tbuckley/cabot-search huggingface dataset:
Abstract 2333: Coronary Magnetic Resonance Angiography with Whole Heart Coverage for The Detection of Coronary Arery Stenoses: A Multicenter Study
Authors: Yasutaka Ichikawa, Hajime Sakuma, Yasuyuki Kobayashi, Masaki Ishida, Kazuhiro Katahira, Yuji Matsumoto, Naoya Fujita, Reiji Ochiai
Journal: Circulation (2007)

Background: Previous single center studies demonstrated that coronary magnetic resonance angiography (MRA) with whole heart coverage allows for noninvasive detection of coronary artery disease. In this prospective, multicenter study, we investigated the accuracy of whole heart coronary MRA in patients with suspected coronary disease. Methods: The subjects were recruited from five institutions. Free-breathing coronary MRA covering the entire heart were obtained in fifty eight patients by using a 3-dimensional, segmented steady-state free precession sequence without contrast injection. Coronary MRA was interpreted by 3 independent observers. Conventional X-ray coronary angiography was analyzed by a separate blinded reviewer. The diagnostic accuracy of coronary MRA was determined in all segments with reference diameter of 2 mm or more on X-ray coronary angiography regardless of the image quality of MRA. Results: Acquisition of coronary MRA was completed in all patients with an averaged imaging time of 9.8 ± 4.8 min. On patient based analysis, coronary MRA showed the sensitivity of 79.4% (range 64.7–88.2%), the specificity of 70.1% (65.9–80.5%), and the negative predictive value of 89.6% (84.6–93.1%). The sensitivity, specificity and negative predictive value in the segmental analysis were 60.6% (53.8–65.4%), 95.5% (94.2–97.6%) and 97.7% (97.4–98.1%). Conclusions: Coronary MRA with whole heart coverage can provide detection of luminal narrowing of the coronary artery with moderate sensitivity, high specificity and high negative predictive value. The high negative predictive value observed in this multicenter study indicates that noninvasive MRA approach is useful in ruling out significant coronary artery disease.
Abstract 4680: Restoration of EGFR-TKI resistance by endocytosis inhibitor PAO in lung cancer with wild-type EGFR
Authors: Boyeon Kim, Jae Sook Sung, Yeul Hong Kim
Journal: Cancer Research (2016)

Abstract Therapeutic efficacy of epithelial growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) is currently limited in selected lung cancer patients who have TKI sensitive EGFR mutation. However, the potential molecular mechanism that expands the therapeutic benefit of EGFT-TKI in patients who have wild-type EGFR non-small cell lung cancer (wtEGFR NSCLC) remains unclear. Recently, several studies revealed EGFR endocytosis mechanism could mediate signal transductions that influence in cancer cell proliferation. Moreover, our previous study demonstrated that EGFR endocytosis is related to gefitinib sensitivity in wtEGFR NSCLC and EGFR endocytosis could be a novel therapeutic target in lung cancer with wtEGFR (Oncotarget. 2014 15;5(5):1265-78). In this study, we investigated whether EGFR-TKI resistance could be restored in wtEGFR NSCLC cell lines by endocytosis inhibitor phenylarsine oxide (PAO). To investigate effects of PAO in vitro, we analyzed EGF-induced EGFR internalization and performed Annexin V and propodium iodide (PI) staining by flow cytometry. As a result, EGF-induced EGFR endocytosis is decreased and apoptotic cell death is induced accompanied by G0/G1 arrest after PAO treatment. In addition, we observed that cell viability is reduced significantly when PAO and EGFR-TKIs (gefitinib, erlotinib) treated together. Furthermore, we verified signaling transduction that associated with proliferation and apoptosis by western blot. To confirm combination effects of PAO and EGFR-TKI in vivo, we established xenograft mouse model using gefitinib-insensitive SNU1327 cell lines. After Tumor sizes reached 100-200mm3, mice were treated with PAO or gefitinib alone, or combined treatment for 3 weeks. We observed that tumor sizes of combination group were more decreased than other groups.In these result, we validate endocytosis inhibitor PAO is potential drug for overcoming therapeutic limitation of EGFR-TKI in gefitinib-insensitive wtEGFR NSCLC cell lines, though further experiment is needed to explain more accurate mechanism. This study was supported by a Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (NRF-2013R1A1A2057538). Citation Format: Boyeon Kim, Jae Sook Sung, Yeul Hong Kim. Restoration of EGFR-TKI resistance by endocytosis inhibitor PAO in lung cancer with wild-type EGFR. [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 4680.
Deep-Sequencing Of The Molecular Landscape In Burkitt Lymphoma/Leukemia
Authors: Alexander Kohlmann, Andreas Roller, Jennifer Kienast, Sabine Denzel, Vera Grossmann, Niroshan Nadarajah, Tamara Alpermann, Wolfgang Kern, Susanne Schnittger, Torsten Haferlach, Claudia Haferlach
Journal: Blood (2013)
Abstract 2526: Regulation of angiogenic factors in glioblastoma progression
Authors: Carolina Larrain, Umadevi V. Wesley, Paul Clark, John S. Kuo, Robert Dempsey
Journal: Cancer Research (2016)

