Results 81 to 90 of about 1,197,742 (268)
Somatic mutational landscape in von Hippel–Lindau familial hemangioblastoma
Molecular Oncology, EarlyView.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
Molecular Oncology, EarlyView.In the present work, we have identified a transcriptional signature based on the differential expression of six genes (BCL2&MAST4, HSH2D&LAT2, METRN&PITPNM2) that would facilitate the early detection of T‐cell acute lymphoblastic leukemia (T‐ALL) patients prone to a poor treatment response and could be implemented at diagnosis, along with other risk ...
Antonio Lahera +11 more
wiley +1 more source
NKCC1: A key regulator of glioblastoma progression
Molecular Oncology, EarlyView.Glioblastoma (GBM) progression is driven by disrupted chloride cotransporter homeostasis. NKCC1 is highly expressed in stem‐like, astrocytic, and progenitor cells, correlating with earlier recurrence, while overall survival remains unaffected. NKCC1 serves as a prognostic marker and potential therapeutic target, linking chloride transporter imbalance ...
Anja Thomsen +5 more
wiley +1 more source
Model-checking Quantitative Alternating-time Temporal Logic on One-counter Game Models [PDF]
, 2014 We consider quantitative extensions of the alternating-time temporal logics ATL/ATLs called quantitative alternating-time temporal logics (QATL/QATLs) in which the value of a counter can be compared to constants using equality, inequality and modulo ...
Vester, Steen
core +1 more source
Molecular Oncology, EarlyView.Here, we demonstrate that HS1BP3 interacts with Cortactin through a proline‐rich region (PRR3.1) and show that this interaction, and HS1BP3 itself, promote cancer cell proliferation and invasion. Inhibition of this interaction leads to build‐up of TKS5 in multivesicular endosomes and altered secretion of CD63 and CD9, providing an explanation for the ...
Arja Arnesen Løchen +9 more
wiley +1 more source
Optimization Procedures in Affine Model Checking
Моделирование и анализ информационных систем, 2011 Symbolic model checking is based on a compact representation of sets of states and transition relations. At present there are three basic approaches of symbolic model checking: BDD-methods, bounded model checking using SAT-solvers, and various algebraic ...
N. O. Garanina
doaj
Probabilistic and Hybrid Model Checking Deployments for Wireless Sensor Networks [PDF]
Mehran University Research Journal of Engineering and Technology, 2012 In the early stages of system development, model checking is a good practice for examining the WSNs (Wireless Sensor Networks). Model checking involves verifying a system\'s properties based on the system\'s finite state model. For varying applications
Mohsin Memon +2 more
doaj
, 2013 Parse trees are fundamental syntactic structures in both computational linguistics and compilers construction. We argue in this paper that, in both fields, there are good incentives for model-checking sets of parse trees for some word according to a ...
Boral, Anudhyan, Schmitz, Sylvain
core +2 more sources
Molecular Oncology, EarlyView.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
Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining
Molecular Oncology, EarlyView.IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis +3 more
wiley +1 more source