tbuckley/cabot-search huggingface dataset:
Type I IFN augments IL-27-dependent TRIM25 expression to inhibit HBV replication
Authors: Guangyun Tan, Qingfei Xiao, Hongxiao Song, Feng Ma, Fengchao Xu, Di Peng, Na Li, Xiaosong Wang, Junqi Niu, Pujun Gao, F Xiao-Feng Qin, Genhong Cheng
Journal: Cellular and Molecular Immunology (2017)
Effects of First and Next-Generation Tyrosine Kinase Inhibitors on Telomere-Mediated Chromosomal Instability in Chronic Myeloid Leukemia Cells
Authors: Tomasz Stoklosa, Anna Deregowska, Joanna Drzewinska-Chanko, Joanna Barankiewicz, Machnicki M Marcin, Pruszczyk Katarzyna, Maciej Wnuk
Journal: Blood (2014)
RNF40 regulates gene expression in an epigenetic context-dependent manner
Authors: Wanhua Xie, Sankari Nagarajan, Simon J. Baumgart, Robyn Laura Kosinsky, Zeynab Najafova, Vijayalakshmi Kari, Magali Hennion, Daniela Indenbirken, Stefan Bonn, Adam Grundhoff, Florian Wegwitz, Ahmed Mansouri, Steven A. Johnsen
Journal: Genome biology (2017)

Monoubiquitination of H2B (H2Bub1) is a largely enigmatic histone modification that has been linked to transcriptional elongation. Because of this association, it has been commonly assumed that H2Bub1 is an exclusively positively acting histone modification and that increased H2Bub1 occupancy correlates with increased gene expression. In contrast, depletion of the H2B ubiquitin ligases RNF20 or RNF40 alters the expression of only a subset of genes. Using conditional Rnf40 knockout mouse embryo fibroblasts, we show that genes occupied by low to moderate amounts of H2Bub1 are selectively regulated in response to Rnf40 deletion, whereas genes marked by high levels of H2Bub1 are mostly unaffected by Rnf40 loss. Furthermore, we find that decreased expression of RNF40-dependent genes is highly associated with widespread narrowing of H3K4me3 peaks. H2Bub1 promotes the broadening of H3K4me3 to increase transcriptional elongation, which together lead to increased tissue-specific gene transcription. Notably, genes upregulated following Rnf40 deletion, including Foxl2, are enriched for H3K27me3, which is decreased following Rnf40 deletion due to decreased expression of the Ezh2 gene. As a consequence, increased expression of some RNF40-"suppressed" genes is associated with enhancer activation via FOXL2. Together these findings reveal the complexity and context-dependency whereby one histone modification can have divergent effects on gene transcription. Furthermore, we show that these effects are dependent upon the activity of other epigenetic regulatory proteins and histone modifications.
A Novel Plant Mannose-Binding Lectin, NTL, Preserves Cord Blood Hematopoietic Stem/Progenitor Cells in Long-Term Culture and Enhances Their Ex Vivo Expansion.
Authors: Karen Kwai Har Li, Kam Tong Leung, Vincent Eng Choon Ooi, Linda Shiou Mei Ooi, Carmen Ka Yee Chuen, Audrey Carmen Lam, Kathy Yuen Yee Chan, Kam Sze Tsang, Lawrence Chi Ming Chiu, Xiao Bing Zhang
Journal: Blood (2007)
Activation and Proliferation of B Cell Chronic Lymphocytic Leukaemia (B-CLL) Cells through Anti-CD180, Anti-CD40 and IL-4.
Authors: Nino Porakishvili, Maria Manoussaka, Nino Kulikova, James Walton, Amit Nathwani, Andrew P. Jewell, Freda Stevenson, Ed Clark, Peter M. Lydyard
Journal: Blood (2004)
EPID-01. STATISTICAL ALTERNATIVES FOR DEVELOPING CLASSIFICATION MODELS IN GLIOMA
Authors: Annette Molinaro, Jeanette Eckel-Passow, Robert Jenkins, Margaret Wrensch
Journal: Neuro-Oncology (2016)

