tbuckley/cabot-search huggingface dataset:
MA 05.08 Very Early Response of Circulating Tumor Derived DNA Predict the Efficacy of Treatment by Nivolumab in Patients with Non-small Cell Lung Cancer
Authors: Y. Iijima, T. Nakagomi, Y. Uchida, Y. Kobayashi, T. Tsutsui, Y. Kakizaki, T. Goto, Y. Miyashita
Journal: Journal of Thoracic Oncology (2017)
EXTH-53. IMPACT OF EGFRvIII AND PTEN DELETION MUTATIONS ON RESPONSE OF Ink4a/Arf-NULL MURINE ASTROCYTES TO EGFR TYROSINE KINASE INHIBITORS
Authors: Erin Smithberger, Alex Flores, Harshil Dhruv, Gary Johnson, Michael Berens, Frank Furnari, C Ryan Miller
Journal: Neuro-Oncology (2017)

Epidermal growth factor receptor (EGFR) represents the most attractive target for personalized medicine of glioblastoma (GBM) due to its frequency in and specificity for the disease, and the availability of multiple inhibitors that target its tyrosine kinase domain. Despite its therapeutic attractiveness, several EGFR-targeted tyrosine kinase inhibitors (TKI) have failed clinically, in part due to multiple molecular mechanisms of resistance. To dissect the genetic contributions to EGFR TKI resistance, we examined the sensitivity of Ink4a/Arf (CDKN2A)-null murine astrocytes engineered to harbor EGFRvIII, the most common activating mutation in GBM where exons 2–7 of the extracellular domain are deleted, to a panel of first (gefitinib, erlotinib), second (lapatinib, afatinib), and third (AZD3759) generation EGFR TKI in vitro. Moreover, we examined the role of PTEN deletion mutations on drug sensitivity. We found that EGFRvIII conferred sensitivity to 4/5 drugs (ΔIC50 1.5-6.5-fold) in the presence of wild-type Pten and 5/5 (ΔIC50 1.5-78.0-fold) when Pten was deleted. In contrast, Pten deletion conferred resistance to 4/5 drugs (ΔIC50 5.6-17.7-fold) in Ink4a/Arf-null astrocytes with wild-type Egfr and 2/5 (ΔIC50 1.4-5.4-fold) when these cells harbored EGFRvIII. Moreover, Ink4a/Arf-null, EGFRvIII-mutated astrocytes developed cross resistance to the other 4 TKI (ΔIC50 2.6-11.0-fold) when grown continuously in the presence of increasing gefitinib (≤ 2 µM). We have previously shown that dynamic kinome responses may be responsible for TKI resistance. Therefore, we are currently using a chemical proteomics method consisting of multiplex inhibitor beads and mass spectrometry (MIB-MS) to assess the functional state of the kinomes of these non-germline genetically engineered mouse (nGEM) models en masse, both in the presence (dynamic profiling) and absence (baseline profiling) of EGFR TKI. Thus, functional kinome analysis using targeted EGFR TKI and MIB-MS will help define the kinase networks required for EGFRvIII-driven GBM pathogenesis and may aid in the identification of novel treatment combinations.
P1.05-003 Impact of Coexisting Pulmonary Diseases on Oncological Outcomes of Patients with pStage I Non-Small Cell Lung Cancer
Authors: H. Tao, H. Onoda, M. Hayashi, A. Hara, R. Miyazaki, D. Murakami, M. Furukawa, K. Okabe
Journal: Journal of Thoracic Oncology (2017)
Prospective translational study investigating circulating predictors of outcome to first-line pazopanib in patients with metastatic renal cell carcinoma (mRCC)
Authors: P. Grassi, E. Verzoni, R. Ratta, A. Martinetti, R. Montone, E. Tagliabue, F. de Braud, G. Procopio
Journal: Annals of Oncology (2017)
Une étude de cas de diphtérie acquise en laboratoire
Authors: H. K. Geiss, W Kiehl, W Thilo
Journal: Eurosurveillance (1997)

