tbuckley/cabot-search huggingface dataset:
Trends in Postpartum Depressive Symptoms — 27 States, 2004, 2008, and 2012
Authors: Jean Y. Ko, Karilynn M. Rockhill, Van T. Tong, Brian Morrow, Sherry L. Farr
Journal: MMWR Morbidity and Mortality Weekly Report (2017)

Postpartum depression is common and associated with adverse infant and maternal outcomes (e.g., lower breastfeeding initiation and duration and poor maternal and infant bonding) (1-3). A developmental Healthy People 2020 objective is to decrease the proportion of women delivering a live birth who experience postpartum depressive symptoms (PDS).* To provide a baseline for this objective, CDC sought to describe self-reported PDS overall, by reporting state, and by selected sociodemographic factors, using 2004, 2008, and 2012 data from the Pregnancy Risk Assessment Monitoring System (PRAMS). A decline in the prevalence of PDS was observed from 2004 (14.8%) to 2012 (9.8%) among 13 states with data for all three periods (p<0.01). Statistically significant (p<0.05) declines in PDS prevalence were observed for eight states, and no significant changes were observed for five states. In 2012, the overall PDS prevalence was 11.5% for 27 states and ranged from 8.0% (Georgia) to 20.1% (Arkansas). By selected characteristics, PDS prevalence was highest among new mothers who 1) were aged ≤19 years or 20-24 years, 2) were of American Indian/Alaska Native or Asian/Pacific Islander race/ethnicity, 3) had ≤12 years of education, 4) were unmarried, 5) were postpartum smokers, 6) had three or more stressful life events in the year before birth, 7) gave birth to term, low-birthweight infants, and 8) had infants requiring neonatal intensive care unit admission at birth. Although the study did not investigate reasons for the decline, better recognition of risk factors for depression and improved screening and treatment before and during pregnancy, including increased use of antidepressants, might have contributed to the decline. However, more efforts are needed to reduce PDS prevalence in certain states and subpopulations of women. Ongoing surveillance and activities to promote appropriate screening, referral, and treatment are needed to reduce PDS among U.S. women.
Comparative investigations of structure and properties of micro-arc wollastonite-calcium phosphate coatings on titanium and zirconium-niobium alloy
Authors: M.B. Sedelnikova, E.G. Komarova, Yu.P. Sharkeev, T.V. Tolkacheva, I.A. Khlusov, L.S. Litvinova, K.A. Yurova, V.V. Shupletsova
Journal: Bioactive Materials (2017)

Investigation results of micro-arc wollastonite-calcium phosphate (W-CaP) biocoatings on the pure titanium (Ti) and Zr-1wt.%Nb (Zr-1Nb) alloy were presented. The voltages of 150-300 V generate the micro-arc oxidation (MAO) process with the initial amplitude current of 150-550 A and 100-350 A for Ti and Zr-1Nb substrates, respectively. The identical dependencies of changes of the coating thickness, surface roughness and adhesion strength on the process voltage were revealed for the both substrates. The W-CaP coatings with the thickness of 10-11 μm were formed on Ti and Zr-1Nb under the low process voltage of 130-150 V. Elongated wollastonite particles with the size in the range of 40-100 μm were observed in such coatings. The structure of the coatings on Ti was presented by the X-ray amorphous and crystalline phases. The X-ray reflexes relating to the crystalline phases of Ti and wollastonite were observed only in XRD patterns of the coatings deposited under 130-200 V on Ti. While, the crystalline structure with phases of CaZr4(PO4)6, β-ZrP2O7, ZrO2, and Zr was detected in the coatings on Zr-1Nb. FT-IRS, XRD, SEM, and TEM data confirmed that the increase of the process voltage to 300 V leads to the dissociation of the wollastonite. No toxic effect of specimens on a viability, morphology and motility of human adipose-derived multipotent mesenchymal stem cells was revealed in vitro.
