tbuckley/cabot-search huggingface dataset:
&lt;italic&gt;In Vitro&lt;/italic&gt; Studies on the Iso-Antigen System in Mice&lt;xref ref-type="fn" rid="fn1"&gt;2&lt;/xref&gt;
Authors: Daniel G. Miller
Journal: JNCI Journal of the National Cancer Institute (1956)

Journal Article In Vitro Studies on the Iso-Antigen System in Mice Get access Daniel G. Miller Daniel G. Miller Tissue Culture Laboratory, The University of Texas—Medical Branch, Galveston, Texas Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 16, Issue 6, June 1956, Pages 1473–1484, https://doi.org/10.1093/jnci/16.6.1473 Published: 01 June 1956 Article history Published: 01 June 1956 Received: 23 November 1966
Effect of Defective Ring Gland on Incidence of Tumors in <italic>Drosophila</italic><xref ref-type="fn" rid="fn1">2</xref>
Authors: Walter J. Burdette, Ph. D.
Journal: JNCI Journal of the National Cancer Institute (1954)

Journal Article Effect of Defective Ring Gland on Incidence of Tumors in Drosophila Get access Walter J. Burdette, Ph. D. Walter J. Burdette, Ph. D. Department of Surgery, Louisiana State University School of Medicine, New Orleans, La. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 15, Issue 2, October 1954, Pages 367–376, https://doi.org/10.1093/jnci/15.2.367 Published: 01 October 1954 Article history Received: 17 May 1954 Published: 01 October 1954
Abstract 18434: Coronary Artery Calcium Progression and Atrial Fibrillation: The Multi-ethnic Study of Atherosclerosis (MESA)
Authors: Wesley T O'Neal, Jimmy T Efird, Waqas T Qureshi, Joseph Yeboah, Alvaro Alonso, Susan R Heckbert, Saman Nazarian, Elsayed Z Soliman
Journal: Circulation (2015)

Introduction: Coronary artery calcium (CAC) measured at a single time point has been associated with an increased risk for atrial fibrillation (AF). It is currently unknown whether CAC progression over time carries a similar risk. Methods: A total of 5,612 study participants (mean age 62 ± 10; 52% women; 39% whites; 27% blacks; 20% Hispanics; 12% Chinese-Americans) from the Multi-Ethnic Study of Atherosclerosis (MESA) were included in this analysis. Phantom-adjusted Agatston scores for baseline and follow-up measurements were used to compute the change in CAC per year (1 to 100, 101 to 300, and &gt;300 units/year) compared with participants with ≤0 change. The mean time between CT scan for study participants was 2.4 ± 0.84 years. AF was ascertained by review of hospital discharge records and from Medicare claims data through December 31, 2010. Cox regression was used to compute hazard ratios (HR) and 95% confidence intervals (95%CI) for the association between CAC progression and AF and models were adjusted for socio-demographics, cardiovascular risk factors, and baseline CAC. Results: At baseline, 2,904 (52%) participants had no evidence of CAC and 2,708 (48%) had CAC values &gt;0. The mean CAC progression for those with baseline CAC was 46.1 ± 85.2 units per year and for those without baseline CAC was 0.84 ± 4.8 units per year. Over a median follow-up of 5.6 years, a total of 203 (3.6%) incident AF cases occurred. Any CAC progression (&gt;0/year) was associated with an increased risk for AF (HR=1.55, 95%CI=1.10, 2.19) and the risk increased with higher levels of CAC progression per year (≤0/year: HR=1.0 [reference]; 1 to 100/year: HR=1.47, 95%CI=1.03, 2.09; 101 to 300/year: HR=1.92, 95%CI=1.15, 3.20; &gt;300/year: HR=3.23, 95%CI=1.48, 7.05). An interaction was observed by age with the association of CAC progression with AF being stronger for younger (&lt;61 years: HR=3.53, 95%CI=1.29, 9.69) compared with older (≥61 years: HR=1.42, 95%CI=0.99, 2.04) participants (p-interaction=0.037). Conclusion: CAC progression during an average of 5-6 years of follow-up is associated with an increased risk for AF. The associated risk is greater in individuals with faster CAC progression.
Effects of Chrysotile Exposure in Human Bronchial Epithelial Cells: Insights into the Pathogenic Mechanisms of Asbestos-Related Diseases
Authors: Giulia Rossana Gulino, Manuela Polimeni, Mauro Prato, Elena Gazzano, Joanna Kopecka, Sebastiano Colombatto, Dario Ghigo, Elisabetta Aldieri
Journal: Environmental Health Perspectives (2015)

