tbuckley/cabot-search huggingface dataset:
CMET-07. VISMODEGIB TREATMENT OF INTRACRANIAL INVASION OF BASAL CELL CARCINOMA
Authors: Evan Jameyfield, Nicholas Blondin
Journal: Neuro-Oncology (2017)

Although basal cell carcinoma (BCC) is one of the most prevalent cancers in the U.S., locally advanced or metastatic BCC was reported to be less than 1% of the cases in a commercially insured U.S. population. Neurological symptoms are rarely reported in association with BCC; however, untreated scalp lesions in patients with metastatic BCC can rarely lead to intracranial complications. Few cases in the literature describe the best treatment options for BCC patients presenting with neurological symptoms due to intracranial invasion. We describe the case of an 84 year old man with a history of scalp BCC diagnosed at age 75. A Mohs surgery was performed as initial treatment but was an incomplete resection. At age 78, he underwent radiation treatment to the region. Despite progressive enlargement of the lesion, he did not seek further medical attention until he suffered a seizure at age 82. An MRI of the brain revealed vasogenic edema and focal enhancement involving the left frontal lobe, consistent with intracranial basal cell carcinoma invasion and associated focal cerebritis. Following initial treatment with an anticonvulsant, corticosteroid and antibiotics, the patient initiated treatment with vismodegib, a small molecule inhibitor marketed for the treatment of metastatic basal cell carcinoma. Within one month of vismodegib treatment, the patient’s scalp wound demonstrated a marked improvement. MRI demonstrated resolution of cerebritis and an apparent regression of intracranial basal cell carcinoma. The patient discontinued vismodegib after 6 months of treatment due to complete response. Now, after an additional 18 months, he has remained disease free. In the rare cases of intracranial invasion of BCC, we present evidence that vismodegib is an effective treatment to reduce cerebritis and prevent further progression of disease.
P3.01-067 TP53 Mutations Could Involve in EGFR-TKI Primary Resistance in Advanced Non-Small Cell Lung Cancer
Authors: X. Li, C. Su, S. Ren, C. Zhao, T. Jiang, X. Chen, J. Li, W. Li, G. Gao, F. Zhou, Y. Shao, C. Zhou
Journal: Journal of Thoracic Oncology (2017)
P3.01-046 Longitudinal Analysis of Plasma CtDNA in EGFR-Mutant NSCLC: SWOG S1403 Trial of Afatinib with or Without Cetuximab
Authors: P. Mack, J. Miao, K. Banks, R. Burich, K. Politi, V. Raymond, D. Dix, R. Lanman, J. Moon, M.A. Melnick, A. Truini, M. Redman, S. Goldberg, D.R. Gandara, K. Kelly
Journal: Journal of Thoracic Oncology (2017)
Gain of function of ASXL1 truncating protein in the pathogenesis of myeloid malignancies
Authors: Hui Yang, Stefan Kurtenbach, Ying Guo, Ines Lohse, Michael A. Durante, Jianping Li, Zhaomin Li, Hassan Al-Ali, Lingxiao Li, Zizhen Chen, Matthew G. Field, Peng Zhang, Shi Chen, Shohei Yamamoto, Zhuo Li, Yuan Zhou, Stephen D. Nimer, J. William Harbour, Claes Wahlestedt, Mingjiang Xu, Feng-Chun Yang
Journal: Blood (2017)
What Constitutes Experience in Surgical Treatment of Valve Disease and How Important Is It?
Authors: Hartzell V. Schaff
Journal: JAMA Cardiology (2017)

