tbuckley/cabot-search huggingface dataset:
Abstract 1603: Highly expressed integrin-α8 in multiple myeloma early relapse induces epithelial to mesenchymal transition-like features
Authors: Jiyeon Ryu, Youngil Koh, Hyun Jung Lee, Hyun Sub Chung, Sung-Soo Yoon
Journal: Cancer Research (2016)

Abstract Multiple myeloma (MM) is characterized by clonal proliferation of malignant plasma cells in the bone marrow niches. Despite the remarkable advances of treatment for MM,still many patients of MM struggle early relapses and its mechanism is not well understood. Patients with early relapse after autologous bone marrow transplantation need to be biologically characterized to better understand and reach complete remission. To define altered gene expression in MM relapse, we performed microarray with whole bone marrow aspirates from 16 relapsed MM patients who underwent auto-BMT. Gene expression profile was compared (P &amp;lt; 0.01) and divided into two groups on the basis of their progression-free survival (PFS) at the point of 12 months. To discern the significance of the result, only four patients with shortest and longest duration of PFS was also nexamined, and interestingly both of the analysis showed common up-regulated genes including PDGFB, ITGA7, and ITGA8. Their associated pathways were focal adhesion, ECM-receptor interaction, and regulation of actin cytoskeleton (P &amp;lt; 0.05). By performing qRT-PCR, we validated three genes and only ITGA8 was corresponded with microarray data that early relapsed patients showed higher expression of ITGA8. Several integrin family members are well documented to involve in MM progression that it mediates MM cell adhesion, migration and homing through BM microenvironment. However, integrin-α8 is largely unknown in MM. Due to ITGA8 was highly expressed in MM relapse, we functionally overexpressed integrin-α8 in MM cell lines. Surprisingly, it activated genes showing stem-like features including HIF1a, VEGF, OCT4, and Nanog and EMT-related genes, such as N-cadherin, Slug, Snail and CXCR4. These, consequently enhanced invasion and migration abilities and reduced adhesion activity, indicating the mechanism of MM progression, metastasis as well as relapse. Our speculated specific gene, integrin-α8, up-regulated in MM early relapse, regulates EMT feature in MM that suggesting a potential marker for relapse and attractive clinical target to achieve complete remission. Citation Format: Jiyeon Ryu, Youngil Koh, Hyun Jung Lee, Hyun Sub Chung, Sung-Soo Yoon. Highly expressed integrin-α8 in multiple myeloma early relapse induces epithelial to mesenchymal transition-like features. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1603.
Use of private sector for NHS hip surgery has reduced NHS provision, study finds
Authors: Gareth Iacobucci
Journal: BMJ (2016)

Private provision of NHS funded hip surgery in Scotland has been associated with a decline in procedures provided by the NHS, a study has found.

The use of private sector providers may also have contributed to a rise in age related and socioeconomic treatment inequalities for patients needing hip surgery in Scotland, the research found.1

The study, by Queen Mary University of London and published in the Journal of Public Health , examined the effects of the 2003 Scottish policy to allow patients to choose to have their NHS funded treatment from a private provider or an NHS provider, to increase capacity and reduce waiting times.2

It found that, between 2006-07 and 2008-09—when private sector NHS activity peaked in Scotland—a rise in the number of procedures commissioned …
Abstract 1611: Epithelial-mesenchymal-epithelial transition induced by long term exposure to TGFB1 creates cellular heterogeneity
Authors: Patricia Oliveira, Joana Carvalho, Sara Rocha, Mafalda Azevedo, Andre F. Vieira, Daniel Ferreira, Nuno Mendes, Ines Reis, Joao Vinagre, Alireza Heravi-Moussavi, Joana B. Nunes, Jorge Lima, Valdemar Máximo, Angela Burleigh, Calvin Roskelley, Joana Paredes, Fatima Carneiro, David Huntsman, Carla Oliveira
Journal: Cancer Research (2016)