Role of epidermal growth factor and its soluble receptor in realization of anti-EGFR monoclonal antibodies effect in patients with head and neck cancer (HNC)
Authors: A. Agieva, O. Kit, E. Frantsiyants, L. Vladimirova, M. Engibaryan, I. Pustovaya, N. Cheryarina, Y. Pogorelova
Journal: Annals of Oncology (2016)
Serial Trough Anti-Xa Levels to Assess Low Molecular Weight Heparin Accumulation in Patients with Chronic Kidney Disease: Analysis of Crcl &lt;30 Ml/Min from the Trivet Study
Authors: Wendy Lim, Mark Crowther, Luqi Wang, James D. Douketis, Terri Schnurr, Cathy Moreau, Catherine Clase, Marc Rodger, Erik Yeo, Martine Leblanc, Philip McFarlane, Christine M. Ribic
Journal: Blood (2016)
Sequencing cabazitaxel and new generation hormonal treatments in metastatic castration resistant prostate cancer patients after first line docetaxel: a retrospective analysis
Authors: M. Tucci, C. Buttigliero, F. Vignani, D. Iaconis, V. Bertaglia, P. Bironzo, D. Pignataro, G.V. Scagliotti, M. Di Maio
Journal: Annals of Oncology (2016)
Characterization of a High-Affinity Fully Human IgG2 Antibody Against Tissue Factor Pathway Inhibitor As a Bypass Agent for the Treatment of Hemophilia
Authors: Maxine Bauzon, Bing Liu, Joanna Grudzinska-Goebel, Jan Tebbe, Junliang Pan, Jill Cifrese, Zhuozhi Wang, Derek Sim
Journal: Blood (2015)
Relationship between Adverse Events and Efficacy of Lenvatinib for Thyroid Cancer
Authors: Hideaki Goto, Naomi Kiyota, Naoko Chayahara, Kei Takenaka, Yoshinori Imamura, Meiko Nishimura, Masanori Toyoda, Toru Mukohara, Hironobu Minami
Journal: Annals of Oncology (2016)
Interactive waiting room project
Authors: L. Riccardi, V. Pozzali, M.T. Simioni, M. Cagnin, M. Soraru', A. Morabito, G. Palazzolo, R. Cavallo, M. Mion, L. Sartor, M. Beda, T. Sava, F. Gaion
Journal: Annals of Oncology (2016)
Biomarker driven combinations for synthetic lethal approaches in KRAS mutant (KRASm) lung adenocarcinoma (LAC)
Authors: C. Lazzari, A. Verlicchi, C. Codony Servat, J. Codony Servat, M.A. Molina Vila, I. Chaib, J.L. Ramírez Serrano, N. Karachaliou, F. de Marinis, R. Rosell
Journal: Annals of Oncology (2016)
Reduced-Intensity Unrelated Cord Blood Transplantation (RICBT) for Over 65 Year-Old Elderly Patients with Myeloid Malignancies
Authors: Aki Chizuka, Rie Kojima, Yoshiki Nakae, Ko Miyamoto, Kazuko Arai, Toshiyuki Noguchi, Shiesaburo Miyakoshi
Journal: Blood (2011)
Hereditary Mutations Are Present As Pathogenic or Predisposition Factors in Otherwise Typical Adult MDS
Authors: Bartlomiej P Przychodzen, Hideki Makishima, Brittney Dienes, Tomas Radivoyevitch, Hetty E. Carraway, Swapna Thota, Bhumika J Patel, Mikkael A. Sekeres, Jaroslaw P. Maciejewski
Journal: Blood (2014)
Birth Center Model of Care
Authors: Lesley Rathbun
Journal: JAMA (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Leukemia Inhibitory Factor (LIF): Marrow-Derived Human Mesenchymal Stem Cell (huMSC) Secretion and Potential Impact on Umbilical Cord Blood (UCB) CD133+ Hematopoietic Stem Cells (HSC) Differentiation.
