garrett, Yanxia Chu, Karen L. Soldano, Kenneth I. Ataga, Marilyn J. Telen, Allison E. Ashley-Koch, Yingze Zhang, Gregory J Kato
Journal: Blood (2016)
A Phase I Study of Escalated Dose Subcutaneous Alemtuzumab Given Weekly with Rituximab In Relapsed CLL/SLL.
Authors: Jennifer R Brown, Bradley Messmer, Lillian Werner, Evgeny Mikler, David C. Fisher, Ann LaCasce, Philippe Armand, Eric D Jacobsen, Virginia Dalton, Bethany Tesar, Stacey M Fernandes, Sean McDonough, Jerome Ritz, Laura Z Rassenti, Thomas J. Kipps, Donna Neuberg, Arnold S. Freedman
Journal: Blood (2010)
Combination of Sorafenib and 5-Azacytidine in Older Patients with Untreated Acute Myeloid Leukemia with FLT3-ITDmutation
Authors: Maro Ohanian, Guillermo Garcia-Manero, Elias J. Jabbour, Naval Daver, Gautam Borthakur, Tapan M. Kadia, Mark Brandt, Sherry Pierce, Jan Burger, Mary Ann Richie, Keyur Patel, Jorge E. Cortes, Hagop M. Kantarjian, Farhad Ravandi
Journal: Blood (2016)
A Unique Recombinant Fluoroprobe Targeting Activated Platelets Allows <i>In Vivo</i> Detection of Arterial Thrombosis and Pulmonary Embolism Using a Novel Three-Dimensional Fluorescence Emission Computed Tomography (FLECT) Technology
Authors: Bock Lim, Yu Yao, Alex Lin-i Huang, May Lin Yap, Ulrike Flierl, Jathushan Palasubramaniam, Maria T.K. Zaldivia, Xiaowei Wang, Karlheinz Peter
Journal: Theranostics (2017)

Progress in pharmaceutical development is highly-dependent on preclinical in vivo animal studies.Small animal imaging is invaluable for the identification of new disease markers and the evaluation of drug efficacy.Here, we report for the first time the use of a three-dimensional fluorescence bioimager called FLuorescence Emission Computed Tomography (FLECT) for the detection of a novel recombinant fluoroprobe that is safe, easily prepared on a large scale and stably stored prior to scan.This novel fluoroprobe (Targ-Cy7) comprises a single-chain antibody-fragment (scFvTarg), which binds exclusively to activated-platelets, conjugated to a near-infrared (NIR) dye, Cy7, for detection.Upon mouse carotid artery injury, the injected fluoroprobe circulates and binds within the platelet-rich thrombus.This specific in vivo binding of the fluoroprobe to the thrombus, compared to its non-targeting control-fluoroprobe, is detected by the FLECT imager.The analyzed FLECT image quantifies the NIR signal and localizes it to the site of vascular injury.The detected fluorescence is further verified using a two-dimensional IVIS ® Lumina scanner, where significant NIR fluorescence is detected in vivo at the thrombotic site, and ex vivo, at the injured carotid artery.Furthermore, fluorescence levels in various organs have also been quantified for biodistribution, with the highest fluoroprobe uptake shown to be in the injured artery.Subsequently, this live animal imaging technique is successfully employed to monitor the response of the induced thrombus to treatment over time.This demonstrates the potential of using longitudinal FLECT scanning to examine the efficacy of candidate drugs in preclinical settings.Besides intravascular thrombosis, we have shown that this non-invasive FLECT-imaging can also detect in vivo pulmonary embolism.Overall, this report describes a novel fluorescence-based preclinical imaging modality that uses an easy-to-prepare and non-radioactive recombinant fluoroprobe.This represents a unique tool to study mechanisms of thromboembolic diseases and it will strongly facilitate the in vivo testing of antithrombotic drugs.Furthermore, the non-radiation nature, low-cost, high sensitivity, and the rapid advancement of optical scanning technologies make this fluorescence imaging an attractive development for future clinical applications.
Uniform Requirements for Manuscripts Submitted to Biomedical Journals
Journal: JAMA (1997)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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
Natural killer cell–mediated inflammation resolution is disabled in severe asthma
Authors: Melody G. Duvall, Cindy Barnig, Manuela Cernadas, Isabell Ricklefs, Nandini Krishnamoorthy, Nicole L. Grossman, Nirav R. Bhakta, John V. Fahy, Eugene R. Bleecker, Mario Castro, Serpil C. Erzurum, Benjamin M. Gaston, Nizar N. Jarjour, David T. Mauger, Sally E. Wenzel, Suzy A. Comhair, Andrea M. Coverstone, Merritt L. Fajt, Annette T. Hastie, Mats W. Johansson, Michael C. Peters, Brenda R. Phillips, Elliot Israel, Bruce D. Levy
Journal: Science Immunology (2017)