Abstract Background &amp; Purpose: Glioblastoma is the most malignant primary brain tumor in humans and has a very low survival rate. The aggressiveness of this cancer can be attributed to the presence of glioblastoma stem cells (GSC), which are highly invasive and therapy resistant. Increased aggressiveness of GSCs is attributed to the release of angiogenic factors, which promotes the formation of new blood vessels that enhances tumor cell survival and proliferation. The neovascularization also provides a scaffold for tumor cells to migrate, enabling metastasis. Therefore, identifying the altered expression of angiogenic factors is of clinical importance. In this study, we examined the changes in the expression of pro-angiogenic factors in GSCs as compared to the original tumor from which they were derived. We also determined if differentiation of GSC towards a less invasive phenotype decreased the levels of these pro-angiogenic factors. Methods: GBM tumor cells were grown in complete media containing 10% Fetal Calf Serum (FCS) and GSCs were grown in media containing B27, heparin, EGF, and FGF. GSCs were differentiated by growing them in media containing 10% FCS and B27 with vitamin A, for about one week. We examined the expression of a panel of pro-angiogenic factors in GSCs (33-GSC) and in the original tumor cells (33-T) from which GSCs were derived. We then examined if differentiation of 33-GSC decreased the levels of these pro-angiogenic factors. Changes in protein levels were evaluated by immunofluorescence staining. The mRNA levels were quantitated using real time Q-PCR. Results: Immunofluorescence staining showed that the GSCs express higher levels of pro-angiogenic factors examined (11 out of 16). GSCs were successfully differentiated into astrocytes as indicated by morphology and GFAP expression. The differentiation of GSCs into astrocytes was sufficient to cause decreased expression of VEGF and c-MYC. Our data showed 27 fold increase in VEGF mRNA levels, 63 fold increase in MMP2 mRNA levels, 11 fold increase in MMP9 mRNA levels, and 2 fold increase in c-MYC mRNA levels in GSCs compared to the tumor line, indicating the regulation of these pro-angiogenic factors at transcriptional level. Conclusions: Increased expression of pro-angiogenic factors in GSCs may render these cells to be more aggressive and invasive, and suggests that differential expression of angiogenic factors in GSC cells may play an important role in the GBM progression, and therapy resistance. Citation Format: Carolina Larrain, Umadevi V. Wesley, Paul Clark, John S. Kuo, Robert Dempsey. Regulation of angiogenic factors in glioblastoma progression. [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 2526.
The Role of Quality Control in Targeted Next-Generation Sequencing Library Preparation
Authors: Rouven Nietsch, Jan Haas, Alan Lai, Daniel Oehler, Stefan Mester, Karen S. Frese, Farbod Sedaghat-Hamedani, Elham Kayvanpour, Andreas Keller, Benjamin Meder
Journal: Genomics Proteomics & Bioinformatics (2016)