Authors: G. Chapman, J.J. Banks, L.R. Fanning, M. Kozik, M.R. Finney, R.P. Weitzel, N.J. Greco, R. Sakthivel, Mary J. Laughlin
Journal: Blood (2006)
MPTH-52. GENOMIC LANDSCAPE OF ADULT MEDULLOBLASTOMAS CLASSIFIED ACCORDING TO WHO 2016 GUIDELINES
Authors: Torsten Pietsch, Tobias Goschzik, Marco Gessi, Andreas Waha, Peter Hau
Journal: Neuro-Oncology (2016)

Medulloblastoma (MB) in adults represents mainly two histological (classic, desmoplastic/nodular) and three genetic groups (WNT; SHH, TP53 wildtype; Non-WNT/non-SHH (neuroblastic) MB). Retrospective case collections indicated different outcomes of specific histological and genetic MB groups. The updated WHO classification of tumors of the CNS 2016 has established an integrated diagnostic system which contains histopathological as well as genetic information. In this study we validated a robust immunostaining algorithm for proper subclassification and studied genomic alterations in each subgroup by genome-wide molecular inversion profiling and NGS panel sequencing of medulloblastoma-associated genes. MB of 29 adult patients enrolled in the NOA-07 trail were tested; further 99 cases were retrieved from the archives of the German Brain Tumor Reference Center in Bonn. Using the protein markers ß-Catenin (WNT), Yap1 (WNT & SHH), p75NGFR (SHH), OTX2 (WNT & Neuroblastic) and p53, a secure annotation to each subgroup was possible in routine diagnostics. In the NOA-07 cohort, 14% were WNT, 70% SHH-TP53wt, and 17% neuroblastic MBs. In the extended cohort, typical genomic alterations were identified: 82% of WNT-MB carried mutations of CTNNB1; 47% showed monosomy of chromosome 6 (30% isolated monosomy 6). SHH-MB with desmoplastic/nodular histology in more than 75% were characterized by frequent chromosome 9q loss or copy-neutral LOH indicating inactivating PTCH1 mutations (41% of cases), chromosome 3q gains (29%) and chromosome 14q losses (24%). Alternative activation of the SHH pathway by PTCH1 or SMO mutations represented a frequent finding in these. Finally, the majority of neuroblastic MBs were characterized by isochromosome 17q and focal gains OTX2. Adult medulloblastomas represent three different disease entities that can be securely diagnosed by immunohistochemistry or alternative genomic methods. They are characterized by different driving oncogenic pathways and may deserve stratified treatment strategies. In addition to the MB classification, upfront panel sequencing allows identification of mutations of components of possible targetable pathways.
Polycomb Repressive Complex 1 Enhances HSC Self-Renewal through Repressing the Canonical Wnt Signaling Pathway
Authors: Sisi Chen, Xicheng Liu, Rui Gao, Michihiro Kobayashi, Hao Yu, Chonghua Yao, Zhijian Qian, Rongwen Xi, Yan Liu
Journal: Blood (2015)
Evaluation of VeriStrat, a serum proteomic test, in the randomized, open-label, Phase 3 LUX-Lung 8 trial of afatinib versus erlotinib for the second-line treatment of advanced squamous cell carcinoma of the lung
Authors: G. Goss, K.H. Lee, E. Felip, M. Cobo, K. Syrigos, E. Goker, V. Georgioulias, S.Z. Guclu, D. Isla, Y.J. Min, A. Morabito, N. Dupuis, V.K. Chand, F. Solca, N. Krämer, N. Gibson, E. Ehrnrooth, J.C. Soria
Journal: Annals of Oncology (2016)
Molecular Characterization of Chronic Lymphocytic Leukemia Patients with a High Number of Losses in 13q14.