Chrysotile asbestos accounts for > 90% of the asbestos used worldwide, and exposure is associated with asbestosis (asbestos-related fibrosis) and other malignancies; however, the molecular mechanisms involved are not fully understood. A common pathogenic mechanism for these malignancies is represented by epithelial-mesenchymal transition (EMT), through which epithelial cells undergo a morphological transformation to assume a mesenchymal phenotype. In the present work, we propose that chrysotile asbestos induces EMT through a mechanism involving a signaling pathway mediated by tranforming growth factor beta (TGF-β).We investigated the role of chrysotile asbestos in inducing EMT in order to elucidate the molecular mechanisms involved in this event.Human bronchial epithelial cells (BEAS-2B) were incubated with 1 μg/cm2 chrysotile asbestos for ≤ 72 hr, and several markers of EMT were investigated. Experiments with specific inhibitors for TGF-β, glycogen synthase kinase-3β (GSK-3β), and Akt were performed to confirm their involvement in asbestos-induced EMT. Real-time polymerase chain reaction (PCR), Western blotting, and gelatin zymography were performed to detect mRNA and protein level changes for these markers.Chrysotile asbestos activated a TGF-β-mediated signaling pathway, implicating the contributions of Akt, GSK-3β, and SNAIL-1. The activation of this pathway in BEAS-2B cells was associated with a decrease in epithelial markers (E-cadherin and β-catenin) and an increase in mesenchymal markers (α-smooth muscle actin, vimentin, metalloproteinases, and fibronectin).Our findings suggest that chrysotile asbestos induces EMT, a common event in asbestos-related diseases, at least in part by eliciting the TGF-β-mediated Akt/GSK-3β/SNAIL-1 pathway.Gulino GR, Polimeni M, Prato M, Gazzano E, Kopecka J, Colombatto S, Ghigo D, Aldieri E. 2016. Effects of chrysotile exposure in human bronchial epithelial cells: insights into the pathogenic mechanisms of asbestos-related diseases. Environ Health Perspect 124:776-784; http://dx.doi.org/10.1289/ehp.1409627.
The prognostic significance of mucinous differentiation in colorectal cancer: A systematic review and meta-analysis.
Authors: J. S. Verhulst, W. P. Ceelen
Journal: Journal of Clinical Oncology (2011)

e14067 Background: Mucinous colorectal adenocarcinoma (MAC) has been known and studied for many years. The prognostic significance of this histological subtype remains controversial. We reviewed the prognostic significance of mucinous differentiation in colorectal cancer (CRC). Methods: A systematic web based search was performed using Web of Knowledge and Medline. Articles Published in English, German or French describing cohort studies, case-control studies or cross-sectional studies comparing survival in patients with MAC and adenocarcinoma not otherwise specified (AC) were included. Data on first author, year of publication, country, number of patients included, prevalence of MAC, % stage IV disease, % disease located in the proximal colon, mean age at presentation, % male patients and 5-year overall survival were extracted from individual studies. A fixed-effects meta-analysis model was used for analysis. The primary outcome was survival expressed as the hazard ratio (HR). Differences between categorical outcome parameters were quantified using the risk ratio (RR) and corresponding 95% confidence interval (95% CI). Results: Forty-four studies, including 222,256 patients, were included. The risk ratio for proximal disease was 1.55 (95%CI 1.53-1.58). Mucinous differentiation was less frequent in males (RR 0.93 [95% CI 0.91-0.94]). Interestingly, the prevalence of stage IV disease was similar in MAC and AC (RR 0.99 [95% CI 0.96-1.02). Thirty-five articles were included in the survival analysis. The hazard ratio (HR) was 1.05 (95% CI 1.02-1.08; P=0.0001) with a worse survival in MAC. Conversely, three out of four studies reported a better survival in MAC with microsatellite instability (MSI). Due to heterogeneity a meta-analysis concerning the interaction of MSI and MAC was not possible. Conclusions: MAC more often originates from the right colon, and is less frequent in males. We did not identify a difference in proportion of stage IV patients at presentation. Mucinous differentiation results in a 2%-8% increased hazard of death, which persists after correction for stage. More research is needed to define the interaction between mucinous differentiation, MSI, and outcome.
Who's Eligible Anyway? Risk Modeling for Clinical Trial Accrual
Authors: Kathryn F. Mileham, Edward S. Kim
Journal: Clinical Cancer Research (2016)