Severe asthma is characterized by decreased NK cell cytotoxicity, and corticosteroids further disable NK cell function.
Abstract A03: Formins stabilize cell-ECM adhesions during invasion onset
Authors: Tim Fessenden, Yvonne Beckham, Mathew Perez-Neut, Guillermina Ramirez-San Juan, Margaret L. Gardel
Journal: Cancer Research (2017)

Abstract The onset of local invasion typically defines the transition from benign to malignant tumors. This pathological definition has clear implications for cell behaviors governing invasion onset, which nonetheless remain mysterious. Thus we asked whether established cytoskeletal regulators contributed specifically to invasion in multicellular ensembles. We investigated roles of actin nucleators from the formin family and the Arp2/3 complex during collective invasion by two cell types: tumor explants from PyMT mice, and acini of Manin-Darby Canine Kidney (MDCK) cells, which initiate collective invasion in response to Hepatocyte Growth Factor (HGF). Contrary to our expectations, inhibition of Arp2/3 did not prevent invasion in either cell type. The pan-formin inhibitor SMIFH2, however, drastically reduced invasive fronts in both cell types. This phenotype was specific to 3D invasion, as formins were dispensable for 2D motility by single cells or cell collectives. We identified Diaphanous 1 (Dia1) and FHOD1 as formin family members required for invasion by MDCK acini. Live imaging of Dia1 knockdown acini revealed that while they formed transient extensions into the collagen, these were too unstable to support invasion. Despite these defects, Dia1 knockdown cells could deform the collagen matrix locally and exerted traction stresses equal to controls. Stiffer, bundled collagen gels potentiated invasion by control acini but could not rescue invasion by Dia1 knockdown acini. We then imaged acini in which GFP-Lifeact and mCherry-Myosin Light Chain were coexpressed as they invaded into labelled collagen. During invasion onset, we observed formation of subcellular actomyosin puncta on minute timescales. These puncta could adhere stably and alter collagen even while the cell continued to change shape and migrate within the acinus. Such adhesions formed rarely and with unstable dynamics in Dia1 knockdown acini. Thus formins may contribute to malignancy through molecular and physical mechanisms distinct from overall cell contractility. Rather, they mediate invasion in 3D contexts where competing cell-cell and cell-ECM interactions make stringent local requirements of adhesion stability. This work provides a bridge between cell motility in 3D and canonical models of 2D migration. Citation Format: Tim Fessenden, Yvonne Beckham, Mathew Perez-Neut, Guillermina Ramirez-San Juan, Margaret L. Gardel. Formins stabilize cell-ECM adhesions during invasion onset. [abstract]. In: Proceedings of the AACR Special Conference on Engineering and Physical Sciences in Oncology; 2016 Jun 25-28; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2017;77(2 Suppl):Abstract nr A03.
BCL6 Overexpression – Regulated By AhR/ARNT and Wild-Type MEF2B – Drives Expression of Germinal Center Markers MYBL1 and LMO2
Authors: Hilmar Quentmeier, Jie Ding, Willy Dirks, Stefan Ehrentraut, Robert Geffers, Rod AF MacLeod, Stefan Nagel, Michaela Scherr, Lea AI Vaas, Hans G Drexler
Journal: Blood (2014)
VDAC1 is a molecular target in glioblastoma, with its depletion leading to reprogrammed metabolism and reversed oncogenic properties
Authors: Tasleem Arif, Yakov Krelin, Itay Nakdimon, Daniel Benharroch, Avijit Paul, Daniela Dadon-Klein, Varda Shoshan-Barmatz
Journal: Neuro-Oncology (2016)