Given the lack of beneficial treatments in glioma, there is a need for prognostic models for therapeutic decision-making and life planning. Recently several studies defining subtypes of glioma have been published. In this talk the statistical considerations of how to build and validate prognostic models is reviewed. The three statistical considerations to establishing clinically useful prognostic models are: study design, model building, and validation. Careful study design helps to ensure that the model is unbiased and generalizable to the population of interest. During model building, a discovery cohort of patients can be used to choose variables, construct models, and estimate prediction performance via internal validation. Via external validation, an independent dataset can assess how well the model performs. It is imperative that published models properly detail the study design and methods for both model building and validation. This provides readers the information necessary to assess the bias in a study, compare other published models, and determine the model’s clinical usefulness. Here we discuss the relevant considerations and illustrate how varying models can be built with different statistical models and the same data. A comparison of the resulting prognostic models is presented and the ramifications explored.
P18.01 Indocyanine green fluorescence endoscope: the useful points in endonasal transsphenoidal surgery
Authors: T. Hide, S. Yano
Journal: Neuro-Oncology (2016)

AbstractIntroduction:For the safe operation, exact orientation during endoscopic endonasal transsphenoidal surgery (ETSS) is essential. Neuronavigation systems can be pointed at exact sites, but their spatial resolution power is too low for the detection of vessels that cannot be seen on MRI images. On Doppler sonographs the shape of concealed arteries and veins cannot be visualized. To solve these problems we evaluated the clinical usefulness of the indocyanine green (ICG) endoscope.Materials and Methods:We enrolled 38 patients with pituitary adenomas (n = 26), tuberculum sellae meningiomas (n = 4), craniopharyngiomas (n = 3), and chordomas (n = 2); there was one patient each with Rathke’s cleft cyst, a dermoid cyst, and fibrous dysplasia. After opening the sphenoid sinus and placing the ICG endoscope, we injected 12.5 mg of ICG into a peripheral vein as a bolus and observed the internal carotid arteries (ICAs), cavernous sinus, intercavernous sinus, and pituitary. Intraoperative real-time measurement of ICG signals was performed in 4 of microadenomas.Results:The ICA was clearly identified by a strong fluorescence signal through the dura mater and the covering thin bone. The cavernous sinus and the attachment of tuberculum sellae meningiomas were identified through the dura matter. At the final inspection after tumor removal, perforators to the brain, optic nerves, chiasm, and pituitary stalk were visualized. ICG fluorescence signals from the hypophyseal arteries were strong enough to see and spread to the area of perfusion with the passage of time. Elevation of ICG signals was relatively delayed in microadenoma compared to the area of normal pituitary.Conclusions:In ETSS, the real time and high resolution image of ICA and cavernous sinus with the ICG endoscope is strongly useful. We suggest that the real-time observation of the blood supply to the optic nerves and pituitary helps to predict the preservation of their function, and different elevation pattern of ICG signal between microadenoma and normal pituitary helps to identify margin of them.
EXTH-26. TARGETING BRAIN TUMOR INITIATING CELL CHEMORESISTANCE WITH THE CARBONIC ANHYDRASE IX INHIBITOR SLC-0111 DELAYS GLIOBLASTOMA GROWTH IN VIVO
Authors: Kiera Walker, Nathaniel Boyd, Paul McDonald, Mark Bevensee, Yancey Gillespie, Burt Nabors, Shoukat Dedhar, Anita Hjelmeland
Journal: Neuro-Oncology (2016)