Abstract Reversible and dynamic transitions between epithelial and mesenchymal cellular states (EMT/MET) contribute to cancer progression and dissemination. Whereas EMT facilitates initial steps of tumour cell detachment, MET is likely required for colonization at distant sites. Although MET is generally perceived as mirroring EMT, we hypothesize that MET entails its own set of novel and/or differentially active molecular circuitries, generating cells with features distinct from the original epithelial state. Using an in vitro TGFβ1-induced EMT/MET model, we demonstrated that MET generates co-existing heterogeneous cell populations (Reverted-Epithelial or RE-cells) with novel phenotypic and functional properties, such as increased self-renewal, in vivo increased tumourigenicity and distinct chemoresistance properties. Overall, our results indicate that MET is a permissive process, driving cellular plasticity towards heterogeneity and with it, creating novel biological signatures of relevance for cancer growth. Citation Format: Patricia Oliveira, Joana Carvalho, Sara Rocha, Mafalda Azevedo, Andre F. Vieira, Daniel Ferreira, Nuno Mendes, Ines Reis, Joao Vinagre, Alireza Heravi-Moussavi, Joana B. Nunes, Jorge Lima, Valdemar Máximo, Angela Burleigh, Calvin Roskelley, Joana Paredes, Fatima Carneiro, David Huntsman, Carla Oliveira. Epithelial-mesenchymal-epithelial transition induced by long term exposure to TGFB1 creates cellular heterogeneity. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1611.
Product Associated Variation in Generic Enoxaparin. Potential Clinical Implications
Authors: Jawed Fareed, Debra Hoppensteadt, Albara Ottman, Omer Iqbal, Walter Jeske, Angel Gray, Jeanine M. Walenga, Evi Kalodiki, Indermohan Thethi, Rakesh Wahi
Journal: Blood (2011)
Abstract 4455: DNA methylation as biomarkers to predict early recurrence of T1-2N0 lung cancer
Authors: Chen Chen, Andrew Yang, Devlin Danielle, Kristen Rodgers, Peng Huang, Zhihao Lu, Candace Griffin, Beverly Lee, Richard Battafarano, Fenglei Yu, Tza-Huei Wang, Stephen Baylin, James Herman, Alicia Hulbert, Malcolm Brock
Journal: Cancer Research (2016)

Abstract Purpose: Many patients die of recurrent NSCLC. Current clinical and molecular tests fail to predict patients at high risk for recurrence. We investigated the relationship between gene promoter methylation and recurrence of NSCLC and its prediction accuracy. Materials and Methods: We prospectively enrolled patients who underwent surgery for T1-2N0 NSCLC. We collected primary tumors, regional lymph nodes (RLN) and mediastinal lymph nodes (MLN). A total of 112 patients were included; cases (n = 39) and controls (n = 73) were defined based on cancer recurrence within 40 months of surgery. Promoter methylation of eight cancer-related genes (CDO1, TAC1, SOX17, p16, CDH13, RASSF1A, APC and MGMT) was obtained by using nanoparticle-based DNA extraction followed by qMSP. Logistic regression analysis adjusted by age, gender, race, tumor size and pack year was used to study the relationship between the gene promoter methylation and the risk of recurrence of NSCLC; machine learning assessed its prediction accuracy. Results: Cases had significantly higher p16 methylation levels than controls in all three tissue types by univariate and multivariate analysis after adjusting for confounders (age, gender, race, tumor size, smoking history, and other gene methylation levels). SOX17 was significantly methylated among cases in both RLN and MLN samples, and remained significant in MLN after adjusting for confounders. Table 1 shows the prediction accuracy of p16 and SOX17 using tumor tissue alone and combined with RLN and/or MLN. Prediction accuracies were increased after adding biomarkers from lymph nodes. Conclusion: Increased methylation status in the promoter region of p16 and SOX17 is associated with an increased risk of cancer recurrence among patients with T1-2N0 NSCLC treated with curative resection. Adding molecular analyses of lymph nodes to primary tumor samples significantly increased the diagnostic accuracy of predicting recurrence in these patients. Table 1.Prediction accuracy using tumor and combined with RLN and/or MLN.Tissue SamplesSensitivitySpecificityPPVNPVTumor0.410.840.520.76Tumor+RLN0.680.960.900.84Tumor+MLN0.560.880.710.79Tumor+RLN+MLN0.690.900.790.85 Citation Format: Chen Chen, Andrew Yang, Devlin Danielle, Kristen Rodgers, Peng Huang, Zhihao Lu, Candace Griffin, Beverly Lee, Richard Battafarano, Fenglei Yu, Tza-Huei Wang, Stephen Baylin, James Herman, Alicia Hulbert, Malcolm Brock. DNA methylation as biomarkers to predict early recurrence of T1-2N0 lung cancer. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 4455.
Abstract 1433: A mobile app for health related quality of life and symptom assessment in patients with primary brain tumors in an outpatient oncology clinic
Authors: Lindsay Rowe, Tuo Dong, Terri Armstrong, Megan Mackey, Mark Gilbert, Andra Krauze, Kevin Camphausen
Journal: Cancer Research (2016)

