Institution
Yonsei University
Education•Seoul, South Korea•
About: Yonsei University is a education organization based out in Seoul, South Korea. It is known for research contribution in the topics: Population & Cancer. The organization has 50162 authors who have published 106172 publications receiving 2279044 citations. The organization is also known as: Yonsei.
Topics: Population, Cancer, Thin film, Breast cancer, Transplantation
Papers published on a yearly basis
Papers
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TL;DR: A novel material that incorporates zinc-doped iron oxide nanocrystals within a mesoporous silica framework that has been surface-modified with pseudorotaxanes is described, which promises to be a noninvasive, externally controlled drug delivery system with cancer-killing properties.
Abstract: Mesoporous silica nanoparticles are useful nanomaterials that have demonstrated the ability to contain and release cargos with mediation by gatekeepers. Magnetic nanocrystals have the ability to exhibit hyperthermic effects when placed in an oscillating magnetic field. In a system combining these two materials and a thermally sensitive gatekeeper, a unique drug delivery system can be produced. A novel material that incorporates zinc-doped iron oxide nanocrystals within a mesoporous silica framework that has been surface-modified with pseudorotaxanes is described. Upon application of an AC magnetic field, the nanocrystals generate local internal heating, causing the molecular machines to disassemble and allowing the cargos (drugs) to be released. When breast cancer cells (MDA-MB-231) were treated with doxorubicin-loaded particles and exposed to an AC field, cell death occurred. This material promises to be a noninvasive, externally controlled drug delivery system with cancer-killing properties.
576 citations
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National Institutes of Health1, Istanbul University2, University of Texas MD Anderson Cancer Center3, University of Birmingham4, Northwestern University5, Athens Regional Medical Center6, King's College London7, Queen Mary University of London8, University of Manchester9, KAIST10, Yonsei University11
TL;DR: The known association of Behçet's disease with HLA-B*51 was confirmed and a second, independent association within the MHC Class I region was identified and the disease-associated IL10 variant was associated with diminished mRNA expression and low protein production.
Abstract: Behcet's disease is a genetically complex disease of unknown etiology characterized by recurrent inflammatory attacks affecting the orogenital mucosa, eyes and skin. We performed a genome-wide association study with 311,459 SNPs in 1,215 individuals with Behcet's disease (cases) and 1,278 healthy controls from Turkey. We confirmed the known association of Behcet's disease with HLA-B*51 and identified a second, independent association within the MHC Class I region. We also identified an association at IL10 (rs1518111, P = 1.88 x 10(-8)). Using a meta-analysis with an additional five cohorts from Turkey, the Middle East, Europe and Asia, comprising a total of 2,430 cases and 2,660 controls, we identified associations at IL10 (rs1518111, P = 3.54 x 10(-18), odds ratio = 1.45, 95% CI 1.34-1.58) and the IL23R-IL12RB2 locus (rs924080, P = 6.69 x 10(-9), OR = 1.28, 95% CI 1.18-1.39). The disease-associated IL10 variant (the rs1518111 A allele) was associated with diminished mRNA expression and low protein production.
576 citations
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TL;DR: Pembrolizumab monotherapy demonstrated durable antitumor activity and manageable safety in patients with advanced cervical cancer and the US Food and Drug Administration granted accelerated approval of pembrolIZumab for patients withAdvanced PD-L1-positive cervical cancer who experienced progression during or after chemotherapy.
Abstract: PURPOSEKEYNOTE-158 (ClinicalTrials.gov identifier: NCT02628067) is a phase II basket study investigating the antitumor activity and safety of pembrolizumab in multiple cancer types. We present inte...
575 citations
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TL;DR: The authors empirically tested five structural models of corporate bond pricing: Those of Merton (1974), Geske (1977), Leland and Toft (1996), Longstaff and Schwartz (1995), and Collin-Dufresne and Goldstein (2001).