Accrual continues to be a challenge for oncology clinical trials. Interventions to enhance accrual after study activation exist, including corrective action plans for NCI-sponsored trials. Clinical trials would benefit from a proactive approach rather than a reactive approach. Accrual strategy planning early in trial development is suggested. Clin Cancer Res; 22(22); 5397-9. ©2016 AACRSee related article by Massett et al., p. 5408.
TNF-a, retinoid acid and STAT4 pathways are differentially regulated by the HDAC inhibitors, SAHA, TSA and Sirtinol in Waldenstrom's Macroglobulinemia
Authors: Z. Hunter, J. Sun, H. Tseng, E. Hatjiharissi, K. Maghsoudi, L. Xu, R. Manning, N. Munshi, K. Anderson, S. Treon
Journal: Journal of Clinical Oncology (2009)

e14582 Background: HDAC inhibitors (HDAC-I) have emerged as a promising class of therapeutics for the treatment of lymphoplasmacytic malignancies, particularly in combination strategies. The basic mechanisms by which these agents modulate malignant cell growth remain to be clarified. In recent studies, we showed that SAHA, TSA, and Sirtinol have significant preclinical activity in Waldenstrom's macroglobulinemia (WM). As part of our effort to identify potential molecular targets for these agents, we performed gene expression profiling (GEP) using WM cells treated with these agents. Methods: We implemented the Bootstrap re-sampling technique on five BCWM1 GEP datasets to characterize the range of gene expression observed. Individual BCWM1 cells were treated with SAHA, TSA and Sirtinol at their established IC50 dosages for 6 and 24 hours prior to gene expression profiling. The genes which changed by two-fold, and fell outside of the 90% range of expression after drug treatment were identified. Results: SAHA upregulated TNF-α and downstream proteins including HSP70, TNFSF9, SERPINB2, as well as STAT4- dependent genes. Sirtinol upregulated metalloproteinase (MMP) and phosphodiesterase (PDE) family members through retinoic acid signaling. We also observed that SAHA, TSA and Sirtinol differentially upregulate elements of the MAP kinase pathways, including signaling through Erk, JNK, and p38 MAPK, indicating a global stress response to HDAC inhibition. Conclusions: The above studies suggest that HDAC inhibitors differentially effect growth of WM cells through both global as well as pathway specific alterations in signaling. Importantly, this data provides a platform for studying the mechanistic role of HDACs in WM, and provide a framework for the use of HDAC-I as single and combination. No significant financial relationships to disclose.
Abstract 16656: Dabigatran is as Safe as Warfarin for Peri-Procedural Anticoagulation in Atrial Fibrillation Ablation: A Meta-Analysis
Authors: Paari Dominic Swaminathan, Arun Prasath, Nader Makki, Prachi Kalamkar, Paras Bhatt, Jude Clancy
Journal: Circulation (2013)