Glioblastoma (GBM), an aggressive brain tumor with frequent relapses and a high mortality, still awaits an effective treatment. Like many cancers, GBM cells acquire oncogenic properties, including metabolic reprogramming, vital for growth. As such, tumor metabolism is an emerging avenue for cancer therapy. One relevant target is the voltage-dependent anion channel 1 (VDAC1), a mitochondrial protein controlling cell energy and metabolic homeostasis.We used VDAC1-specific short interfering (si)RNA (si-VDAC1) to treat GBM cell lines and subcutaneous or intracranial-orthotopic GBM xenograft mouse models. Tumors were monitored using MRI, immunohistochemistry, immunoblotting, immunofluorescence, quantitative real-time PCR, transcription factor expression, and DNA microarray analyses.Silencing VDAC1 expression using si-VDAC1 in 9 glioblastoma-related cell lines, including patient-derived cells, led to marked decreases in VDAC1 levels and cell growth. Using si-VDAC1 in subcutaneous or intracranial-orthotopic GBM models inhibited tumor growth and reversed oncogenic properties, such as reprogrammed metabolism, stemness, angiogenesis, epithelial-mesenchymal transition, and invasiveness. In cells in culture, si-VDAC1 inhibits cancer neurosphere formation and, in tumors, targeted cancer stem cells, leading to their differentiation into neuronal-like cells. These VDAC1 depletion-mediated effects involved alterations in transcription factors regulating signaling pathways associated with cancer hallmarks.VDAC1 offers a target for GBM treatment, allowing for attacks on the interplay between metabolism and oncogenic signaling networks, leading to tumor cell differentiation into neuron- and astrocyte-like cells. Simultaneously attacking all of these processes, VDAC1 depletion overcame GBM heterogeneity and can replace several anticancer drugs that separately target angiogenesis, proliferation, or metabolism.
Abstract A31: Proteomic characterization of stromal contribution to tumor using patient-derived xenografts
Authors: Jason E. McDermott, Tao Liu, Vladislav Petyuk, Richard Smith, Karin Rodland
Journal: Clinical Cancer Research (2016)

Abstract Patient-derived xenografts (PDXs) are an important and powerful tool to study many types of cancer and provide valuable insight into potential drug response and development of resistance. Due to the differences in tissue lineage PDXs also allow the dissection of stromal contribution to the tumor that is not easily obtainable from examination of the original tumor itself. We have applied mass-spectrometry enabled proteomics, phosphoproteomics, and RNAseq to compare primary metastasis, and PDXs derived from several metastatic sites from the same original tumor which was a colorectal adenocarcinoma. Comparing our results with a large-scale proteomic characterization of tumors performed under the clinical tumor analysis consortium (CPTAC) shows that the original metastasis, and PDXs from different sites, are significantly similar, regardless of metastasis site. Proteomic profiles of these samples are enriched in proteins expressed in the tissue of origin, rather than the site of metastasis. Pathway analysis from proteomics revealed enrichment in complement cascade, extracellular matrix receptors, and focal adhesion. These were different than the pathways indicated by the transcriptomics, which included cell cycle, focal adhesion, and MAP signaling, but not complement or extracellular matrix. We found in the case of complement and focal adhesion the original metastasis sample was very different from the PDX samples, if we only considered human protein contributions. Considering mouse proteins we found that the mouse stromal contribution complemented the human tumor contribution in the PDXs, aligning the functional analysis in both types of samples. Combining these results with subsequent analysis of driver mutations revealed that the proteomic contribution of stroma was as high as 40%. We have extended these observations to additional pairs of clinical tumor specimens and paired PDXs, including different tumor types. In all cases, there is greater similarity among the same sample type (resected tumor, metastatic lesion, or PDX) than between different sample types from the same patient. Citation Format: Jason E. McDermott, Tao Liu, Vladislav Petyuk, Richard Smith, Karin Rodland. Proteomic characterization of stromal contribution to tumor using patient-derived xenografts. [abstract]. In: Proceedings of the AACR Special Conference: Patient-Derived Cancer Models: Present and Future Applications from Basic Science to the Clinic; Feb 11-14, 2016; New Orleans, LA. Philadelphia (PA): AACR; Clin Cancer Res 2016;22(16_Suppl):Abstract nr A31.
What are the critical elements of sideline screening that can be used to establish the diagnosis of concussion? A systematic review
Authors: Jon Patricios, Gordon Ward Fuller, Richard Ellenbogen, Stanley Herring, Jeffrey S Kutcher, Mike Loosemore, Michael Makdissi, Michael McCrea, Margot Putukian, Kathryn J Schneider
Journal: British Journal of Sports Medicine (2017)