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OA 17.01 Pemetrexed-Carboplatin Plus Pembrolizumab as First-Line Therapy for Advanced Nonsquamous NSCLC: KEYNOTE-021 Cohort G Update
Authors: H. Borghaei, C. Langer, S. Gadgeel, V. Papadimitrakopoulou, A. Patnaik, S. Powell, R. Gentzler, R. Martins, J. Stevenson, S. Jalal, A. Panwalkar, J.C. Yang, M. Gubens, L. Sequist, M. Awad, J. Fiore, S. Saraf, H. Raftopoulos, L. Gandhi
Journal: Journal of Thoracic Oncology (2017)
Abstract 20376: Inhibition of Farnesylation of Ras-GTPases Ameliorates Inflammation-Induced Loss of Endothelial Barrier Integrity and Leukocyte Transmigration
Authors: Dursun Gündüz, Samina Mahmood, Neslihan Sevinc, Christoph Liebetrau, Christian Troidl, Christian Hamm, Muhammad Aslam
Journal: Circulation (2017)

Background and Aims: The family of small GTPases (Rho- and Ras-GTPases) is known to regulate endothelial cytoskeleton dynamics and hence barrier integrity. The role of Rho GTPases (RhoA and Rac1) i...
OA 16.07 Radiological Feature on TSCT for Predicting a Pathological Less-Invasive Lung Cancer According to the 8th TNM Classification
Authors: S. Katsumata, K. Aokage, T. Sakai, S. Okada, K. Sekihara, T. Miyoshi, K. Tane, G. Ishii, M. Tsuboi
Journal: Journal of Thoracic Oncology (2017)
Brote prolongado de enfermedades meningocócicas B en Seine Maritime, Francia, enero 2003 a junio 2005
Authors: Pascale Rouaud, A Perrocheau, M K Taha, C Sesboué, A M Forgues, I Parent du Châtelet, D Lévy-Bruhl
Journal: Eurosurveillance (2006)

Entre enero de 2003 y junio de 2005, se produjo un brote prolongado de enfermedades meningococicas en el distrito de Seine-Maritime en Francia. Se declararon 86 casos, dando una incidencia media anual de 2,7 casos por 100.000 habitantes, comparado con una incidencia anual nacional de 1,6. Se identifico un area especialmente afectada, que incluia la ciudad de Dieppe y sus alrededores (26 casos, con una incidencia anual de 12 casos por 100.000). Este brote era debido a N. meningitidis fenotipo B:14:P1.7,16 perteneciente al complejo clonal ST-32/ET-5. Se confirmaron por fenotipado 31 casos de B14:P1.7,16 en el Centro Nacional de Referencia de Meningococos (CNR), asociados a una tasa de mortalidad (19%) y una proporcion de purpura fulminans (42%) particularmente altas. Los grupos de edad mas afectados fueron los jovenes de 15 a 19 anos y los ninos entre uno y nueve anos. En 2003, las autoridades sanitarias llevaron a cabo una vigilancia epidemiologica reforzada, junto con campanas de informacion hacia los medicos y el publico. En 2004, el comite nacional de vacunaciones evaluo la oportunidad de utilizar una vacuna no autorizada, basada en vesiculas de membranas externas de N. meningitis B y desarrollada en Noruega, que podria proporcionar proteccion contra la cepa B14:P1.7,16. En 2006, el Ministerio de Sanidad decide proponer la vacunacion con dicha vacuna en las personas entre uno y 19 anos en Seine Maritime.
IMMU-16. EFFECT OF ANTI-PD-1 THERAPY COMBINATION ON TEMOZOLOMIDE IN MOUSE GLIOBLASTOMA
Authors: Junseong Park, Chang Gon Kim, Jin-Kyong Shim, Jae Eun Lee, Jong Hee Chang, Eui-Cheol Shin, Seok-Gu Kang
Journal: Neuro-Oncology (2017)

