12 research outputs found

    Large expert-curated database for benchmarking document similarity detection in biomedical literature search

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    Document recommendation systems for locating relevant literature have mostly relied on methods developed a decade ago. This is largely due to the lack of a large offline gold-standard benchmark of relevant documents that cover a variety of research fields such that newly developed literature search techniques can be compared, improved and translated into practice. To overcome this bottleneck, we have established the RElevant LIterature SearcH consortium consisting of more than 1500 scientists from 84 countries, who have collectively annotated the relevance of over 180 000 PubMed-listed articles with regard to their respective seed (input) article/s. The majority of annotations were contributed by highly experienced, original authors of the seed articles. The collected data cover 76% of all unique PubMed Medical Subject Headings descriptors. No systematic biases were observed across different experience levels, research fields or time spent on annotations. More importantly, annotations of the same document pairs contributed by different scientists were highly concordant. We further show that the three representative baseline methods used to generate recommended articles for evaluation (Okapi Best Matching 25, Term Frequency-Inverse Document Frequency and PubMed Related Articles) had similar overall performances. Additionally, we found that these methods each tend to produce distinct collections of recommended articles, suggesting that a hybrid method may be required to completely capture all relevant articles. The established database server located at https://relishdb.ict.griffith.edu.au is freely available for the downloading of annotation data and the blind testing of new methods. We expect that this benchmark will be useful for stimulating the development of new powerful techniques for title and title/abstract-based search engines for relevant articles in biomedical research.Peer reviewe

    ELLIOT Project Presentation #4

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    44 pages, Delivrable D6.3.4 (M32)The fourth and final version of the FP7 ICT ELLLIOT Project Public presentation is provided in this deliverable. Its aim is to serve for facilitating the dissemination efforts of all consortium partners, by providing common background information on the project objectives and expected resul

    ELLIOT Project Presentation #4

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    44 pages, Delivrable D6.3.4 (M32)The fourth and final version of the FP7 ICT ELLLIOT Project Public presentation is provided in this deliverable. Its aim is to serve for facilitating the dissemination efforts of all consortium partners, by providing common background information on the project objectives and expected resul

    Common Assets identification and Characterisation

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    FP7 Fireball coordination Action, http://www.fireball4smartcities.eu/Smart Cities innovation ecosystems are based on an infrastructure forinnovation. This infrastructure is built upon what within FIREBALL we are calling "common assets": resources of various types that can be selected, combined,shared and used by those who want to engage in living labs innovation projects.In this report, common assets types such as technical infrastructures, userdriven open innovation methods and tools, test bed facilities and usercommunities are identified and characterized based on a number of cases. Thecharacterization results into an overview and analysis how configurations of suchcommon assets can be tailored to the needs and requirements of Smart Cities.The work reported in this deliverable forms the basis for describing mechanismsfor access and governance of the common assets (D1.3). Also it is of relevanceto, and has been developed in close coordination with, the Landscape andRoadmap as developed in D2.1, which contains a number of "Smart City" casestudies where common assets are being studied as well.The work presented in this deliverable has been subject of several FIREBALLworkshops where the concept of common assets has been discussed andelaborated: * Future Interne Assembly (FIA) conference, Ghent, December 2010, workshopon "Smart Cities and Future Internet Experimentation". Workshop jointlyorganized with FIRESTATION. * Future Internet Assembly (FIA) conference, Budapest, May 2011, workshopon "Smart Cities and FIRE: Experimentation and Living Labs for the FutureInternet". Workshop jpointly organized with FIRESTATION. * ICE 2011 conference, June 2011, Aachen: workshop "Common Assets forSmart Cities Living Labs Innovation: IT Infrastructures, methods and usercommunities".The work has been subject of elaborate discussions with FIA members and alsohas resulted in a joint proposal for a Support Action in FP7-ICT (currently underevaluation)

    Targeting metastasis-initiating cancer stem cells in gastric cancer with leukaemia inhibitory factor