Introduction: Newer anticoagulants offer an alternative to warfarin in patients with atrial fibrillation. Studies and meta-analyses have shown that these drugs are at least as safe and efficacious ...
CR-18A REVIEW OF VISUAL OUTCOMES IN CHILDHOOD CRANIOPHARYNGIOMA TREATED WITH A HYPOTHALAMIC SPARING, SURGICAL AND RADIATION STRATEGY
Authors: Victoria Smith, Bronwen Walters, Alki Liasis, Kristian Acquilina, Helen Spoudeas, Katrina Prise, Christos Moraitis, Richard Bowman
Journal: Neuro-Oncology (2016)

CR-18. A REVIEW OF VISUAL OUTCOMES IN CHILDHOOD CRANIOPHARYNGIOMA TREATED WITH A HYPOTHALAMIC SPARING, SURGICAL AND RADIATION STRATEGY Victoria Smith1, Bronwen Walters1, Alki Liasis1, Kristian Acquilina1, Helen Spoudeas1, Katrina Prise1, Christos Moraitis1, and Richard Bowman1,2; Great Ormond Street Hospital, London, UK; UCL Institute of Child Health, London, UK AIM: To review visual outcomes in childhood craniopharyngioma. METHOD: Retrospective longitudinal case review. RESULTS: 27 (19M) patients diagnosed at mean age 88 months and followed for 26 months. VISUAL ACUITY: At first assessment 2 patients were classified as blind, (light perception & 1.325) and one having low vision (limited following) employing the WHO classification (binocular vision). Post-intervention one patient remained blind (no light perception) and 2 had low vision (1.10, 0.60). A further 6 patients had monocular vision loss (worse than 1.30) at presentation versus 7 post-intervention. Older children tended to have better visual acuity pre and post treatment (p 1⁄4 0.05). 20 (74%) patients retained final binocular vision of 0.20 LogMAR or better. VISUAL FIELDS: 9 children underwent Goldmann kinetic perimetry in at least one eye (17 eyes) graded by Wall and George classification. At diagnosis 6 (36%) eyes had minimal or mild loss, 9 eyes (53%) had moderate loss and 2 eyes (11%) had marked loss. Post-intervention 3 (17%) eyes showed no visual field loss, 6 (36%) eyes had minimal or mild loss and 8 (47%) eyes showed moderate loss. Grades improved/ were stable in 15 eyes (89%) and deteriorated in 2 (11%). OPTIC ATROPHY: Optic disc pallor was similar between first and last visit, 56% versus 50%. CONCLUSIONS: Although visual field loss and optic pallor are common most children retain good vision in at least one eye and where formal testing was possible, field deficits improved/ stabilised in most eyes (15/17). Neuro-Oncology 18:iii18–iii23, 2016. doi:10.1093/neuonc/now068.18 #The Author(s) 2016. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
Partial remission and resectability.
Authors: M H Cohen
Journal: Journal of Clinical Oncology (1990)

Article Tools Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.1990.8.8.1443 Journal of Clinical Oncology - published online before print September 22, 2016 PMID: 2166144 Partial remission and resectability. M H CohenxM H CohenSearch for articles by this author https://doi.org/10.1200/JCO.1990.8.8.1443 PDF "Partial remission and resectability.." Journal of Clinical Oncology, 8(8), pp. 1443–1444© 1990 by American Society of Clinical Oncology
Pharmacological and psychotherapeutic interventions for management of obsessive-compulsive disorder in adults: a systematic review and network meta-analysis
Authors: Petros Skapinakis, Deborah M Caldwell, William Hollingworth, Peter Bryden, Naomi A Fineberg, Paul Salkovskis, Nicky J Welton, Helen Baxter, David Kessler, Rachel Churchill, Glyn Lewis
Journal: The Lancet Psychiatry (2016)