Glioblastoma (GBM) is the most common and aggressive primary brain tumor with a poor prognosis despite multimodal interventions. For brain tumors, immunotherapy has not yet fully proved their potential. The central nervous system has historically been regarded as an immune privileged organ, throwing doubt on application of immunotherapy to GBM. However, growing evidences suggest that immune cells can traverse the blood-brain barrier and affect immune responses in the brain. Although immunotherapy by programmed cell death protein 1 (PD-1) blockade has dramatically improved the survival rate of some types of cancer patients, its application to GBM still needs further investigation. To improve efficacy of immunotherapy, there have been many attempts for finding effective combination partner in several types of tumors. We hypothesized that TMZ could work synergistically with PD-1 blockade to generate a robust antitumor response against GBM. Here, we evaluated therapeutic responses of PD-1 blockade and its combination with temozolomide (TMZ) in mouse GBM model. PD-1 blockade remarkably showed long-term antitumor effects, and combined use of TMZ further improved survival rate. However, distinct working mechanisms operated in these two therapeutic strategies. Anti-PD-1 monotherapy significantly augmented the number of tumor-infiltrating lymphocytes and protected them from exhaustion. In comparison, TMZ combination abrogated these effects, suggesting that superior therapeutic efficacy did not originated from increased immune responses. Microarray experiments revealed that anti-PD-1 and combination groups differentially converted transcriptional programs, particularly emphasized by mutually exclusive functional annotation by ImmuneSigDB gene sets. Moreover, tumor rechallenge study showed that immunologic memory was generated only in the anti-PD-1 monotherapy group. Although TMZ did not facilitate anti-PD-1-mediated immune response or memory function, these data suggest that combined treatment of anti-PD-1 and TMZ exert robust antitumor efficacy with therapeutic benefits in GBM. In addition, our data suggest possibility of immunotherapy to be added in standard treatment modalities of GBM.
PDTM-03. SURPRISING ROLE FOR WNT SIGNALING IN Trp53-MUTANT SHH MEDULLOBLASTOMA
Authors: Jezabel Rodriguez-Blanco, Lina Pednekar, Clara Penas, Bin Li, Vanesa Martin, Jun Long, Ethan Lee, William Weiss, Carmen Rodriguez, Nadji Merhdad, Dao Nguyen, Nagi Ayad, Priyamvada Rai, Anthony Capobianco, David J Robbins
Journal: Neuro-Oncology (2017)

The classification of specific cancers into distinct subgroups, based on emerging genomic technologies, has ushered in a new era of targeted therapeutics and companion diagnostics. This promise, however, is inconsistent with a model in which the growth of solid tumors, and their resistance to various chemotherapeutics, is driven by a small number of tumor-propagating cells whose transcriptome is unlikely to be captured by these technologies. We isolated such tumor propagating cells from a mouse model for SONIC HEDGEHOG (SHH)-subgroup medulloblastoma. Medulloblastoma sphere cultures were enriched for the medulloblastoma progenitor marker SOX2, resistant to SHH inhibitors, and formed tumors in vivo. Surprisingly, these cultures, and their ability to self-renew were WNT-dependent. We show that Trp53 loss in these sphere cultures activated canonical WNT signaling and a small molecule WNT inhibitor was able to reduce the propagation and growth of SHH-subgroup medulloblastoma in vivo, in an on-target manner, leading to increased survival. Our results suggest that the tumor propagating cells driving the growth of bulk SHH-dependent medulloblastoma are themselves WNT dependent. Further, these results suggest WNT pathway inhibition as a novel therapeutic strategy to treat TRP53 deficient SHH-subgroup medulloblastoma patients, for whom few therapeutic options exist.
Viabilidad de la vigilancia de resistencias a fármacos antituberculosos: Europa, 1997
Authors: V Schwoebel, D Antoine, J Veen
Journal: Eurosurveillance (2000)