En mars 1996, une technicienne de laboratoire âgee de 41 ans presenta des malaises, une fievre moderee, un mal de gorge, une voix rauque et une dysphagie. Elle recut initialement un traitement symptomatique. Un jour plus tard, elle fut admise dans le service d'urgence d'une clinique d'oto-rhino-laryngologie avec des signes de dyspnee, un gonflement important du pharynx, une fausse membrane s'etendant au-dela de l'amygdale droite jusqu'au voile du palais, une adenopathie et un oedeme cervical. Une diphterie probable fut alors diagnostiquee. Une tracheotomie fut immediatement pratiquee.
PDTM-36. FUNCTIONAL GENOMIC ANALYSIS OF MYC-AMPLIFIED MEDULLOBLASTOMA NOMINATES THE TGFB PATHWAY AS A CLINICALLY VIABLE TARGET
Authors: Jacob Henderson, Hyeyoung Cho, Monika Davare, Aviad Tsherniak, Glenn Cowley, Barbara Weir, William C Hahn, Yoon-Jae Cho
Journal: Neuro-Oncology (2017)

Group 3, MYC-amplified medulloblastomas (MB) remain exceedingly difficult to treat despite maximum tolerable doses of chemotherapy and radiation. Additionally, strategies to directly target MYC are not readily available for clinical use in pediatrics. Thus, to identify novel genetic dependencies and potential therapeutic targets in MYC-amplified MB tumors, we screened MB cell lines using a high-throughput shRNA library of 102,000 unique hairpins targeting nearly all genes in the coding genome. As expected, we observed genes such as MYC and components of the PI3K and FOXO pathways as statistically significant genetic dependencies in MYC-amplified MB cells relative to >70 non-MB cancer cell lines. However, we also observed consistent and marked sensitivity to hairpins targeting genes in the TGFb pathway. Supporting these findings, a meta-analysis of multiple genomic profiling studies showed mutations and/or copy number variations in several components of the TGFb pathway in Group 3 MBs and we further confirmed the presence of activated TGFb/SMAD pathway in Group 3/MYC-amplified MB tumors. Treatment of MYC-amplified MB cells with the FDA-approved TGFb inhibitor, LY-2157299, resulted in marked inhibition of phospho-SMAD2/3 levels as well as inhibition of non-canonical targets of the TGFb pathway. Proliferation assays showed LY-2157299 preferentially inhibited growth in MYC-amplified MB cells compared to non-MYC-amplified MB lines. This growth inhibition was accompanied by loss of markers of epithelial to mesenchymal transition, a known proxy for infiltrative and metastatic phenotype. Lastly, mice harboring patient-derived orthotopic xenografts treated with LY-2157299 lived significantly longer relative to vehicle-treated mice with immunohistochemical confirmation of downregulated phospho-SMAD2 and increased cleaved caspase, in vivo. Thus, our functional genomic and pre-clinical validation studies nominate TGFb pathway inhibitors as a therapeutic strategy for patients with Group 3/MYC-amplified medulloblastomas.
A Tale of Two Countries
Authors: Dawn E. DeWitt
Journal: Annals of Internal Medicine (2017)

Letters7 November 2017A Tale of Two CountriesDawn E. DeWitt, MD, MScDawn E. DeWitt, MD, MScFrom Washington State University, Spokane, Washington.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/L17-0393 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:Dr. Kumar's experience in the United Kingdom and the United States validates the idea that other systems with outcomes as good as or better than those in the United States may function better for both physicians and patients. I respectfully disagree that we cannot have the best of both worlds. Why should the United States not identify and improve upon the most effective systems in the world while eliminating barriers and waste? Our best innovations improve upon the work and experience of experts to make them more user friendly (for example, the Apple iPhone).I also propose that ...References1. Erickson SM, Rockwern B, Koltov M, McLean RM; Medical Practice and Quality Committee of the American College of Physicians. Putting patients first by reducing administrative tasks in health care: a position paper of the American College of Physicians. Ann Intern Med. 2017;166:659-61. [PMID: 28346948]. doi:10.7326/M16-2697 LinkGoogle Scholar2. Sinsky CA. Designing and regulating wisely: removing barriers to joy in practice. Ann Intern Med. 2017;166:677-8. [PMID: 28346949]. doi:10.7326/M17-0524 LinkGoogle Scholar3. Wible P. I just lost my son to suicide. What can I do? KevinMD. 20 June 2017. Accessed at www.kevinmd.com/blog/2017/06/just-lost-son-suicide-can.html on 19 September 2017. Google Scholar Author, Article, and Disclosure InformationAffiliations: From Washington State University, Spokane, Washington.Disclosures: Disclosures can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M17-0244. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoA Tale of Two Countries: How I Saw More Patients With More Joy in Internal Medicine Practice Dawn E. DeWitt A Tale of Two Countries Vaibhav Kumar Metrics 7 November 2017Volume 167, Issue 9Page: 687KeywordsComplex systemsDisclosureHealth careInternational Classification of DiseasesPatientsSuicide ePublished: 7 November 2017 Issue Published: 7 November 2017 Copyright & PermissionsCopyright © 2017 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
CSIG-18. RALOXIFENE SENSITIZES GLIOBLASTOMA CELLS TO HYPOXIA-INDUCED DEATH THROUGH INHIBITION OF RNA STRESS GRANULE DISSOLUTION
Authors: Aaron Robichaud, Michel Roberge, Aruna Balgi, Craig McCormick, Adrienne Weeks
Journal: Neuro-Oncology (2017)