BackgroundSeveral interventions are available for management of obsessive-compulsive disorder in adults, but few studies have compared their relative efficacy in a single analysis. We aimed to simultaneously compare all available treatments using both direct and indirect data.MethodsIn this systematic review and network meta-analysis, we searched the two controlled trials registers maintained by the Cochrane Collaboration Common Mental Disorders group for trials published up to Feb 16, 2016. We selected randomised controlled trials in which an active psychotherapeutic or pharmacological intervention had been used in adults with obsessive-compulsive disorder. We allowed all comorbidities except for schizophrenia or bipolar disorder. We excluded studies that focused exclusively on treatment-resistant patient populations defined within the same study. We extracted data from published reports. The primary outcome was symptom severity as measured by the Yale-Brown Obsessive Compulsive Scale. We report mean differences with 95% credible intervals compared with placebo. This study is registered with PROSPERO, number CRD42012002441.FindingsWe identified 1480 articles in our search and included 53 articles (54 trials; 6652 participants) in the network meta-analysis. Behavioural therapy (mean difference −14·48 [95% credible interval −18·61 to −10·23]; 11 trials and 287 patients), cognitive therapy (−13·36 [–18·40 to −8·21]; six trials and 172 patients), behavioural therapy and clomipramine (−12·97 [–19·18 to −6·74]; one trial and 31 patients), cognitive behavioural therapy and fluvoxamine (−7·50 [–13·89 to −1·17]; one trial and six patients), cognitive behavioural therapy (−5·37 [–9·10 to −1·63]; nine trials and 231 patients), clomipramine (−4·72 [–6·85 to −2·60]; 13 trials and 831 patients), and all SSRIs (class effect −3·49 [95% credible interval −5·12 to −1·81]; 37 trials and 3158 patients) had greater effects than did drug placebo. Clomipramine was not better than were SSRIs (−1·23 [–3·41 to 0·94]). Psychotherapeutic interventions had a greater effect than did medications, but a serious limitation was that most psychotherapeutic trials included patients who were taking stable doses of antidepressants (12 [80%] of the 15 psychotherapy trials explicitly allowed antidepressants).InterpretationA range of interventions is effective in the management of obsessive-compulsive disorder, but considerable uncertainty and limitations exist regarding their relative efficacy. Taking all the evidence into account, the combination of psychotherapeutic and psychopharmacological interventions is likely to be more effective than are psychotherapeutic interventions alone, at least in severe obsessive-compulsive disorder.FundingNational Institute for Health Research.
Characterization of patients at high risk of melanoma in Austria
Authors: C. Müller, J. Wendt, S. Rauscher, S. Burgstaller‐Muehlbacher, R. Sunder‐Plassmann, C. Scheurecker, E. Richtig, I. Fae, G. Fischer, H. Pehamberger, I. Okamoto
Journal: British Journal of Dermatology (2016)

Risk of melanoma is determined by genetic and exogenous factors. Only a few studies have included both characteristics in a comprehensive multivariable analysis.To find determinants of patients at high risk of melanoma in Austria, including phenotype, genotype and lifestyle characteristics in comprehensive analyses.In total, 1668 patients with melanoma from the M3 case-control study were studied. Overall, 567 participants were sequenced for CDKN2A, 232 for CDK4, 123 for MITF encoding the variant E318K and 964 for MC1R.Patients with melanoma with a positive family history (n = 190, 11·6%), multiple primary melanomas (n = 261, 15·7%) and younger age (< 50 years, n = 675, 40·5%) were defined as being at high risk. All other patients with melanoma were defined as the reference group. We found significant differences between those two groups and between the high-risk subgroups (positive family history, multiple primary melanomas and younger age). Pigmentation phenotype was associated with the high-risk group in general (childhood freckling, odds ratio 1·46, P = 0·007; blond/reddish hair colour, odds ratio 1·43, P = 0·011). Patients with a positive family history and patients with early-onset disease were similar regarding both their phenotypic characteristics and external factors. Established high-risk mutations in CDKN2A were found in cases with a positive family history (n = 12) or multiple melanomas (n = 2). Moreover, we found three patients carrying the MITF p.E318K variant, two with a CDK4 variant and seven with nonsynonymous MC1R variants with undescribed biological significance, of which four were predicted as damaging.Austrian patients could represent a reservoir for novel genetic variants. Further investigation of populations in Central and Eastern Europe might reveal more novel and disease-relevant variants.
CMS-02MRI AND SURGICAL PARAMETERS TO DETERMINE THE RISK OF A CEREBELLAR MUTISM
Authors: Anjali Sergeant, Brij Karmur, Arjuna Maharaj, Nikunj Patel, Cheryl Alyman, Saleh Almenawer, JoAnn Duckworth, Adam Fleming, Katrin Scheinemann, Forough Farrokhyar, Sheila Singh, Nina Stein
Journal: Neuro-Oncology (2016)
Thoracic aortic aneurysms due to giant cell aortitis
Authors: Muhammad A Cheema, David H MacIver
Journal: Journal of the Royal Society of Medicine (2016)