En 1997, entre el 28% y el 100% de los aislamientos notificados en diez paises participantes en la Red EuroTB presentaba datos sobre susceptibilidad a medicamentos antituberculosos. La resistencia a los farmacos fue mas habitual en casos nacidos en el extranjero y, en general, en casos previamente tratados contra la tuberculosis.
P2.03-048 Mixed Response of Non-Small Cell Lung Cancer Harboring the EGFR T790M Mutation to Osimertinib
Authors: Y. Shinno, Y. Goto, J. Sato, R. Morita, Y. Matsumoto, S. Murakami, S. Kanda, H. Horinouchi, Y. Fujiwara, N. Yamamoto, Y. Ohe
Journal: Journal of Thoracic Oncology (2017)
f-scLVM: scalable and versatile factor analysis for single-cell RNA-seq
Authors: Florian Buettner, Naruemon Pratanwanich, Davis J. McCarthy, John C. Marioni, Oliver Stegle
Journal: Genome biology (2017)

Single-cell RNA-sequencing (scRNA-seq) allows studying heterogeneity in gene expression in large cell populations. Such heterogeneity can arise due to technical or biological factors, making decomposing sources of variation difficult. We here describe f-scLVM (factorial single-cell latent variable model), a method based on factor analysis that uses pathway annotations to guide the inference of interpretable factors underpinning the heterogeneity. Our model jointly estimates the relevance of individual factors, refines gene set annotations, and infers factors without annotation. In applications to multiple scRNA-seq datasets, we find that f-scLVM robustly decomposes scRNA-seq datasets into interpretable components, thereby facilitating the identification of novel subpopulations.
DDIS-07. TG02, AN ORAL CDK INHIBITOR, INDUCES MULTIPLE CELL DEATH PATHWAYS IN HUMAN GLIOMA CELL LINES AND GLIOMA-INITIATING CELLS
Authors: Emilie Le Rhun, Caroline Von Achenbach, Emese Szabo, Michael Weller
Journal: Neuro-Oncology (2017)

TG02 is an orally bioavailable, multikinase inhibitor which potently inhibits cyclin-dependent kinases (CDK) 1, 2, 5, 7 and 9. CDK9-dependent depletion of short-lived oncoproteins such as MCL-1 and MYC has been proposed as its primary mechanism of cytotoxicity. Here we report that TG02 exhibits strong anti-tumor activity in both human long-term cell lines (LN-18, LN-428, D247MG, LN-319, A172, U87MG, T98G, LN-308, LN-229) and in glioma-initiating cell lines (T-325, T-269, ZH-161, ZH-305, S-24) regardless of MGMT promoter methylation status. This activity was observed in acute growth inhibition assays at EC50 concentrations between 42.5 nM and 187.5 nM and in clonogenic survival assays at EC50 concentrations between 14 nM and 73.3 nM. Baseline expression of direct TG02 targets (CDK-9, CDK-5) and indirect TG02 targets (MCL-1, MYC) was detected in all cell lines by immunoblot, but did not correlate with sensitivity to TG02. Similarly, p53 mutation or PTEN inactivation status showed no association with TG02 sensitivity. Under hypoxic cell culture conditions, TG02 was less active against the glioma-initiating cell lines, ZH-161 and ZH-305, but not against the long-term cell lines, LN-229 and LN-308. Blocking the extrinsic cell death pathway by gene transfer of the viral gene product, cytokine response modifier (crma)-A, abrogated CD95 ligand-induced apoptosis, but had no effect on cell death induced by TG02. High concentrations of TG02 induced annexin V positivity on the cell membrane and minor caspase 3 cleavage, but co-exposure to the pan-caspase inhibitor, zVAD-fmk, did not attenuate TG02-induced cell death. High concentrations of TG02 also induced autophagy as assessed by LC3 cleavage, but inhibition of autophagy by 3-methyladenine reduced only caspase cleavage, but not cell death. These data suggest that TG02 is a highly potent anti-glioma agent in vitro that may induce cell death in a non-apoptotic, non-autophagic manner. Early clinical trials of TG02 in glioblastoma are ongoing.
P3.01-062 The Perceived Value of Avoiding Biopsy: Patients' Willingness to Pay for Circulating Tumor DNA T790M Testing
Authors: T. Barnes, J. Laskin, P. Cheema, G. Liu, M. Iqbal, J. Rothenstein, R. Burkes, S. Owen, D. Laurence, I. Carvalhana, L. Markin, L. Wong, N. Perera-Low, M. Sawczak, M. Tsao, N. Leighl
Journal: Journal of Thoracic Oncology (2017)
Molecular and enzoinformatics perspectives of targeting Polo-like kinase 1 in cancer therapy
Authors: Shazi Shakil, Mohammad H. Baig, Shams Tabrez, Syed M. Danish Rizvi, Syed K. Zaidi, Ghulam M. Ashraf, Shakeel A. Ansari, Aftab Aslam Parwaz Khan, Mohammad H. Al-Qahtani, Adel M. Abuzenadah, Adeel G. Chaudhary
Journal: Seminars in Cancer Biology (2017)
Políticas de inmunización contra el virus de la varicela-zoster y estrategias de vigilancia en Europa
Authors: A Pinot de Moira, A Nardone
Journal: Eurosurveillance (2005)