Glioblastoma (GBM) is the most common primary malignant brain tumour, and carries a uniformly poor prognosis. Despite aggressive therapy, median survival is only 14 months. Death typically results from treatment failure and local recurrence. The GBM microenvironment is highly hypoxic, and previous work has shown that cells residing in this region are more resistant to treatment. Cytoplasmic RNA stress granules (SGs) form in response to hypoxic stress and act as sites of mRNA triage, allowing translational machinery to focus on the translation of pro-survival mRNA during stress thus increasing the probability of cell survival. We hypothesize that SGs may play a role in hypoxia-induced resistance to therapy. We therefore conducted a drug screen to identify drugs that altered the formation or dissolution of SGs in hypoxia. Utilizing high content array scanning, we screened 1280 currently approved compounds (the Prestwick Drug Library) to identify drugs that inhibited formation or dissolution of SGs. We identified 99 candidate drugs inhibiting SG formation and 129 candidate drugs inhibiting SG dissolution. Our screen identified three selective estrogen receptor modulators (SERMs) as potential novel inhibitors of SG dissolution. The most potent effect was observed with raloxifene, which delays SG dissolution in a dose-dependent manner. When raloxifene was administered to U251 glioma cells prior to hypoxia, the combination achieved synergistic killing of tumour cells. Western blotting for cleaved PARP and LC3II demonstrated increased levels of apoptosis and autophagy, respectively, in combination treatment conditions. Taken together, this data would suggest that raloxifene induces apoptotic and autophagic death in GBM cells through its inhibitory effects on SG dissolution. As raloxifene is a currently approved drug already in use in humans, promising data could lead to a phase III clinical trial in GBM patients.
P3.02-085 Sphingosine Kinase 1 (SPHK1) Promotes Proliferation and Survival in Non-Small Cell Lung Cancer
Authors: N. Motono, Y. Ueda, A. Funasaki, T. Matsui, R. Maeda, A. Sekimura, K. Usuda, H. Uramoto
Journal: Journal of Thoracic Oncology (2017)
ACTR-68. CONCORDANCE OF EGFR AND MGMT ANALYSES BETWEEN LOCAL AND CENTRAL LABORATORIES: IMPLICATIONS FOR CLINICAL TRIAL DESIGN AND PRECISION MEDICINE FOR DEPATUXIZUMAB-MAFODOTIN (ABT-414) IN GLIOBLASTOMA (GBM)
Authors: Andrew Lassman, Cara Dimino, Mahesh Mansukhani, Vundavalli Murty, Peter J Ansell, Earle Bain, Kyle D Holen, Lisa A Roberts-Rapp, James Lee, Walter Curran, Minesh P Mehta, Peter Canoll
Journal: Neuro-Oncology (2017)