Abstract Purpose: Primary brain tumors, and their treatments, can have a significant impact on patient quality of life due to altered mentation, mood changes, memory loss, and neurologic deficits. It has therefore been suggested that patient related outcomes need to be included as endpoints for treatment efficacy. The objective of this project was to develop and evaluate a mobile application (GlioNCI), in reporting health-related quality of life measures and symptom scoring in patients with primary brain tumors treated and followed in an outpatient oncology clinic. Experimental Procedures and Results: Apple's Xcode Integrated Development Environment (IDE) was used to develop GlioNCI using the Swift programming language. The parameters and scores chosen had previously been validated in primary CNS tumors. Medication and steroid use is captured at each encounter, as are seizure characteristics, frequency and management. Health related quality of life questionnaires included portions of the EORTC QLQ-C30, and EORTC QLQ-BN20, and MD Anderson Symptom Inventory Brain Tumor Module, which have been validated in patients with cancer and primary CNS tumors respectively. Patients’ symptoms and effects on function are collected with the Activities of Daily Living scale, and the Instrumental Activities of Daily Living Scale. Mood and mental state were addressed using the Hospital Anxiety and Depression Scale. Separate questionnaires for different encounters and time points in outpatient treatment were included to assess care provider, as well as patient related measures, allowing for flexibility of the app to the needs of both. A mobile app was developed to collect, and archive in a database, input and feedback from both patients and care providers in oncology clinics. Conclusion: The creation of a patient centered quality of life and symptom assessment mobile app, following patients with primary brain tumors over their course of treatment and in follow-up is feasible. Pilot testing and patient evaluation of the application in an oncology clinic will be used to validate GlioNCI as a tool in outpatient clinics. Citation Format: Lindsay Rowe, Tuo Dong, Terri Armstrong, Megan Mackey, Mark Gilbert, Andra Krauze, Kevin Camphausen. A mobile app for health related quality of life and symptom assessment in patients with primary brain tumors in an outpatient oncology clinic. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1433.
Use of Diffusion-Weighted Magnetic Resonance Imaging in Sporadic Creutzfeldt-Jakob Disease—Reply
Authors: Laura Eisenmenger, Simon Mead, Harpreet Hyare
Journal: JAMA Neurology (2016)

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Abstract 838: Natural plant extracts induced DNA damage and apoptosis through oxidative stress in transgenic mouse model
Authors: Clement G. Yedjou, Paul B. Tchounwou, Lucio Miele, Marinelle Payton
Journal: Cancer Research (2016)