Background Sideline detection is the first and most significant step in recognising a potential concussion and removing an athlete from harm. This systematic review aims to evaluate the critical elements aiding sideline recognition of potential concussions including screening tools, technologies and integrated assessment protocols. Data sources Bibliographic databases, grey literature repositories and relevant websites were searched from 1 January 2000 to 30 September 2016. A total of 3562 articles were identified. Study selection Original research studies evaluating a sideline tool, technology or protocol for sports-related concussion were eligible, of which 27 studies were included. Data extraction A standardised form was used to record information. The QUADAS-2 and Newcastle-Ottawa tools were used to rate risk of bias. Strength of evidence was assessed using the Grades of Recommendation, Assessment, Development and Evaluation Working Group system. Data synthesis Studies assessing symptoms, the King-Devick test and multimodal assessments reported high sensitivity and specificity. Evaluations of balance and cognitive tests described lower sensitivity but higher specificity. However, these studies were at high risk of bias and the overall strength of evidence examining sideline screening tools was very low. A strong body of evidence demonstrated that head impact sensors did not provide useful sideline concussion information. Low-strength evidence suggested a multimodal, multitime-based concussion evaluation process incorporating video review was important in the recognition of significant head impact events and delayed onset concussion. Conclusion In the absence of definitive evidence confirming the diagnostic accuracy of sideline screening tests, consensus-derived multimodal assessment tools, such as the Sports Concussion Assessment Tool, are recommended. Sideline video review may improve recognition and removal from play of athletes who have sustained significant head impact events. Current evidence does not support the use of impact sensor systems for real-time concussion identification.
PGE2-treated macrophages inhibit development of allergic lung inflammation in mice
Authors: C. Draijer, C. E. Boorsma, C. Reker-Smit, Eduard Post, K. Poelstra, B. N. Melgert
Journal: American Journal of Respiratory and Critical Care Medicine (2016)

In healthy lungs, many macrophages are characterized by IL-10 production, and few are characterized by expression of IFN regulatory factor 5 (formerly M1) or YM1 and/or CD206 (formerly M2), whereas in asthma, this balance shifts toward few producing IL-10 and many expressing IFN regulatory factor 5 or YM1/CD206. In this study, we tested whether redressing the balance by reinstating IL-10 production could prevent house dust mite-induced allergic lung inflammation. PGE2 was found to be the best inducer of IL-10 in macrophages in vitro. Mice were then sensitized and challenged to house dust mites during a 2 wk protocol while treated with PGE2 in different ways. Lung inflammation was assessed 3 d after the last house dust mite challenge. House dust mite-exposed mice treated with free PGE2 had fewer infiltrating eosinophils in lungs and lower YM1 serum levels than vehicle-treated mice. Macrophage-specific delivery of PGE2 did not affect lung inflammation. Adoptive transfer of PGE2-treated macrophages led to fewer infiltrating eosinophils, macrophages, (activated) CD4(+), and regulatory T lymphocytes in lungs. Our study shows that the redirection of macrophage polarization by using PGE2 inhibits development of allergic lung inflammation. This beneficial effect of macrophage repolarization is a novel avenue to explore for therapeutic purposes.