Next-generation sequencing (NGS) is getting routinely used in the diagnosis of hereditary diseases, such as human cardiomyopathies. Hence, it is of utter importance to secure high quality sequencing data, enabling the identification of disease-relevant mutations or the conclusion of negative test results. During the process of sample preparation, each protocol for target enrichment library preparation has its own requirements for quality control (QC); however, there is little evidence on the actual impact of these guidelines on resulting data quality. In this study, we analyzed the impact of QC during the diverse library preparation steps of Agilent SureSelect XT target enrichment and Illumina sequencing. We quantified the parameters for a cohort of around 600 samples, which include starting amount of DNA, amount of sheared DNA, smallest and largest fragment size of the starting DNA; amount of DNA after the pre-PCR, and smallest and largest fragment size of the resulting DNA; as well as the amount of the final library, the corresponding smallest and largest fragment size, and the number of detected variants. Intriguingly, there is a high tolerance for variations in all QC steps, meaning that within the boundaries proposed in the current study, a considerable variance at each step of QC can be well tolerated without compromising NGS quality.
C型肝炎関連混合クリオグロブリン血症におけるリツキシマブ+Peg-インターフェロンα/リバビリンとPeg-インターフェロンα/リバビリンの比較
Authors: Saadoun David, Rigon Mathieu Resche, Sene Damien, Terrier Benjamin, Karras Alexandre, Perard Laurent, Schoindre Yoland, Coppere Brigitte, Blanc Francois, Musset Lucile, Piette Jean-Charles, Rosenzwajg Michele, Cacoub Patrice
Journal: Blood (2010)
Preoperative Anemia and Neonates
Authors: Rosemary D. Higgins, Ravi Mangal Patel, Cassandra D. Josephson
Journal: JAMA Pediatrics (2016)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Pediatrics HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Pediatrics journal
Abstract 2951: A comprehensive analysis of proteins involved in innate and acquired resistance to molecularly-targeted drugs in breast cancer cells
Authors: Hamid Montazeri
Journal: Cancer Research (2016)