We present three cases of thoracic aortic aneurysms caused by giant cell aortitis. Thoracic aortic aneurysms are common and usually related to hypertension, a bicuspid aortic valve or connective tissue diseases such as Marfan syndrome. Our report serves as a reminder that giant cell aortitis is an unusual yet very important cause of thoracic aortic aneurysm.
HG-29K27M MUTATION IN HISTONE H3.3 DEFINES A DIFFERENT DISEASE IN PEDIATRIC AND YOUNG ADULT HIGH GRADE GLIOMAS WITH UNIQUE CLINICAL FEATURES: THE FLORENTINE EXPERIENCE WITH LITERATURE REVIEW
Authors: Maurizio Lucchesi, Milena Guidi, Laura Giunti, Anna Maria Buccoliero, Carla Fonte, Silvia Farina, Claudio Favre, Lorenzo Genitori, Iacopo Sardi
Journal: Neuro-Oncology (2016)
QOS-18SPECIFIC INTERVENTION CARE IN CHILDREN TREATED FOR BRAIN TUMOURS: A PILOT STUDY IN GUSTAVE ROUSSY CANCER CAMPUS
Authors: Clémentine Lopez, Audrey Longaud-Vales, Camille Pouchepadass, Anne Laure Domer, Christelle Dufour, Dominique Valteau-Couanet, Sarah Dauchy
Journal: Neuro-Oncology (2016)

QOS-18. SPECIFIC INTERVENTION CARE IN CHILDREN TREATED FOR BRAIN TUMOURS: A PILOT STUDY IN GUSTAVE ROUSSY CANCER CAMPUS Clementine Lopez1, Audrey Longaud-Vales1,2, Camille Pouchepadass1, Anne Laure Domer1, Christelle Dufour2, Dominique Valteau-Couanet2, and Sarah Dauchy1; Gustave Roussy, Supportive Care Department, Villejuif, France; Gustave Roussy, Pediatric Department, Villejuif, France BACKGROUND: Childhood brain tumors, the second most common type of childhoodcancer, account forapproximately20%of thepediatriconcology population. Several neuropsychological studies have shown cognitive deficits in these children.Thosedifficulties areresponsible for schoolproblemsandcan disrupt their social outcome. The links with emotional difficulties or behavioral problems, also more common in these children, appear complex. In this context, the overall assessment of neurocognitive sequelae and their impact on education in particular, of emotional /behavior disturbance of children in remission from a brain tumour seems a major challenge. METHOD: The goal of this project is to implement a new individualized care plan, on a 4-days short hospital session to conduct a comprehensive assessment of the child’s difficulties. Depending on the needs of each child, several assessments will be performed (neuropsychological, psychomotor, speech therapy, child psychiatry, education). This time of hospitalization will also allow the observation of the child’s behavior, his autonomy and sleep. A psycho-educational work will also be made to parents. OBJECTIVES: This new care plan will allow a comprehensive and multidisciplinary reflection after which the child’s needs will be defined. Then, parents will be accompanied to the implementationand coordination of various rehabilitations and liaison work will be done with the school. CONCLUSION: This innovative, collaborative project (Departments of Pediatrics and Supportive Care) should simplify and improve theoverall careof childrenwith TC, to facilitate their integration bypromoting the pursuit of education and in fine improve their quality of life. Neuro-Oncology 18:iii145–iii158, 2016. doi:10.1093/neuonc/now081.18 #The Author(s) 2016. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.