Authors: Ana E Rodríguez, Jose Ángel Hernández-Rivas, Alberto Risueño, Encarna Fermiñán, Natalia de las Heras, Alfonso Garcia de Coca, Carlos Aguilar, Juan Nicolás Rodríguez, Josefina Galende, Javier de las Rivas, Jesús F San Miguel, Marcos González, Jesús M Hernández-Rivas
Journal: Blood (2012)
Ectopic Expression of Mir-125a or Mubritinib Treatment of Human Acute Promyelocytic Leukemia t(15; 17) NB4 Cells Containing Epigenitically Silenced Mir-125a Results in Inhibition of Cell Cycle Progression Through Targeting the Erbb2 Pathway.
Authors: Melanie Ufkin, Pradeep Sathyanarayana
Journal: Blood (2012)
Mutation and Single-Nucleotide Polymorphism (rs16754) in Wilms Tumor-1 Gene Are Independent Prognostic Factors in Acute Myeloid Leukemia.
Authors: Wanlong Ma, Hagop Kantarjian, XI Zhang, Xiuqiang Wang, Zhong Zhang, Chen-Hsiung Yeh, Anthony Sferruzza, Susan O'Brien, Maher Albitar
Journal: Blood (2009)
AG-221, a First-in-Class Therapy Targeting Acute Myeloid Leukemia Harboring Oncogenic <i>IDH2</i> Mutations
Authors: Katharine Yen, Jeremy Travins, Fang Wang, Muriel D. David, Erin Artin, Kimberly Straley, Anil Padyana, Stefan Gross, Byron DeLaBarre, Erica Tobin, Yue Chen, Raj Nagaraja, Sung Choe, Lei Jin, Zenon Konteatis, Giovanni Cianchetta, Jeffrey O. Saunders, Francesco G. Salituro, Cyril Quivoron, Paule Opolon, Olivia Bawa, Véronique Saada, Angelo Paci, Sophie Broutin, Olivier A. Bernard, Stéphane de Botton, Benoît S. Marteyn, Monika Pilichowska, YingXia Xu, Cheng Fang, Fan Jiang, Wentao Wei, Shengfang Jin, Lee Silverman, Wei Liu, Hua Yang, Lenny Dang, Marion Dorsch, Virginie Penard-Lacronique, Scott A. Biller, Shin-San Michael Su
Journal: Cancer Discovery (2017)

Abstract Somatic gain-of-function mutations in isocitrate dehydrogenases (IDH) 1 and 2 are found in multiple hematologic and solid tumors, leading to accumulation of the oncometabolite (R)-2-hydroxyglutarate (2HG). 2HG competitively inhibits α-ketoglutarate–dependent dioxygenases, including histone demethylases and methylcytosine dioxygenases of the TET family, causing epigenetic dysregulation and a block in cellular differentiation. In vitro studies have provided proof of concept for mutant IDH inhibition as a therapeutic approach. We report the discovery and characterization of AG-221, an orally available, selective, potent inhibitor of the mutant IDH2 enzyme. AG-221 suppressed 2HG production and induced cellular differentiation in primary human IDH2 mutation–positive acute myeloid leukemia (AML) cells ex vivo and in xenograft mouse models. AG-221 also provided a statistically significant survival benefit in an aggressive IDH2R140Q-mutant AML xenograft mouse model. These findings supported initiation of the ongoing clinical trials of AG-221 in patients with IDH2 mutation–positive advanced hematologic malignancies. Significance: Mutations in IDH1/2 are identified in approximately 20% of patients with AML and contribute to leukemia via a block in hematopoietic cell differentiation. We have shown that the targeted inhibitor AG-221 suppresses the mutant IDH2 enzyme in multiple preclinical models and induces differentiation of malignant blasts, supporting its clinical development. Cancer Discov; 7(5); 478–93. ©2017 AACR. See related commentary by Thomas and Majeti, p. 459. See related article by Shih et al., p. 494. This article is highlighted in the In This Issue feature, p. 443
The Effects of Imatinib on the Function of Monocyte Derived Dendritic Cells Are Mediated Via the Inhibition of Akt and NF-kappaB Signal Transduction Pathways.