Brain tumor initiating cells (BTICs) are resistant to chemo- and radiotherapy, providing a cellular reserve for tumor recurrence and an important target for anti-glioma treatments. Standard of care for glioblastoma (GBM; grade IV astrocytoma) includes the chemotherapy temozolomide, which prolongs life expectancy but is not curative. Prior studies suggested the efficacy of chemotherapies including temozolomide was increased by reducing expression of carbonic anhydrase 9 (CA9). CA9 is a hypoxia responsive gene elevated in tumors that is important for regulating intracellular pH and contributing to the acidic extracellular microenvironment. After confirming basal and hypoxia-induced expression of CA9 in GBM BTICs, we targeted CA9 activity with the small molecule inhibitor SLC-0111 alone or in combination with temozolomide. In multiple GBMs, SLC-0111 reduced cell growth in vitro and showed additional benefit when used concurrently with temozolomide. Importantly, SLC-0111 inhibited the enrichment of BTICs after temozolomide treatment as determined via BTIC marker expression and neurosphere formation capacity. These data suggested the potential of SLC-0111 as a chemosensitizer, which we next evaluated in preclinical studies using a subcutaneous recurrent GBM model. GBMs treated with SLC-0111 in combination with temozolomide significantly regressed and the resulting in vivo growth delay was greater than that of temozolomide or SLC-0111 alone. Together, our data suggest that SLC-0111 can sensitize GBM BTICs to the chemotherapy temozolomide and significantly delay disease progression.
Remodeling Specific Immunity by Use of MHC-Tetramers Distinguishes Graft-Versus-Tumor Activity from Graft-Versus-Host-Disease.
Authors: Barry J. Kappel, Javier Pinilla-Ibarz, Adam A. Kochman, Jeffrey M. Eng, Vanessa M. Hubbard, Ingrid M. Leiner, Eric G. Pamer, Marcel R.M. van den Brink, David A. Scheinberg
Journal: Blood (2005)
Dual Targeted Therapy with the AKT Inhibitor Perifosine and the Multikinase Inhibitor Sorafenib in Patients with Relapsed/Refractory Lymphomas: Final Results of a Phase II Trial
Authors: Anna Guidetti, Simonetta Viviani, Alfonso Marchianò, Anna Dodero, Lucia Farina, Silvia L Locatelli, Domenico Russo, Pietro Bulian, Roberto Sorasio, Massimo Di Nicola, Laura Giordano, Paolo Corradini, Alessandro M. Gianni, Carmelo Carlo-Stella
Journal: Blood (2012)
Comparison of BuCy (Busulfan plus Cyclophosphamide) Versus FluBu4 (Fludarabine plus Busulfan) As a Conditioning Regimen for Allogeneic Stem Cell Transplantation
Authors: Silvia Park, Jung Yong Hong, Moon Ki Choi, Young Saing Kim, Ji Yun Lee, Sung Hee Lim, Chul Won Jung, Jun Ho Jang, Kihyun Kim
Journal: Blood (2012)
HER2 positive breast cancer with central nervous system metastases: Pathological features and clinical outcome
Authors: G. Masci, L. Santarpia, G. Bottai, L. Giordano, M. Zuradelli, R. Torrisi, L. Di Tommaso, A. Sagona, V. Errico, W. Gatzemeier, A. Testori, P. Navarria, L. Bello, C. Tinterri, M. Scorsetti, A. Santoro
Journal: Annals of Oncology (2016)
Challenges of managing chronic pain
Authors: Jianren Mao
Journal: BMJ (2017)

Start by ensuring realistic expectations

Chronic pain is an individualised experience with multifactorial aetiology.1 It can cause unexpectedly prolonged suffering when, for example, an initial injury evolves into a complex disease state. A transient ankle sprain may turn into a complex regional pain syndrome lasting for months to years; or a week long episode of shingles may cause post-herpetic neuralgia with disabling pain for months or years. Moreover, chronic pain can be an accompanying symptom of largely irreversible underlying disease, such as degenerative arthritis (osteoarthritis), spinal stenosis, or compression fracture resulting from osteoporosis in older people. Chronic pain can also be a primary complaint of clinical conditions such as fibromyalgia and trigeminal neuralgia, for which neither the aetiology nor mechanism is currently well understood.