En Europa, la inclusion de la inmunizacion contra el virus de la varicela-zoster (VVZ) en el calendario vacunal infantil es una opcion cada vez mas frecuente. El estudio siguiente es parte del analisis sobre el VVZ llevado a cabo en el marco de la Red europea de vigilancia serologica 2 (ESEN 2), y describe las politicas de inmunizacion pasivas actuales, las estrategias de inmunizacion activa actuales y propuestas, y los sistemas de vigilancia de las enfermedades debidas al virus de varicela zoster en los paises participantes de la Red. Se elaboro un cuestionario, el cual se envio a los 23 paises participantes. Actualmente, 14 de los 20 paises participantes tienen comercializada una vacuna contra el VVZ. Alemania es el unico pais que incluyo la vacuna anti VVZ en su calendario de vacunacion infantil de rutina. Tres paises mas recomiendan la vacuna contra el VVZ en ninos y cinco paises tienen el proyecto de incluir esta vacuna en el calendario vacunal infantil. Sin embargo, de los ocho paises que introdujeron esta vacuna en los ninos o que van a hacerlo, solo seis tienen una notificacion obligatoria de casos de varicela, y solo dos paises tienen datos de vigilancia de atencion primaria para el herpes-zoster.
Revised STandards for Reporting Interventions in Clinical Trials of Acupuncture (STRICTA): Extending the CONSORT Statement
Authors: Hugh MacPherson, Douglas G. Altman, Richard Hammerschlag, Li Youping, Wu Taixiang, Adrian White, David Moher
Journal: PLoS Medicine (2010)

The STandards for Reporting Interventions in Clinical Trials of Acupuncture (STRICTA) were published in five journals in 2001 and 2002. These guidelines, in the form of a checklist and explanations for use by authors and journal editors, were designed to improve reporting of acupuncture trials, particularly the interventions, thereby facilitating their interpretation and replication. Subsequent reviews of the application and impact of STRICTA have highlighted the value of STRICTA as well as scope for improvements and revision. To manage the revision process a collaboration between the STRICTA Group, the CONSORT Group, and the Chinese Cochrane Centre was developed in 2008. An expert panel with 47 participants was convened that provided electronic feedback on a revised draft of the checklist. At a subsequent face-to-face meeting in Freiburg, a group of 21 participants further revised the STRICTA checklist and planned dissemination. The new STRICTA checklist, which is an official extension of CONSORT, includes six items and 17 sub-items. These set out reporting guidelines for the acupuncture rationale, the details of needling, the treatment regimen, other components of treatment, the practitioner background, and the control or comparator interventions. In addition, and as part of this revision process, the explanations for each item have been elaborated, and examples of good reporting for each item are provided. In addition, the word "controlled" in STRICTA is replaced by "clinical," to indicate that STRICTA is applicable to a broad range of clinical evaluation designs, including uncontrolled outcome studies and case reports. It is intended that the revised STRICTA, in conjunction with both the main CONSORT Statement and extension for nonpharmacologic treatment, will raise the quality of reporting of clinical trials of acupuncture.
GENE-43. LIQUID BIOPSY FOR MONITORING OF TUMOR RESPONSE IN CHILDREN WITH DIFFUSE MIDLINE GLIOMA
Authors: Eshini Panditharatna, Madhuri Kambhampati, Sridevi Yadavilli, Jordana Sandy, Xiaodong Yang, Lindsay Kilburn, John Crawford, Suresh Magge, Roger Packer, Michael Prados, Sabine Mueller, Javad Nazarian
Journal: Neuro-Oncology (2017)
A p190BRhoGAP mutation and prolonged RhoB activation in fatal systemic capillary leak syndrome
Authors: Richard W. Pierce, Jonathan Merola, John Paul Lavik, Martin S. Kluger, Anita Huttner, Mustafa K. Khokha, Jordan S. Pober
Journal: The Journal of Experimental Medicine (2017)