Authors: Anette Rupf, Silke Appel, Markus M. Weck, Frank Grünebach, Lothar Kanz, Oliver Schoor, Tim H. Brümmendorf, Toni Weinschenk, Peter Brossart
Journal: Blood (2004)
Scalp Cooling to Prevent Chemotherapy-Induced Alopecia
Authors: Dawn L. Hershman
Journal: JAMA (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors 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
Autologous bone marrow transplantation for low-grade non-Hodgkin's lymphoma: The European Bone Marrow Transplant Group experience
Authors: H.C. Schouten, P.h. Colombat, L.F. Verdonck, N.C. Gorin, B. Björkstrand, G. Taghipour, A.H. Goldstone
Journal: Annals of Oncology (1994)
Soldiers’ load carriage performance in high mountains: a physiological study
Authors: Tirthankar Chatterjee, Debojyoti Bhattacharyya, Anilendu Pramanik, Madhusudan Pal, Deepti Majumdar, Dhurjati Majumdar
Journal: Military Medical Research (2017)

The present study was designed to evaluate load carriage performance at extremely high altitudes with different loads and walking speeds in terms of physiological evaluation. The degree of maximum oxygen consumption changes at high altitudes was also examined. Twelve Indian Army soldiers were acclimatized at altitudes of 3,505 m and 4,300 m. They walked for 10 minutes on a motorized treadmill at 2.5 km/h and 3.5 km/h speeds during carrying no loads and three magnitudes of load (10.7 kg, 21.4kg, 30 kg) at both altitudes. Physiological parameters such as oxygen consumption, energy expenditure, heart rate, and ventilation were recorded for each breath using a gas analyzer. The rating of perceived exertion was also noted after each load carriage session. Maximal oxygen consumption (VO2max) was measured at sea level and the two high altitudes, and respective relative workloads (% of VO2max) were calculated from oxygen consumption. Repeated measure ANOVA was applied to reveal the significant effects of the independent variables. The participants had significant reductions in VO2max with rising altitude. Marked increases in almost all physiological parameters were observed with increasing load, altitude, and speed. The soldiers expressed heavy perceived exertion levels with higher loads at 3.5 km/h at the two high altitudes. Considering the physiological responses, expressions of perceived exertion and changes in relative work load at both of the high altitudes Indian soldiers are advised to walk slowly with adequate rest in between their schedules and to carry not more than 32% of their body weight.
P01.11 The transcriptional coactivator PGC-1a promotes defence against reactive oxygen species (ROS) and proliferation in human glioma cells
Authors: I. Hartel, B. Sauer, M. Burger, M. W. Ronellenfitsch, J. P. Steinbach, J. Rieger
Journal: Neuro-Oncology (2016)

AbstractGene expression of many signalling pathways and metabolic programs is regulated at the transcriptional level by DNA binding coactivators. These coactivators act in a tissue-specific-manner and are responsive to different physiological stimuli like nutrient supply and temperature. One of these coactivators, Peroxisome proliferator-activated receptor- coactivator (PGC)-1α, is a master regulator of mitochondrial biogenesis, controls antioxidative responses and coordinates posttranscriptional events. The activity of PGC-1a is regulated by growth factor receptor signaling and the AMP-activated protein kinase (AMPK) pathway, both of which are crucial for the growth and metabolism of tumors. Further, because variable nutritional environments require tumor cells to adapt their energy metabolism, we asked whether PGC-1α is involved in growth, resistance against nutrient depletion and metabolic flexibility of glioma cells.We found that PGC-1α is expressed in a subset of established and primary glioma cells. Surprisingly, while suppression of PGC-1α expression by sh-RNA in U343MG glioma cells reduced glucose consumption and lactate production, it did not reduce oxygen consumption or mitochondrial mass. PGC-1α-sh cells had impaired proliferation and migration in vitro. Compatible to the known PGC-1α’s functions in reactive oxygen species (ROS) metabolism, glioma cells lacking PGC-1α expression had reduced RNA levels of proteins involved in (ROS) detoxification mechanism, and these cells were more susceptible to death induction by H2O2 compared to control cells. Interestingly, the PGC-1α-knock-down conferred protection against hypoxia-induced cell death. In an in-vivo-xenograft experiment, tumors formed by PGC-1α-suppressed glioma cells grew much slower than control tumors.In summary, PGC-1α is expressed in glioma cells and has an important role in growth and resistance against ROS in these cells. As the oxygen consumption in PGC-1α-sh cells was not significantly impaired, the presented effects of PGC-1α seemingly do not depend on the well-established functions of PGC-1α on mitochondrial oxidative phosphorylation. Further experiments are underway to analyse in more detail the metabolic and cellular functions of PGC-1α.