Abstract One of the most frightening events that women will ever face is being diagnosed with breast cancer. One in eight women in the United States will be diagnosed with this life-threatening disease during her lifetime. Even with all the advances in pharmaceutical technology, mortality rates for breast cancer have remained stagnant for the past few decades. The development of new drugs from natural products is considered important. The specific aim of the present study was to use transgenic mouse mammary tumors as a test model to explore the therapeutic mechanisms of a novel natural product as anti-cancer agent in the treatment of breast cancer. To achieve our specific aim, we performed both in vitro and in vivo studies. Acridine orange and propidium iodide (AO/PI) staining were used to visualize live and dead cells with the means of Cellometer Vision. Tumor volume and weight were measured. Tumor histology was assessed by immunohistochemistry, and enzymatic activities were determined by spectrophotometry. The extent of DNA damage was evaluated by the Comet assay. Cell/tissue apoptosis was measured by the flow cytometry. Data obtained from the AO/PI dye assessment indicated that the tested natural product significantly reduced the number of live cells in a dose-dependent manner, showing a gradual increase in the loss of viability in treated cells. We observed tumor growth inhibition after 4 weeks of daily intraperitoneal administration of plant extracts to trangenic mice. There was a significant increase in DNA damage in treated mice compared to the control mice. Flow cytometry data showed a strong dose-response relationship between plant extracts treatment and annexin V/PI positive cells. Similarly, a statistically significant and dose-dependent increase (p&amp;lt; 0.05) was recorded with regard to caspase 3 activity. Data from enzyme analysis (alaninine transaminase, aspartate transaminase, and creatinine) revealed that plant extract administration is not toxic to treated mice. These results suggest that induction of cell death, DNA damage, and cell/tissue apoptosis may be involved in the therapeutic mechanisms of plant extracts in breast cancer. Collectively, the findings from this study provide convincing evidence that the tested plant extracts may represent a potential anticancer candidate against breast cancer. Research supported by NIH Grant No. NIMHD-G12MD007581) and Grant No. P20GM103476. Citation Format: Clement G. Yedjou, Paul B. Tchounwou, Lucio Miele, Marinelle Payton. Natural plant extracts induced DNA damage and apoptosis through oxidative stress in transgenic mouse model. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 838.
The Psychology and Neuroscience of Financial Decision Making
Authors: Cary Frydman, Colin F. Camerer
Journal: Trends in Cognitive Sciences (2016)

TrendsA boom in accumulated evidence over the past several decades shows that financial decision-making at all levels in the economy often departs from the predictions of models of rational information-processingNew data from a variety of sources, including the human brain, corporate conference calls, genetics, and online trading activity, allow researchers to uncover new facts about the cognitive processes that influence financial decision-makingEvidence from these new data sources, and vigorous randomized field experiments, are already being used for prescriptive purposes to test out low cost practical "nudges" by governments around the worldCloser collaboration between behavioral economic theory and methodologies from cognitive science is likely to generate important new insights on financial decision-making from households to corporate managersAbstractFinancial decisions are among the most important life-shaping decisions that people make. We review facts about financial decisions and what cognitive and neural processes influence them. Because of cognitive constraints and a low average level of financial literacy, many household decisions violate sound financial principles. Households typically have underdiversified stock holdings and low retirement savings rates. Investors overextrapolate from past returns and trade too often. Even top corporate managers, who are typically highly educated, make decisions that are affected by overconfidence and personal history. Many of these behaviors can be explained by well-known principles from cognitive science. A boom in high-quality accumulated evidence–especially how practical, low-cost 'nudges' can improve financial decisions–is already giving clear guidance for balanced government regulation.
The bright side of dark matter: lncRNAs in cancer
Authors: Joseph R. Evans, Felix Y. Feng, Arul M. Chinnaiyan
Journal: Journal of Clinical Investigation (2016)

The traditional view of genome organization has been upended in the last decade with the discovery of vast amounts of non–protein-coding transcription. After initial concerns that this “dark matter” of the genome was transcriptional noise, it is apparent that a subset of these noncoding RNAs are functional. Long noncoding RNA (lncRNA) genes resemble protein-coding genes in several key aspects, and they have myriad molecular functions across many cellular pathways and processes, including oncogenic signaling. The number of lncRNA genes has recently been greatly expanded by our group to triple the number of protein-coding genes; therefore, lncRNAs are likely to play a role in many biological processes. Based on their large number and expression specificity in a variety of cancers, lncRNAs are likely to serve as the basis for many clinical applications in oncology.
Abstract 5109: MDM2 regulates intracellular pathways in TNBC and osteosarcoma that affect osteoclastogenesis
Authors: David J. Olivos, Lindsey D. Mayo
Journal: Cancer Research (2016)

