Results 111 to 120 of about 317,964 (264)

Developmental programmes drive cellular plasticity, disease progression and therapy resistance in lung adenocarcinoma

open access: yesMolecular Oncology, EarlyView.
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

Auxetic dihedral Escher tessellations

open access: yesGraphical Models
The auxetic structure demonstrates an unconventional deployable mechanism, expanding in transverse directions while being stretched longitudinally (exhibiting a negative Poisson’s ratio).
Xiaokang Liu   +4 more
doaj   +1 more source

Stimulator of interferon genes agonist augmented antitumor immunity of osimertinib in Egfr‐mutated lung cancer

open access: yesMolecular Oncology, EarlyView.
Combining osimertinib with the STING agonist ADU‐S100 activates innate and adaptive immunity to overcome the non‐inflamed microenvironment of Egfr‐mutant lung cancer. This combination increases NK and CD8+ T‐cell infiltration, associated with activation of the STING‐IRF3 pathway and local immunogenic cell death.
Jun Nishimura   +19 more
wiley   +1 more source

Rod-Bonded Discrete Element Method

open access: yesGraphical Models
The Bonded Discrete Element Method (BDEM) has raised interests in the graphics community in recent years because of its good performance in fracture simulations.
Kangrui Zhang   +3 more
doaj   +1 more source

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

open access: yesMolecular 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

On the Identification of ARMA Graphical Models

open access: yesIEEE Transactions on Automatic Control
The paper considers the problem to estimate a graphical model corresponding to an autoregressive moving-average (ARMA) Gaussian stochastic process. We propose a new maximum entropy covariance and cepstral extension problem and we show that the problem admits an approximate solution which represents an ARMA graphical model whose topology is determined ...
openaire   +3 more sources

Clusterpath Gaussian Graphical Modeling

open access: yesJournal of Computational and Graphical Statistics
Graphical models serve as effective tools for visualizing conditional dependencies between variables. However, as the number of variables grows, interpretation becomes increasingly difficult, and estimation uncertainty increases due to the large number of parameters relative to the number of observations.
D.J.W. Touw   +3 more
openaire   +4 more sources

Persistent geometry-topology descriptor for porous structure retrieval based on Heat Kernel Signature

open access: yesGraphical Models
Porous structures are essential in a variety of fields such as materials science and chemistry. To retrieve porous materials efficiently, novel descriptors are required to quantify the geometric and topological features. In this paper, we present a novel
Peisheng Zhuo, Zitong He, Hongwei Lin
doaj   +1 more source

Finding novel vulnerabilities of hypomorphic BRCA1 alleles

open access: yesMolecular Oncology, EarlyView.
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

open access: yesMolecular Oncology, EarlyView.
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

Home - About - Disclaimer - Privacy