Chronic pain is therefore not simply a chronological extension of acute pain and requires different diagnostic approaches and management strategies. For example, …
Libro Blu: a tool to coordinate Oncology practice and to rationalise resource employment
Authors: I.G. Rapposelli, O. Fusco, P. Deligiannis, A. Pastorini, M.S. Fiumanò, E. Menatti, V. Viaggi, F. Stiglich, R. Palazzolo, A.M. Soccodato, M. Volpi, F. Antoniazzi, C. Pedrotti, F. Malugani, F. De Filippi, E. Libera, C. Songini, E. Tavasci, K. Dell'Agostino, T. Bazza, A. Bertolini
Journal: Annals of Oncology (2016)
A phase 1B study of pegylated liposomal mitomycin-C prodrug with or without capecitabine and bevacizumab in third line chemotherapy of colorectal cancer
Authors: A.A. Gabizon, T. Grenader, E. Tahover, H. Shmeeda, T. Golan, R. Berger, R. Geva, I. Wolf, R. Perets, Y. Amitay, P. Ohana
Journal: Annals of Oncology (2016)
Next generation sequencing identifies actionable mutations in EGFR-wild type and KRAS mutant non-small cell lung cancer patients
Authors: A. Voutsina, A. Kalikaki, A. Koutsopoulos, M. Sfakianaki, M. Trypaki, E. Tsakalaki, S. Agelaki, V. Georgoulias, D. Mavroudis
Journal: Annals of Oncology (2016)
High incidence of cetuximab-related infusion reactions in head and neck cancer pts (real life data)
Authors: V. Palomar, M. Annereau, N. Lezghed, C. Even, L. Mayache-Badis, M. Iacob, C. Leibu, M. Matias, P. Bravo, C. Ferte
Journal: Annals of Oncology (2016)
Prominent Oncogenic Roles of EVI1 in Breast Carcinoma
Authors: Hui Wang, Thorsten Schaefer, Martina Konantz, Martin Braun, Zsuzsanna Varga, Anna M. Paczulla, Selina Reich, Francis Jacob, Sven Perner, Holger Moch, Tanja N. Fehm, Lothar Kanz, Klaus Schulze-Osthoff, Claudia Lengerke
Journal: Cancer Research (2017)

Abstract Overexpression of the EVI1 oncogene is associated typically with aggressive myeloid leukemia, but is also detectable in breast carcinoma where its contributions are unexplored. Analyzing a tissue microarray of 608 breast carcinoma patient specimens, we documented EVI1 overexpression in both estrogen receptor–positive (ER+) and estrogen receptor–negative (ER−) breast carcinomas. Here, we report prognostic relevance of EVI1 overexpression in triple-negative breast carcinoma but not in the HER2-positive breast carcinoma subset. In human breast cancer cells, EVI1 silencing reduced proliferation, apoptosis resistance, and tumorigenicity, effects rescued by estrogen supplementation in ER+ breast carcinoma cells. Estrogen addition restored ERK phosphorylation in EVI1-silenced cells, suggesting that EVI1 and estradiol signaling merge in MAPK activation. Conversely, EVI1 silencing had no effect on constitutive ERK activity in HER2+ breast carcinoma cells. Microarray analyses revealed G-protein–coupled receptor (GPR) signaling as a prominent EVI1 effector mechanism in breast carcinoma. Among others, the GPR54-ligand KISS1 was identified as a direct transcriptional target of EVI1, which together with other EVI1-dependent cell motility factors such as RHOJ regulated breast carcinoma cell migration. Overall, our results establish the oncogenic contributions of EVI1 in ER- and HER2-negative subsets of breast cancer. Cancer Res; 77(8); 2148–60. ©2017 AACR.
Progressing G1-G2 neuroendocrine tumors (WD NET) in treatment with capecitabine (Cp) plus somatostatin analog (SSA): a single center experience
Authors: R. Marconcini, S. Ricci, L. Galli, A. Antonuzzo, C. Orlandini, E. Vasile, A. Falcone
Journal: Annals of Oncology (2016)
Phase Ib/II study to evaluate the efficacy and tolerability of PM01183 (lurbinectedin) in combination with olaparib in patients with advanced solid tumors
Authors: A.M. Poveda, A. Oaknin, I. Romero, A. Guerrero, L. Fariñas Madrid, A. Soto, C. Peris, J.A. Lopez Guerrero
Journal: Annals of Oncology (2016)
SURG-25. STABILITY OF SHUNT PROGRAMMABLE VALVE SETTINGS WITH SIMULTANEOUS USE OF THE OPTUNE TRANSDUCER ARRAY
Authors: Andrew Chan, Harjus Birk
Journal: Neuro-Oncology (2016)