Abstract: This paper empirically tests five structural models of corporate bond pricing: Those of Merton (1974), Geske (1977), Leland and Toft (1996), Longstaff and Schwartz (1995), and Collin-Dufresne and Goldstein (2001). We implement the models using a sample of 182 bond prices from firms with simple capital structures during the period 1986-1997. The conventional wisdom is that structural models do not generate spreads as high as those seen in the bond market, and true to expectations we find that the predicted spreads in our implementation of the Merton model are too low. The compound option approach of Geske comes much closer to the spreads observed in the market, on average, but still underpredicts spreads. In contrast, the Leland and Toft model substantially overestimates credit risk on most bonds, and especially so for high coupon bonds. The Longstaff and Schwartz model modifies Merton to incorporate a stochastic interest rate and a correlation between interest rates and firm value. While the correlation and the level of interest rates have little effect, higher interest rate volatility leads to higher predicted spreads. However, this and other features of this model result in spreads that are often too high for risky bonds and too low for safe bonds. The target leverage ratio model of Collin-Dufresne and Goldstein helps to raise the spreads on the bonds that were considered very safe by the Longstaff and Schwartz model, but overall tends toward overestimation of credit risk. We conclude that structural models do not systematically underpredict spreads, as the previous literature implies, but accuracy is a problem. Moreover, some of the simplifications made to date lead to overestimation of credit risk on the riskier bonds while scarcely affecting the spreads of the safest bonds.
574 citations
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TL;DR: In this paper, the authors demonstrate that canonical Wnt signalling engages tumour cell dedifferentiation and tissue-invasive activity through an Axin2-dependent pathway that stabilizes the Snail1 zinc-transcription factor, a key regulator of normal and neoplastic EMT programs.
Abstract: Accumulating evidence indicates that hyperactive Wnt signalling occurs in association with the development and progression of human breast cancer. As a consequence of engaging the canonical Wnt pathway, a beta-catenin-T-cell factor (TCF) transcriptional complex is generated, which has been postulated to trigger the epithelial-mesenchymal transition (EMT) that characterizes the tissue-invasive phenotype. However, the molecular mechanisms by which the beta-catenin-TCF complex induces EMT-like programmes remain undefined. Here, we demonstrate that canonical Wnt signalling engages tumour cell dedifferentiation and tissue-invasive activity through an Axin2-dependent pathway that stabilizes the Snail1 zinc-transcription factor, a key regulator of normal and neoplastic EMT programmes. Axin2 regulates EMT by acting as a nucleocytoplasmic chaperone for GSK3beta, the dominant kinase responsible for controlling Snail1 protein turnover and activity. As dysregulated Wnt signalling marks a diverse array of cancerous tissue types, the identification of a beta-catenin-TCF-regulated Axin2-GSK3beta-Snail1 axis provides new mechanistic insights into cancer-associated EMT programmes.
573 citations
Authors
Showing all 50632 results
Name | H-index | Papers | Citations |
---|---|---|---|
Younan Xia | 216 | 943 | 175757 |
Peer Bork | 206 | 697 | 245427 |
Ralph Weissleder | 184 | 1160 | 142508 |
Hyun-Chul Kim | 176 | 4076 | 183227 |
Gregory Y.H. Lip | 169 | 3159 | 171742 |
Yongsun Kim | 156 | 2588 | 145619 |
Jongmin Lee | 150 | 2257 | 134772 |
James M. Tiedje | 150 | 688 | 102287 |
Guanrong Chen | 141 | 1652 | 92218 |
Kazunori Kataoka | 138 | 908 | 70412 |
Herbert Y. Meltzer | 137 | 1148 | 81371 |
Peter M. Rothwell | 134 | 779 | 67382 |
Tae Jeong Kim | 132 | 1420 | 93959 |
Shih-Chang Lee | 128 | 787 | 61350 |
Ming-Hsuan Yang | 127 | 635 | 75091 |