Abstract Advanced cancer cells infiltrate and colonize new organ microenvironments through transformation of the dynamic metastatic niche. In bone, tumor cells secrete soluble factors that distort and manipulate normal bone remodeling leading to osteolytic lesions and inflammation. Clinically, primary high-grade bone sarcomas and secondary metastatic cancers exhibit elevated levels of murine double minute 2 (Mdm2), the principal cellular antagonist and E3 ubiquitin ligase of tumor suppressor p53. We demonstrate a novel function of mdm2, independent of p53, to drive osteolytic disease influenced by the signaling cascade of RANKL, ICAM1, and RANTES. To elucidate the direct influence of Mdm2 in cancer cells on osteoclast differentiation, several cell lines were created to overexpress or silence Mdm2. We found that osteoblast-like osteosarcoma (MG63, Saos2) and metastatic breast cancer cell lines (MDA468, MDA231, TMD-231, T47D, and BT474) lead to significant increased osteoclast differentiation, proliferation, and bone resorption. Co-cultures of Mdm2 over-expressing cancers and normal monocytes resulted in increased numbers of osteoclasts. In cancer cell lines where Mdm2 is silenced, we observed lower number of osteoclasts. The presence of Mdm2 in cancer cells also increased osteoclast resorption in an in vitro organ model. To determine the effects of ICAM1, we used an ICAM antibody to block ICAM1 in the media and showed a decrease in osteoclastogenesis. Understanding the role of Mdm2 in osteoclastogenesis may be amendable to translational benefit in disease models of advanced bone resorption and bone metastases. Citation Format: David J. Olivos, Lindsey D. Mayo. MDM2 regulates intracellular pathways in TNBC and osteosarcoma that affect osteoclastogenesis. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 5109.
Atherothrombotic Risk Stratification and the Efficacy and Safety of Vorapaxar in Patients With Stable Ischemic Heart Disease and Previous Myocardial Infarction
Authors: Erin A. Bohula, Marc P. Bonaca, Eugene Braunwald, Philip E. Aylward, Ramon Corbalan, Gaetano M. De Ferrari, Ping He, Basil S. Lewis, Piera A. Merlini, Sabina A. Murphy, Marc S. Sabatine, Benjamin M. Scirica, David A. Morrow
Journal: Circulation (2016)

Background: Patients with stable ischemic heart disease and previous myocardial infarction (MI) vary in their risk for recurrent cardiovascular events. Atherothrombotic risk assessment may be useful to identify high-risk patients who have the greatest potential to benefit from more intensive secondary preventive therapy such as treatment with vorapaxar. Methods: We identified independent clinical indicators of atherothrombotic risk among 8598 stable, placebo-treated patients with a previous MI followed up for 2.5 years (median) in TRA 2°P-TIMI 50 [Thrombin Receptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events–TIMI 50]. The efficacy and safety of vorapaxar (SCH 530348; MK-5348) were assessed by baseline risk among patients with previous MI without prior stroke or transient ischemic attack for whom there is a clinical indication for vorapaxar. End points were cardiovascular death, MI, or ischemic stroke and GUSTO (Global Use of Strategies to Open Occluded Coronary Arteries) severe bleeding. Results: The 9 independent risk predictors were age, diabetes mellitus, hypertension, smoking, peripheral arterial disease, previous stroke, previous coronary bypass grafting, heart failure, and renal dysfunction. A simple integer-based scheme using these predictors showed a strong graded relationship with the rate of cardiovascular death/MI/ischemic stroke and the individual components ( P for trend &lt;0.001 for all). High-risk patients (≥3 risk indicators; 20% of population) had a 3.2% absolute risk reduction in cardiovascular disease/MI/ischemic stroke with vorapaxar, and intermediate-risk patients (1–2 risk indicators; 61%) had a 2.1% absolute risk reduction ( P &lt;0.001 each), translating to a number needed to treat of 31 and 48. Bleeding increased across risk groups ( P for trend&lt;0.01); however, net clinical outcome was increasingly favorable with vorapaxar across risk groups. Fatal bleeding or intracranial hemorrhage was 0.9% with both treatments in high-risk patients. Conclusions: Stratification of baseline atherothrombotic risk can assist with therapeutic decision making for vorapaxar use for secondary prevention after MI. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT00526474.