Depatuxizumab-mafodotin is an EGFR-directed monoclonal antibody that targets activated EGFR (wild type or EGFRvIII) conjugated to a microtubule inhibitor. EGFRamp correlated with recurrent GBM response in a phase I trial (M12-356, NCT01800695), thus becoming a centrally determined inclusion criterion in an ensuing phase II/III randomized study for newly diagnosed disease now accruing (RTOG 3508, M13-813, NCT02573324). Centrally detected EGFRvIII mutation and MGMT promoter methylation are also stratification factors in RTOG 3508 to balance randomization for biomarkers of potential predictive or prognostic significance. Allowing use of locally determined molecular profiling may reduce accrual barriers by avoiding added time of tissue shipping and repeat central testing. However, discordant results between local and central tests could confound interpretation of clinical trial results. Therefore, we compared local vs. central biomarker results among patients screened for M12-356 or RTOG 3508 at Columbia University Medical Center (CUMC). We retrospectively tabulated local and central EGFRamp, EGFRvIII, and MGMT results. EGFRamp was analyzed by FISH/CISH and EGFRvIII and MGMT by PCR, although the assays for each differed slightly between laboratories. 109 GBMs were molecularly profiled from 73 patients who underwent 1–4 resection(s) and screened for M12-356 (n=44) or RTOG 3508 (n=29) at CUMC. EGFRamp, EGFRvIII, and MGMT promoter methylation each was observed in 54, 36, and 27% of tumors tested locally vs. 68, 33, and 43% centrally, respectively. Concordance between laboratories was observed 88%, 86%, and 61%. EGFRamp and EGFRvIII results were mainly concordant (over 85%) between local and central laboratories. EGFRamp frequency was higher centrally, likely biased by investigators who preferentially sent cases known to harbor EGFRamp locally for central testing. Of concern, MGMT results were discordant in 39%. Allowing local MGMT testing for stratification could unacceptably imbalance randomization if confirmed in a larger dataset.
P3.03-028 WINTHER – a Study of Cancer Therapy Based on Tumor and Normal-Matched Biopsies – the Sheba Medical Center Lung Cancer Experience
Authors: T. Sella, A. Ackerstein, S. Halperin, G. Hout-Siloni, S. Lieberman, I. Barshack, H. Nechushatan, R. Berger, J. Bar, A. Onn
Journal: Journal of Thoracic Oncology (2017)
GENE-22. CORRELATION BETWEEN PIK3R1MET326ILE MUTATION, CYSTEINE-RICH PROTEIN 61 EXPRESSION AND POOR PROGNOSIS IN GLIOBLASTOMA
Authors: Kentaro Fujii, Yoshihiro Otani, Joji Ishida, Kazuhiko Kurozumi, Tetsuo Oka, Toshihiko Shimizu, Yusuke Tomita, Yasuhiko Hattori, Atsuhito Uneda, Yuji Matsumoto, Hiroyuki Michiue, Tomotsugu Ichikawa, Isao Date
Journal: Neuro-Oncology (2017)

In spite of the development of treatments, long-term survival in patients with glioblastoma is very rare. Recently, studies about clarifying prognostic markers for glioblastoma have been growing. Previously we reported that median progression-free survival and overall survival (OS) of patients with high cysteine-rich protein 61 (CCN1) expression were significantly shorter than those of patients with low CCN1 expression. To investigate the molecular mechanisms that regulate CCN1 expression, we analysed 147 tumor samples from 80 glioblastoma patients and 67 lower grade glioma patients using next-generation and Sanger sequencing. Sequencing analysis showed that CCN1 high expression group includes PIK3R1Met326Ile more frequently (10/37 cases, 27.0%) than CCN1 low expression group (3/38 cases, 7.9%) in glioblastoma. We also found this mutation in corresponding blood samples. And multivariate analysis indicated that, high CCN1 expression and PIK3R1Met326Ile in glioblastoma patients were prognostic factors for OS ([HR=2.488 (1.298–4.769), p=0.006] and [HR=2.089 (1.020–4.277), p=0.0439], respectively. According to our results, the PIK3R1Met326Ile mutation related to CCN1 expression and poor prognosis in glioblastoma.
La légionellose associée au voyage en Europe : 2003
Authors: K D Ricketts, C Joseph
Journal: Eurosurveillance (2004)

En 2003, 632 cas de legionellose associee au voyage ont ete declares au reseau de surveillance EWGLINET par 24 pays. Sur les 89 foyers de cas detectes, 35 (39%) n'auraient pas ete identifies sans le programme EWGLINET.
CD4+ T Cell Help Confers a Cytotoxic T Cell Effector Program Including Coinhibitory Receptor Downregulation and Increased Tissue Invasiveness
Authors: Tomasz Ahrends, Aldo Spanjaard, Bas Pilzecker, Nikolina Bąbała, Astrid Bovens, Yanling Xiao, Heinz Jacobs, Jannie Borst
Journal: Immunity (2017)