The Optune transducer array is an FDA-approved noninvasive regional therapy that aims to inhibit growth of glioblastoma multiforme (GBM) cells via utilization of alternating electric fields. Some patients with GBM may develop hydrocephalus and benefit from subsubsequent shunt placement, but special attention must be paid in patients in whom programmable valves are utilized given the potential effect of the magnetic fields on valve settings. We present the first case report illustrating the stability of programmable shunt valve settings in a neurosurgical patient undergoing therapy with the Optune device. In this study, shunt valve settings were stable over a period of five days despite concurrent Optune therapy. This is reassuring for patients with GBM that require simultaneous treatment with both the Optune device and a programmable shunt system.
Trastuzumab plus chemotherapy in the treatment of HER-2 –positive, advanced, gastric or gastro-esophageal junction cancer: a single center experience
Authors: L.R. Martella, I. Toma, L. Belluomini, F. Lancia, F. Daniel, I. Carandina, A. Frassoldati
Journal: Annals of Oncology (2016)
The Vitiligo Working Group recommendations for narrowband ultraviolet B light phototherapy treatment of vitiligo
Authors: Tasneem F. Mohammad, Mohammed Al-Jamal, Iltefat H. Hamzavi, John E. Harris, Giovanni Leone, Raúl Cabrera, Henry W. Lim, Amit G. Pandya, Samia M. Esmat
Journal: Journal of the American Academy of Dermatology (2017)
Primary non-Hodgkin lymphoma of the colon among patients in the Veterans Affairs Health System.
Authors: T. Tashi, R. Thota, J. Krishnamurthy, A. R. Sama, I. T. Aldoss, W. Gonsalves, A. Ganti, P. Townley, P. T. Silberstein, S. Subbiah
Journal: Journal of Clinical Oncology (2011)

554 Background: Primary non-Hodgkin lymphoma (NHL) of the colon is rare. There are no randomized controlled trials describing treatment outcomes for this tumor. We provide the largest descriptive study of this tumor to date. Methods: Retrospective analysis of 109 patients diagnosed with primary non-Hodgkin lymphoma of the colon from 1995 to 2008 was done via the Veteran's Affairs Central Cancer Registry. By definition, all cases presented with a lymphomatous involvement of the colon as the first manifestation of their disease with no previous diagnosis of NHL of any type or site. Demographic, staging, histology, treatment, and outcome data was recorded. Lymphomas were classified as aggressive versus indolent based on their histology. Results: There were 36,260 colon cancers diagnosed in 1995-2008 of which 109 (0.3%) were primary non-Hodgkin colon lymphomas. The median age of diagnosis was 67 years. 55 pts had aggressive disease, 27 pts had indolent disease, and 27 pts had inadequate histological data. Diffuse large B cell lymphoma (73%) was the most common aggressive lymphoma whereas it was marginal zone (56%) in the indolent group. The indolent group had 5- year survival rate of 76.9% compared to 48.6% for the aggressive group. Both groups had received different treatment regimens as seen in the Table with variable mean survival outcomes. Conclusions: Our data suggests addition of postoperative adjuvant chemotherapy appears superior to surgery alone in the treatment of aggressive disease whereas it does not appear to provide any benefit in the treatment of indolent disease. However, patient numbers are too small to draw definite conclusions and warrant future investigation in multinational randomized fashion. [Table: see text] No significant financial relationships to disclose.
A phase 1b study of the nanoparticle-drug conjugate (NDC) CRLX101 in combination with weekly paclitaxel in patients (pts) with platinum-resistant ovarian cancer (OC)
Authors: C.N. Krasner, R.J. Schilder, W.E. Brady, L.R. Duska, D. O'Malley, P.A. Disilvestro, J. Li, W. Downing, A. Senderowicz
Journal: Annals of Oncology (2016)
Surf: Open label, randomized multi-centre phase II study to assess the efficacy and tolerability of sunitinib by dose administration regimen (dose modification or dose interruptions) in patients with advanced or metastatic renal cell carcinoma (mRCC)
Authors: G. Mouillet, T. Maurina, M.-J. Paillard, P. Montcuquet, T. Nguyen Tan Hon, H. Almotlak, U. Stein, D. Berthod, E. Robert, A. Meurisse, F. Bonnetain, A. Thiery-Vuillemin
Journal: Annals of Oncology (2016)
Differential Diagnosis of Hereditary and Acquired Thrombocytopenia By the Immature Platelet Fraction and Thrombopoietin Levels
Authors: Fabio Luiz Bandeira Ferreira, Marina Pereira Colella, Samuel de Souza Medina, Maiara Marx Luz Fiusa, Loredana Nilkenes Gomes da Costa, Carolina Costa-Lima, Fernanda Andrade Orsi, Joyce Maria Annichino-Bizzacchi, Kleber Yotsumoto Fertrin, Maria de Fatima Pereira Gilberti, Margareth C Ozelo, Erich Vinicius De Paula
Journal: Blood (2015)
High dose oral amiodarone added to doxorubicin and vindesine for overcoming multidrug resistance in solid tumors
Authors: W.T.A. van der Graaf, J. Buter, E.G.E. de Vries, P.H.B. Willemse, D.Th. Sleijfer, N.H. Mulder
Journal: Annals of Oncology (1994)
Time course of selected treatment emergent adverse events (TEAEs) in NAPOLI-1: A phase 3 study of nal-IRI (MM-398) ± 5-fluorouracil and leucovorin (5-FU/LV) vs 5-FU/LV in metastatic pancreatic cancer (mPAC) previously treated with gemcitabine-based therapy
Authors: R.A. Hubner, L.-T. Chen, J.T. Siveke, C.-P. Li, G. Bodoky, A. Dean, Y.-S. Shan, G.S. Jameson, T. Macarulla, K.-H. Lee, D. Cunningham, J.-F. Blanc, C.-F. Chiu, G. Schwartsmann, F. Braiteh, K. Mamlouk, B. Belanger, F. de Jong, D.D. von Hoff, A. Wang-Gillam
Journal: Annals of Oncology (2016)
Impact of searching clinical trial registries in systematic reviews of pharmaceutical treatments: methodological systematic review and reanalysis of meta-analyses
Authors: Marie Baudard, Amélie Yavchitz, Philippe Ravaud, Elodie Perrodeau, Isabelle Boutron
Journal: BMJ (2017)

