Results 121 to 130 of about 959,893 (266)
Lipidome Analysis of Cancer Cells and Their Extracellular Vesicles Reveals Cancer-Type-Specific Lipid Signatures and Enables the Design of EV-Mimetic Liposomes. [PDF]
Douanne N +14 more
europepmc +1 more source
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
Implicit 3D geological modeling method based on expert knowledge constraints: A case study from the Songshugang Mining District, Hengfeng County, Jiangxi Province, China. [PDF]
Jin W +9 more
europepmc +1 more source
Radiotherapy (RT) response depends on the DNA repair capacity of tumor and host cells. We show that circulating tumor cell (CTC) counts and apoptosis rates before and after RT predict treatment response and outcome, which can be accessed via easily accessible liquid biopsy approaches. Created in BioRender. Wikman, H.
Yvonne Goy +10 more
wiley +1 more source
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
X-ray line profile analysis of BaTiO3 thin film prepared by sol-gel deposition [PDF]
Zeen Vee Ooi +3 more
openalex +1 more source
Beyond chromatin accessibility: bulk ATAC-seq as an integrative assay to portray genomes and epigenomes. [PDF]
Toumi I +4 more
europepmc +1 more source
Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining
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