CD4+ T cells optimize the cytotoxic T cell (CTL) response in magnitude and quality, by unknown molecular mechanisms. We here present the transcriptomic changes in CTLs resulting from CD4+ T cell help after anti-cancer vaccination or virus infection. The gene expression signatures revealed that CD4+ T cell help during priming optimized CTLs in expression of cytotoxic effector molecules and many other functions that ensured efficacy of CTLs throughout their life cycle. Key features included downregulation of PD-1 and other coinhibitory receptors that impede CTL activity, and increased motility and migration capacities. "Helped" CTLs acquired chemokine receptors that helped them reach their tumor target tissue and metalloprotease activity that enabled them to invade into tumor tissue. A very large part of the "help" program was instilled in CD8+ T cells via CD27 costimulation. The help program thus enhances specific CTL effector functions in response to vaccination or a virus infection.
P1.17-017 Usefulness of FDG-PET for Differentiating Thymic Epithelial Tumors from Malignant Lymphomas
Authors: H. Sakamaki, T. Otsuka, M. Suzuki, S. Omura, H. Tanaka, Y. Suzuki, S. Kuriyama, K. Hamada, M. Yotsukura, K. Kaseda, K. Masai, T. Hishida, H. Asamura
Journal: Journal of Thoracic Oncology (2017)
El control de la tuberculosis en Letonia: los programas DOTS integrados y DOTS-plus
Authors: V Leimane, J Leimans
Journal: Eurosurveillance (2006)

Entre 1991 y 1998, el numero de pacientes con tuberculosis en Letonia aumento 2,5 veces con un aumento simultaneo de la tuberculosis resistente y multirresistente (TB-MDR). Se llevo a cabo un analisis descriptivo de los servicios, actividades y estrategias de los programas de TB, incluyendo los DOTS (Directly Observed Therapy Short-course, terapia corta directamente observada) para la tuberculosis y el tratamiento de la TB-MDR (DOTS-plus). Se utilizaron los datos del registro nacional de la tuberculosis, de la vigilancia de la resistencia a los farmacos antituberculosos y de la base de datos sobre TB-MDR. En 1996 se implemento en Letonia el programa nacional de control de la tuberculosis (NTAP, Nacionālā Tuberkulozes Apkarosanas Programma), financiado por el Estado, basado en la estrategia DOTS recomendada por la Organizacion Mundial de la Salud (OMS). Ese programa incluia pruebas tuberculinicas en las prisiones. El tratamiento de la TB-MDR con farmacos de segunda linea fue iniciado en 1997 (DOTS-plus). Las tasas de curacion aumentaron del 59,5% en 1996 al 77,5% en 2003. Durante este periodo, mas de 200 pacientes por ano iniciaron un tratamiento de TB-MDR con una tasa de curacion del 66% al 73%. Durante el periodo, el numero de pacientes multirresistentes disminuyo mas de la mitad. Los resultados de los tratamientos incluyendo el de la TB-MDR alcanzaron el objetivo de la OMS, con tasas de curacion del 85% para nuevos casos. Estos resultados muestran que el tratamiento y el manejo de la TB multirresistente de forma individualizada pueden ser aplicados de modo eficaz en el marco de un programa de TB a escala nacional, para tratar con exito un numero elevado de pacientes con TB-MDR. 
Los metodos de diagnostico rapido, junto con la deteccion rapida de casos con medidas de aislamiento y control de la infeccion, pueden permitir una disminucion de la transmision de la tuberculosis y de la tuberculosis multirresistente en los hospitales y en la comunidad. Es fundamental que el manejo de los casos de tuberculosis multirresistente se adapte a las recomendaciones de la OMS para evitar la aparicion de resistencias a los farmacos antituberculosos de primera y segunda linea.
MNGI-08. HIGH-RISK MENINGIOMA: INITIAL OUTCOMES FROM NRG ONCOLOGY/RTOG-0539
Authors: Leland Rogers, Peixin Zhang, Michael Vogelbaum, Arie Perry, Lynn S Ashby, Jignesh Modi, Anthony Alleman, James Galvin, Shannon Fogh, Emad Youssef, Nimsha Deb, Young Kwok, Clifford G Robinson, Hui-Kuo Shu, Barbara J Fisher, Valerie Panet-Raymond, William McMillan, John de Groot, Minesh P Mehta
Journal: Neuro-Oncology (2017)