Patient preference of trastuzumab administration (SC versus IV) in HER2-positive metastatic breast cancer: Results of the randomised Metaspher study
Authors: X. Pivot, J.-P. Spano, E. Marc, P. Cottu, C. Jouannaud, V. Pottier, L. Moreau, J.-M. Extra, A. Lortholary, P. Rivera, D. Spaeth, H. Attar-Rabia, C. Benkamoun, L. Dima-Martinez, N. Esposito, J. Gligorov
Journal: Annals of Oncology (2016)
TMOD-16. BIOMATHEMATICAL MODEL OF PRONEURAL TUMORS SUGGESTS BEST CANDIDATES FOR PDGF-INHIBITOR THERAPIES
Authors: Susan Massey, Peter Canoll, Kristin Swanson
Journal: Neuro-Oncology (2016)

Platelet Derived Growth Factor (PDGF) is often over-expressed in gliomas, where it can drive tumor growth via autocrine stimulation of PDGF receptor (PDGFR) expressing glioma cells and via paracrine stimulation of non-neoplastic oligodendrocyte progenitor cells (OPCs), which also express PDGFRa. To date, the use of PDGF inhibitors has remained largely unsuccessful at improving patient outcomes in glioblastoma; however, this may be due to inadequate targeting of these agents to the best candidates. In particular, these therapies have been given in the recurrent setting, when tumors that had been predominantly comprised by OPCs and OPC-like glioma cells (e.g., proneural subtype) have transformed to a mesenchymal phenotype with fewer OPC-like cells, thereby precluding the opportunity to target OPC-like cells with these agents. Using a mathematical model of PDGF-driven glioma, we explore which patients might receive the greatest benefit from PDGF-targeted therapies. The results of our mathematical model show that tumors with higher levels PDGF signaling recruit more OPCs and grow faster, resulting in larger but less infiltrating tumors. By incorporating different treatment simulations in our model, we show that PDGF inhibition results in decreased OPC recruitment, which leads to slower growing, but more diffusely infiltrating tumors. This suggests that PDGF inhibitors may be most effective at treating patients with more rapidly proliferating, less infiltrative tumors which show a predominance of OPCs on immunohistochemistry. Further, the model suggests that they should be given earlier in the disease course, i.e., prior to recurrence, but following resection.
EXTH-37. CHEMOTHERAPY-INDUCED METABOLIC STRESS IN IDH1 MUTANT GLIOMAS
Authors: Kensuke Tateishi, Hiroaki Wakimoto, Fumi Higuchi, Julie Miller, Mara V. A. Koerner, Nina Lelic, Ganesh Shankar, Shota Tanaka, William T. Curry, David E. Fisher, Tracy T. Batchelor, A. John Iafrate, Andrew S. Chi, Daniel P. Cahill
Journal: Neuro-Oncology (2016)