We describe a fatal case of pediatric systemic capillary leak (Clarkson’s disease) associated with a point mutation in p190BRhoGAP. Dermal microvascular endothelial cells (ECs) isolated from this patient form monolayers with similar levels and distribution of junctional proteins and transendothelial electrical resistance compared with normal human dermal microvascular ECs. However, patient-derived ECs demonstrate a greater increase in permeability and impaired recovery of barrier function in response to tumor necrosis factor (TNF) compared with normal donor EC cultures. TNF transiently activates RhoB in ECs coincident with developing leak, and inactivation of RhoB correlates with barrier recovery. The mutation in p190BRhoGAP impairs RhoB inactivation, and the mutant phenotype of patient-derived ECs is replicated by siRNA knockdown of p190BRhoGAP in normal ECs. These data suggest a previously unknown function for p190BRhoGAP in control of capillary EC barrier function that may also be important in acquired systemic capillary leak associated with critical illness in humans.
Neuropeptide Y regulates a vascular gateway for hematopoietic stem and progenitor cells
Authors: Pratibha Singh, Jonathan Hoggatt, Malgorzata M. Kamocka, Khalid S. Mohammad, Mary R. Saunders, Hongge Li, Jennifer Speth, Nadia Carlesso, Theresa A. Guise, Louis M. Pelus
Journal: Journal of Clinical Investigation (2017)

Endothelial cells (ECs) are components of the hematopoietic microenvironment and regulate hematopoietic stem and progenitor cell (HSPC) homeostasis. Cytokine treatments that cause HSPC trafficking to peripheral blood are associated with an increase in dipeptidylpeptidase 4/CD26 (DPP4/CD26), an enzyme that truncates the neurotransmitter neuropeptide Y (NPY). Here, we show that enzymatically altered NPY signaling in ECs caused reduced VE-cadherin and CD31 expression along EC junctions, resulting in increased vascular permeability and HSPC egress. Moreover, selective NPY2 and NPY5 receptor antagonists restored vascular integrity and limited HSPC mobilization, demonstrating that the enzymatically controlled vascular gateway specifically opens by cleavage of NPY by CD26 signaling via NPY2 and NPY5 receptors. Mice lacking CD26 or NPY exhibited impaired HSPC trafficking that was restored by treatment with truncated NPY. Thus, our results point to ECs as gatekeepers of HSPC trafficking and identify a CD26-mediated NPY axis that has potential as a pharmacologic target to regulate hematopoietic trafficking in homeostatic and stress conditions.
Cardiovascular disease (CVD) markers in patients(pts) with prostate cancer(PCa) treated with GN-RH agonists(AG) or antagonist(AN): a prospective cohort study
Authors: A. Cavo, A. Rubagotti, A. Bellodi, E. Zanardi, L. Zinoli, P. Spallarossa, P. Bagnato, B. Pane, S. Favorini, S. Barra, C. Arboscello, E. Arboscello, D. Palombo, F. Boccardo
Journal: Annals of Oncology (2017)