Unified management of multi-model data : (Vision paper)

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Measure-Based Inconsistency-Tolerant Maintenance of Database Integrity

[EN] To maintain integrity, constraint violations should be prevented or repaired. However, it may not be feasible to avoid inconsistency, or to repair all violations at once. Based on an abstract concept of violation measures, updates and repairs can be checked for keeping inconsistency bounded, such that integrity violations are guaranteed to never get out of control. This measure-based approach goes beyond conventional methods that are not meant to be applied in the presence of inconsistency. It also generalizes recently introduced concepts of inconsistency-tolerant integrity maintenance.Partially supported by FEDER and the Spanish grants TIN2009-14460-C03 and TIN2010-17139Decker, H. (2013). Measure-Based Inconsistency-Tolerant Maintenance of Database Integrity. Lecture Notes in Computer Science. 7693:149-173. https://doi.org/10.1007/978-3-642-36008-4_7S1491737693Abiteboul, S., Hull, R., Vianu, V.: Foundations of Databases. 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Elevated Expression of Stromal Palladin Predicts Poor Clinical Outcome in Renal Cell Carcinoma

The role that stromal renal cell carcinoma (RCC) plays in support of tumor progression is unclear. Here we sought to determine the predictive value on patient survival of several markers of stromal activation and the feasibility of a fibroblast-derived extracellular matrix (ECM) based three-dimensional (3D) culture stemming from clinical specimens to recapitulate stromal behavior in vitro. The clinical relevance of selected stromal markers was assessed using a well annotated tumor microarray where stromal-marker levels of expression were evaluated and compared to patient outcomes. Also, an in vitro 3D system derived from fibroblasts harvested from patient matched normal kidney, primary RCC and metastatic tumors was employed to evaluate levels and localizations of known stromal markers such as the actin binding proteins palladin, alpha-smooth muscle actin (α-SMA), fibronectin and its spliced form EDA. Results suggested that RCCs exhibiting high levels of stromal palladin correlate with a poor prognosis, as demonstrated by overall survival time. Conversely, cases of RCCs where stroma presents low levels of palladin expression indicate increased survival times and, hence, better outcomes. Fibroblast-derived 3D cultures, which facilitate the categorization of stromal RCCs into discrete progressive stromal stages, also show increased levels of expression and stress fiber localization of α-SMA and palladin, as well as topographical organization of fibronectin and its splice variant EDA. These observations are concordant with expression levels of these markers in vivo. The study proposes that palladin constitutes a useful marker of poor prognosis in non-metastatic RCCs, while in vitro 3D cultures accurately represent the specific patient's tumor-associated stromal compartment. Our observations support the belief that stromal palladin assessments have clinical relevance thus validating the use of these 3D cultures to study both progressive RCC-associated stroma and stroma-dependent mechanisms affecting tumorigenesis. The clinical value of assessing RCC stromal activation merits further study

Efficient Targeting of Head and Neck Squamous Cell Carcinoma by Systemic Administration of a Dual uPA and MMP-Activated Engineered Anthrax Toxin

Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide. Although considerable progress has been made in elucidating the etiology of the disease, the prognosis for individuals diagnosed with HNSCC remains poor, underscoring the need for development of additional treatment modalities. HNSCC is characterized by the upregulation of a large number of proteolytic enzymes, including urokinase plasminogen activator (uPA) and an assortment of matrix metalloproteinases (MMPs) that may be expressed by tumor cells, by tumor-supporting stromal cells or by both. Here we explored the use of an intercomplementing anthrax toxin that requires combined cell surface uPA and MMP activities for cellular intoxication and specifically targets the ERK/MAPK pathway for the treatment of HNSCC. We found that this toxin displayed strong systemic anti-tumor activity towards a variety of xenografted human HNSCC cell lines by inducing apoptotic and necrotic tumor cell death, and by impairing tumor cell proliferation and angiogenesis. Interestingly, the human HNSCC cell lines were insensitive to the intercomplementing toxin when cultured ex vivo, suggesting that either the toxin targets the tumor-supporting stromal cell compartment or that the tumor cell requirement for ERK/MAPK signaling differs in vivo and ex vivo. This intercomplementing toxin warrants further investigation as an anti-HNSCC agent

Endo180 modulation by bisphosphonates and diagnostic accuracy in metastatic breast cancer

We thank the patients who participated in this study; Professor Gerry Thomas and the Imperial College Healthcare NHS Trust, Human Biomaterials Resource Centre (Tissue Bank); Professor Clare M Isacke (Institute of Cancer Research, London) for Endo180 antibodies; Dr Richard Harvey (Department of Medical Oncology, Imperial College Healthcare NHS Trust) for CA 15-3 antigen measurement. The Division of Cancer at Imperial College London, Imperial College Healthcare NHS Trust is an Experimental Cancer Medicine Centre (ECMC) supported by funds from Cancer Research UK and the Department of Health (C37/A7283) and forms part of Imperial Cancer Research UK Centre (C42671/A12196). CP is recipient of a CRUK Clinician Scientist award. JW is The Flow Foundation Professor of Oncology at Imperial College London. MPC and GK were supported by donations from Tony and Rita Gallagher and Imperial College NHS Healthcare Trust Special Trustees (to JW and JS). MPC was funded by The Rosetrees Trust (Grant JS16/M59; to JW and JS). A-VF was funded by Fundação para a Ciência e Tecnologia fellowship (project supervisor: JS) and Imperial College NHS Healthcare Special Trustees (to JW and JS). MR-T was funded by the Association of International Cancer Research (Grant 08-0803 to JS)