Abstract Cancer is the second leading cause of death among Americans, and despite advances in diagnosis, new technologies for early detection, and development of potent molecularly-targeted drugs, survival rates in advanced disease have not been improving at desired rates. Perseverance of cancer cells seem to rely both on their significant heterogeneity at the onset of treatment, and the inherent plasticity (genetic instability) to adopt to environmental conditions and exogenous agents. Cancer is known as a heterogeneous disease. In fact, extensive genetic diversity has been revealed not only between different types of cancer, but also within a single tumor (as diversity in the expression of protein biomarkers). This intra-tumor heterogeneity could be a major obstacle in cancer treatment due to a wide range of responsivity to any specific anticancer agent. This study aims to analyze the heterogeneity and plasticity among a small panel of breast cancer cell lines as a reaction to exposure to a variety of molecularly-targeted agents, which could lead us to identification of the proteins that play major roles in drug resistance in cancer cells. After initial evaluation of the LC50, we exposed five different breast cancer cell lines to high doses of erlotinib (selective ErbB1/EGFR-inhibitor), vemurafenib (pan Raf inhibitor), everolimus (selective mTORC1 inhibitor), and ruxolitinib (pan JAK inhibitor), an collected the survivors. Using an in-house designed microarray and real-time PCR analysis, we analyzed the protein expression profile of the survivors compared to the untreated population, which revealed proteins involved in innate resistance and the heterogeneity among the population. In an alternative approach, we exposed the cells to gradually increasing doses of these selected agents, affording the cells the opportunity to adapt to the treatment. The resistant cells were then analyzed in a similar fashion to reveal proteins involved in acquired resistance. Citation Format: Hamid Montazeri. A comprehensive analysis of proteins involved in innate and acquired resistance to molecularly-targeted drugs in breast cancer cells. [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 2951.
Nivolumab for classical Hodgkin's lymphoma after failure of both autologous stem-cell transplantation and brentuximab vedotin: a multicentre, multicohort, single-arm phase 2 trial
Authors: Anas Younes, Armando Santoro, Margaret Shipp, Pier Luigi Zinzani, John M Timmerman, Stephen Ansell, Philippe Armand, Michelle Fanale, Voravit Ratanatharathorn, John Kuruvilla, Jonathon B Cohen, Graham Collins, Kerry J Savage, Marek Trneny, Kazunobu Kato, Benedetto Farsaci, Susan M Parker, Scott Rodig, Margaretha G M Roemer, Azra H Ligon, Andreas Engert
Journal: The Lancet Oncology (2016)
P0848 : Efficacy of response-guided pegylated interferon and ribavirin therapy for people who inject drugs with HCV genotype 2/3 infection: The activate study
Authors: J. Grebely, O. Dalgard, B. Conway, G. Foster, P. Bruggmann, M. Backmund, G. Robaeys, T. Swan, B. Hajarizadeh, J. Amin, P. Marks, S. Quiene, M. Weltman, D. Shaw, A. Dunlop, M. Hellard, J. Bruneau, S. Bourgeois, C. Thurnheer, G.J. Dore
Journal: Journal of Hepatology (2015)
Abstract 704: Hyperglycemia stimulates glycolysis and enhances migratory/invasive potential in tongue squamous cell carcinoma
Authors: Anxun Wang, Wei Wang, Luodan Zhao, Qianting He, Jingjing Sun, Zhonghua Liu, Zujian Chen, Xiaofeng Zhou
Journal: Cancer Research (2016)

Abstract Objective: The aim of this study was to investigate the role of glycolysis (HK2/PKM2) in the development of tongue squamous cell carcinoma (TSCC) and elucidate how hyperglycaemia stimulate HK2 and PKM2 and enhance migration/invasion potential in TSCC. Methods: A total of 501 patients which diagnosed as TSCC between 1998 and 2004 were enrolled in the retrospective study. The expression of HK2/PKM2 was examined by IHC and the relationship between TSCC and diabetes mellitus (DM) was investigated. We then investigated the role of HK2/PKM2 in the migration and invasion of TSCC and relevant pathways (the SOD2-H2O2 pathway and miR-138 pathway). Finally, we investigated whether hyperglycaemia enhance migratory/invasive potential of TSCC through stimulating glycolysis. Results: The prevalent rate of TSCC patients with diabetes was 13.97%, which was significantly higher than the incidence rate of DM (11.6%) in China. Cox analysis revealed that the HR for patients with DM vs without DM was 1.32. IHC results confirmed that the up-regulation of PKM2/HK2 expression was correlated with tumor stage, clinical stages, diabetes, lymph node metastasis and associated with reduced overall survival. PKM2/HK2/AKT1 overexpression increased cell migration and invasion, SOD2 activities and intracellular H2O2. The siRNA-based PKM2/HK2 knockdown inhibited cell migration and invasion, reduced activities of SOD2 and intracellular H2O2, and also inhibited tumor growth and lung metastasis in vivo. Luciferase assays revealed that PKM2/AKT1 was directly targeted by miR-138 and miR-138 can reduce the expression of the PKM2/AKT1 gene. High glucose enhanced the migration/invasion ability, miR-138/PKM2/HK2 expression and increased SOD2 activities and intracellular H2O2. Conclusions: Our results confirm that DM may be a risk factor in the development of TSCC. PKM2/HK2 plays an important role in the progression of TSCC, and may serve as a biomarker or therapeutic target for patients with TSCC. High glucose stimulates glycolysis (PKM2/HK2) and enhances migration/invasion potential in TSCC. Citation Format: Anxun Wang, Wei Wang, Luodan Zhao, Qianting He, Jingjing Sun, Zhonghua Liu, Zujian Chen, Xiaofeng Zhou. Hyperglycemia stimulates glycolysis and enhances migratory/invasive potential in tongue squamous cell carcinoma. [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 704.
Abstract 4053: A unique nutrient mixture suppresses ovarian cancer growth of A-2780 by inhibiting invasion and MMP-9 secretion
Authors: M. Waheed Roomi, Matthias Rath, Aleksandra Niedzwiecki
Journal: Cancer Research (2016)

