Results 191 to 200 of about 25,147,248 (249)
Dormant cancer cells can hide in distant organs for years, evading treatment and the immune system. This review highlights how signals from the surrounding tissue and immune environment keep these cells inactive or trigger their reawakening. Understanding these mechanisms may help develop therapies to eliminate or control dormant cells and prevent ...
Kanishka Tiwary +1 more
wiley +1 more source
Comparative molecular dynamics of two cyclic peptide inhibitors bound to the Zika virus NS2B/NS3 protease. [PDF]
Marinho CVS, de Oliveira MVD, Lima AH.
europepmc +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
HLA-DRB1 Polymorphisms Modulate the Dynamic Compatibility between the Presentation of EBNA1<sub>400-413</sub> and MBP<sub>85-99</sub>. [PDF]
Alves LB, Giuliatti S.
europepmc +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
Confirmation and Extension of the HLA-DPB1*1000:01 Allele by Next-Generation and Oxford Nanopore Sequencing. [PDF]
Merschman J +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
De Novo MFN2 p.Arg95Met in Severe Charcot-Marie-Tooth Disease Type 2A. [PDF]
Lee HY +5 more
europepmc +1 more source
Pair‐wise comparison of the CellSearch and FETCH enrichment technologies for circulating tumor cells (CTCs) from metastatic breast, prostate, and small cell lung cancer patients shows an increased capture of CTCs using FETCH enrichment. The clinical implementation of circulating tumor cells (CTCs) as a predictive tool for therapy efficacy in the ...
Michiel Stevens +6 more
wiley +1 more source