<b>Objective</b>&nbsp;To evaluate the impact of searching clinical trial registries in systematic reviews. <b>Design</b>&nbsp;Methodological systematic review and reanalyses of meta-analyses. <b>Data sources</b>&nbsp;Medline was searched to identify systematic reviews of randomised controlled trials (RCTs) assessing pharmaceutical treatments published between June 2014 and January 2015. For all systematic reviews that did not report a trial registry search but reported the information to perform it, the World Health Organization International Trials Registry Platform (WHO ICTRP search portal) was searched for completed or terminated RCTs not originally included in the systematic review. <b>Data extraction</b>&nbsp;For each systematic review, two researchers independently extracted the outcomes analysed, the number of patients included, and the treatment effect estimated. For each RCT identified, two researchers independently determined whether the results were available (ie, posted, published, or available on the sponsor website) and extracted the data. When additional data were retrieved, we reanalysed meta-analyses and calculated the weight of the additional RCTs and the change in summary statistics by comparison with the original meta-analysis. <b>Results</b>&nbsp;Among 223 selected systematic reviews, 116 (52%) did not report a search of trial registries; 21 of these did not report the information to perform the search (key words, search date). A search was performed for 95 systematic reviews; for 54 (57%), no additional RCTs were found and for 41 (43%) 122 additional RCTs were identified. The search allowed for increasing the number of patients by more than 10% in 19 systematic reviews, 20% in 10, 30% in seven, and 50% in four. Moreover, 63 RCTs had results available; the results for 45 could be included in a meta-analysis. 14 systematic reviews including 45 RCTs were reanalysed. The weight of the additional RCTs in the recalculated meta-analyses ranged from 0% to 58% and was greater than 10% in five of 14 systematic reviews, 20% in three, and 50% in one. The change in summary statistics ranged from 0% to 29% and was greater than 10% for five of 14 systematic reviews and greater than 20% for two. However, none of the changes to summary effect estimates led to a qualitative change in the interpretation of the results once the new trials were added. <b>Conclusions</b>&nbsp;Trial registries are an important source for identifying additional RCTs. The additional number of RCTs and patients included if a search were performed varied across systematic reviews.