Results 21 to 30 of about 1,131 (222)
Loss of the miR‐214/199a cluster is associated with recurrence in ovarian cancer. Engineered small extracellular vesicles (m214‐sEVs) elevate miR‐214‐3p/miR‐199a‐5p in tumor cells, suppress β‐catenin, TLR4, and YKT6 signaling, reprogram tumor‐derived sEV cargo, reduce chemoresistance and migration, and enhance carboplatin efficacy and survival in ...
Weida Wang +12 more
wiley +1 more source
Organisational Ontology Framework for Semantic Business Process Management [PDF]
The field of Semantic Business Process Management (SBPM) has refuelled interest in using ontologies for the representation of the static and dynamic aspects of an enterprise and value chains. Putting the SBPM vision into practice, however, requires a consistent and operational network of ontologies reflecting the various spheres of enterprise ...
Agata Filipowska +3 more
openaire +1 more source
Somatic mutational landscape in von Hippel–Lindau familial hemangioblastoma
The causes of central nervous system (CNS) hemangioblastoma in Von Hippel–Lindau (vHL) disease are unclear. We used Whole Exome Sequencing (WES) on familial hemangioblastoma to investigate events that underlie tumor development. Our findings suggest that VHL loss creates a permissive environment for tumor formation, while additional alterations ...
Maja Dembic +5 more
wiley +1 more source
D4.2 - Methodological framework for ontology management
This document describes the Linked Open Terms (LOT) methodology, the methodological framework for OntoCommons. This document introduces the activities that should be performed in the ontology development process and includes recommendations and guidelines to put them into practice.The document first presents the state of the art in ontology development
openaire +2 more sources
Both cg12821679MAPRE3 methylation and MAPRE3 expression are significantly associated with overall survival (OS) of non‐small cell lung cancer. Meanwhile, MAPRE3 expression significantly modified the effect of smoking cessation on OS. Smoking cessation benefits OS merely for patients with high MAPRE3 expression.
Chao Chen +14 more
wiley +1 more source
This study shows that lung adenocarcinomas exploit developmental branching morphogenesis to acquire a therapy resistant basal‐like tumour cell state. This process was found to be regulated by combined TP53 loss‐of‐function and type‐I interferon signalling, identifying a novel axis for biomarker and therapeutic target discovery.
Kamila J Bienkowska +13 more
wiley +1 more source
Finding novel vulnerabilities of hypomorphic BRCA1 alleles
Synthetic lethality screens performed to identify novel vulnerabilities often model complete gene loss, thereby overlooking patient‐derived hypomorphic mutations. In this study, we have performed genome‐wide CRISPR screens on BRCA1 hypomorphic mutations, showing BRCA1I26A behaves like wild‐type, while BRCA1R1699Q mimics deficiency. Furthermore, we have
Anne Schreuder +10 more
wiley +1 more source
MITF maintains genome stability in nonmelanocyte lineages
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir +13 more
wiley +1 more source
Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization
In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu +13 more
wiley +1 more source
BCL9 and BCL9L drive bladder cancer progression by enhancing β‐catenin signaling, promoting proliferation, migration, invasion, and organoid growth. Genetic depletion of BCL9(L) suppresses malignant phenotypes, while pharmacological disruption of the β‐catenin/BCL9(L) complex with ZW4864 inhibits canonical Wnt signaling and tumor‐associated cellular ...
Roland Kotolloshi +11 more
wiley +1 more source