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    Abstract Gastric cancer’s (GC) bad prognosis is usually associated with metastatic spread. Invasive cancer stem cells (CSC) are considered to be the seed of GC metastasis and not all CSCs are able to initiate metastasis. Targeting these aggressive metastasis-initiating CSC (MIC) is thus vital. Leukaemia inhibitory factor (LIF) is hereby used to target Hippo pathway oncogenic members, found to be induced in GC and associated with CSC features. LIF-treated GC cell lines, patient-derived xenograft (PDX) cells and/or CSC tumourspheres underwent transcriptomics, laser microdissection-associated proteomics, 2D and 3D invasion assays and in vivo xenograft in mice blood circulation. LIFR expression was analysed on tissue microarrays from GC patients and in silico from public databases. LIF-treated cells, especially CSC, presented decreased epithelial to mesenchymal transition (EMT) phenotype and invasion capacity in vitro, and lower metastasis initiation ability in vivo. These effects involved both the Hippo and Jak/Stat pathways. Finally, GC’s high LIFR expression was associated with better clinical outcomes in patients. LIF treatment could thus represent a targeted anti-CSC strategy to fight against metastatic GC, and LIFR detection in primary tumours could constitute a potential new prognosis marker in this disease

    CD44v3 is a marker of invasive cancer stem cells driving metastasis in gastric carcinoma

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    International audienceBackground: Cancer stem cells (CSCs) are at the origin of tumour initiation and progression in gastric adenocarcinoma (GC). However, markers of metastasis-initiating cells remain unidentified in GC. In this study, we characterized CD44 variants expressed in GC and evaluated the tumorigenic and metastatic properties of CD44v3+ cells and their clinical significance in GC patients.Methods: Using GC cell lines and patient-derived xenografts, we evaluated CD44+ and CD44v3+ GC cells molecular signature and their tumorigenic, chemoresistance, invasive and metastatic properties, and expression in patients-derived tissues.Results: CD44v3+ cells, which represented a subpopulation of CD44+ cells, were detected in advanced preneoplastic lesions and presented CSCs chemoresistance and tumorigenic properties in vitro and in vivo. Molecular and functional analyses revealed two subpopulations of gastric CSCs: CD44v3+ CSCs with an epithelial-mesenchymal transition (EMT)-like signature, and CD44+/v3- CSCs with an epithelial-like signature; both were tumorigenic but CD44v3+ cells showed higher invasive and metastatic properties in vivo. CD44v3+ cells detected in the primary tumours of GC patients were associated with a worse prognosis.Conclusion: CD44v3 is a marker of a subpopulation of CSCs with metastatic properties in GC. The identification of metastasis-initiating cells in GC represents a major advance for further development of anti-metastatic therapeutic strategies

    Nrf2 Downregulation Contributes to Epithelial-to-Mesenchymal Transition in Helicobacter pylori-Infected Cells

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    Background: Gastric cancer, the fifth most common cancer worldwide, is mainly linked to Helicobacter pylori infection. H. pylori induces chronic inflammation of the gastric mucosa associated with high oxidative stress. Our study aimed at assessing the implication of Nrf2, a major regulator of cellular redox homeostasis, in H. pylori-induced gastric carcinogenesis. Methods: Using three different gastric epithelial cell lines, a non-cancerous (HFE-145) and two different subtypes of gastric cancer (AGS and MKN74), we analyzed the modulation of Nrf2 expression over time. After invalidation of Nrf2 by CRISPR-cas9, we assessed its role in H. pylori-induced epithelial-to-mesenchymal transition (EMT). Finally, we evaluated the expression of Nrf2 and ZEB1, a central EMT transcription factor, in human gastric tissues. Results: We first demonstrated that the Nrf2 signaling pathway is differentially regulated depending on the infection stage. Rapidly and transiently activated, Nrf2 was downregulated 24 h post-infection in a VacA-dependent manner. We then demonstrated that Nrf2 invalidation leads to increased EMT, which is even exacerbated after H. pylori infection. Finally, Nrf2 expression tended to decrease in human patients’ gastric mucosa infected with H. pylori. Conclusions: Our work supports the hypothesis that Nrf2 downregulation upon H. pylori infection participates in EMT, one of the most important events in gastric carcinogenesis
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