Initial analysis of high-risk meningioma on NRG Oncology/RTOG-0539, outlining 3yPFS, overall survival (OS) and adverse events (AEs) This phII trial apportioned patients to 1 of 3 risk groups and management strategies by WHO grade, recurrence status, and resection extent. High-risk included newly diagnosed or recurrent WHOIII or recurrent WHOII of any resection extent, or newly diagnosed WHOII with subtotal resection (STR). Pathology and imaging were centrally reviewed. Patients were treated with RT, 60 Gy/30. 53 received protocol therapy, 28 (52.8%) female. 22 (41.5%) were WHOIII, 8 (15.1%) recurrent WHOII, 11 (20.8%) newly diagnosed WHOII after STR, and 12 (22.6%) imaging progression of prior WHO II/III meningioma. Median FU was 4.0y, 4.8y for living patients. 3yPFS was 58.8% comparable to literature-based estimate, 50% (p=0.13). 3yLC was 68.9%, and 3yOS 78.6%. 5yPFS, LC, and OS were 47.2, 62.4, and 59.1%. Among 51 evaluable for 3yPFS, there were 21 PFS events within 3y: 16 (31.4%) true progressors, and 5 (9.8%) who died without progression. These included 6 of 17 (35.3%) new WHOIII, 3 of 5 (60%) recurrent WHOIII, 4 of 7 (57.1%) recurrent WHOII, 3 of 11 (27.3%) new WHOII, and 5 of 11 (45.5%) with progressive tumor identified by imaging. Combined acute and late AEs (definitely, probably or possibly related to protocol treatment) included 1 (1.9%) grade 5 necrosis-related event. All others were grade 1-3: highest grade 1 in 13 (24.5%), 2 in 24 (45.3%), and 3 in 6 (11.3%). Patients with high-risk meningioma treated with RT experienced 3yPFS 58.8%. Acute and late AEs were limited to grades 1-3, excepting a single necrosis-related grade 5 event. These results support post-operative IMRT for WHOIII, recurrent WHOII, or newly diagnosed subtotally resected WHOII meningioma. They also confirm suboptimal outcome for this cohort, and strongly support further investigations to optimize management.
OrthoGNC: A Software for Accurate Identification of Orthologs Based on Gene Neighborhood Conservation
Authors: Soheil Jahangiri-Tazehkand, Limsoon Wong, Changiz Eslahchi
Journal: Genomics Proteomics & Bioinformatics (2017)

Orthology relations can be used to transfer annotations from one gene (or protein) to another. Hence, detecting orthology relations has become an important task in the post-genomic era. Various genomic events, such as duplication and horizontal gene transfer, can cause erroneous assignment of orthology relations. In closely-related species, gene neighborhood information can be used to resolve many ambiguities in orthology inference. Here we present OrthoGNC, a software for accurately predicting pairwise orthology relations based on gene neighborhood conservation. Analyses on simulated and real data reveal the high accuracy of OrthoGNC. In addition to orthology detection, OrthoGNC can be employed to investigate the conservation of genomic context among potential orthologs detected by other methods. OrthoGNC is freely available online at http://bs.ipm.ir/softwares/orthognc and http://tinyurl.com/orthoGNC.
P2.03-021 A Phase I Study Evaluating the Combination of Afatinib, Carboplatin and Pemetrexed after Failure of 1st Generation EGFR-TKIs
Authors: O. Yamaguchi, S. Watanabe, A. Masumoto, Y. Maeno, Y. Kawashima, O. Ishimoto, S. Sugawara, H. Yoshizawa, K. Kobayashi, T. Nukiwa
Journal: Journal of Thoracic Oncology (2017)
TMIC-13. ELUCIDATION OF MicroRNA-OSTEOPONTIN CIRCUIT IN GLIOBLASTOMA ASSOCIATED INFILTRATING MACROPHAGES
Authors: Anantha Marisetty, Jun Wei, Konrad Gabrusiewicz, Yuuri Hashimoto, Ling-Yuan Kong, Martina Ott, Amy Heimberger
Journal: Neuro-Oncology (2017)
P3.16-011 Correlation Between Pulmonary Vein Stump Thrombus and Cerebral Infarction After Left Upper Lobectomy of the Lung
Authors: Y. Yasuura, Y. Terada, K. Sato, S. Hayashi, K. Mizuno, H. Kayata, H. Kojima, S. Takahashi, M. Isaka, Y. Ohde
Journal: Journal of Thoracic Oncology (2017)