Abstract Ovarian cancer is the deadliest gynecological malignancy in women, and fifth leading cause of death. The American Cancer Society estimated that it would claim 14,250 lives in 2013. Despite the advances made in chemotherapy and surgery, the average time of clinical remission is approximately 2 years and the 5-year survival rate is 45%. Thus, there is an urgent need for the development of a novel therapeutic approach to ovarian cancer treatment. We investigated the effect of a unique nutrient mixture (NM) containing ascorbic acid, lysine, proline and green tea extract on human ovarian cancer cell A-2780 in vivo and in vitro. Athymic female nude mice (n = 12) were inoculated by I.P. with 2×106 cells in 0.1ml PBS and randomly divided into two groups. Group A (n = 6) was fed a regular diet and group B (n = 6) a regular diet supplemented with 0.5% NM. Four weeks later, the mice were sacrificed and tumors that developed in the ovary were excised, weighed and processed for histology. In vitro, A-2780 cells were cultured in Dulbecco modified Eagle medium supplemented with 10% FBS and antibiotics. At near confluence, cells were treated with NM in triplicate at concentrations between 0-1000 μg/ml. Cell proliferation was measured by MTT assay, MMP-9 secretion by gelatinase zymography, invasion through Matrigel and morphology by H&amp;E staining. All control mice (Group A) developed large ovarian tumors, whereas 5 out of 6 mice in group B developed no tumors, and one, a small tumor. Zymography demonstrated only MMP-9 expression, which NM inhibited in a dose dependent fashion, with virtual total block at 250 μg/ml concentration. NM significantly inhibited invasion through Matrigel with total block at 250 μg/ml concentration. MTT showed dose dependent inhibition of cell proliferation with NM and H&amp;E staining showed no morphological changes below 500 μg/ml NM. These results suggest that NM has therapeutic potential in treatment of ovarian cancer by significantly suppressing tumor growth and by inhibiting MMP-9 secretion and invasion of A-2780 ovarian cancer cells. Citation Format: M. Waheed Roomi, Matthias Rath, Aleksandra Niedzwiecki. A unique nutrient mixture suppresses ovarian cancer growth of A-2780 by inhibiting invasion and MMP-9 secretion. [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 4053.
Stress is unlikely to increase breast cancer risk, study finds
Authors: Jacqui Wise
Journal: BMJ (2016)

A large prospective study, published in Breast Cancer Research , has found no association between breast cancer risk and stress levels or adverse life events.1 Women with breast cancer have often attributed their cancer to psychological stress, although the scientific evidence for this has been inconclusive.

The Generations study, set up by Breast Cancer Now, the United Kingdom’s largest breast cancer research charity, included 106 000 women in the UK who were asked how frequently they had …
Race and Poverty Status as a Risk for Overall Mortality in Community-Dwelling Middle-Aged Adults
Authors: Alan B. Zonderman, Nicolle A. Mode, Ngozi Ejiogu, Michele K. Evans
Journal: JAMA Internal Medicine (2016)

This study uses data from the Healthy Aging in Neighborhoods of Diversity across the Life Span study to examine the contributions of sex, race, and socioeconomic differences to overall mortality in middle-aged adults.