Results 181 to 190 of about 1,503,887 (312)
Unveiling Risk Profiles: A Latent Profile Analysis of 21st-Century Skills, Resistance to Change, and Cognitive Flexibility. [PDF]
Uras MC, Kaya S, Kaya A, Yildirim M.
europepmc +1 more source
Effects of response preference on resistance to change. [PDF]
Ringdahl JE +8 more
europepmc +1 more source
While some resistance to change is inevitable, this article suggests that inept management strategies can often cause the normal unease associated with a change to accelerate into more severe problems.
Baker, Sharon L.
core
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
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
Do Organism Profile and Resistance Patterns Change between First and Subsequent Two-Stage Revision for Periprosthetic Joint Infection? [PDF]
Ahrens H +6 more
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
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
[Resistance to change: nurse prescription]. [PDF]
Ruiz Sánchez JJ.
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

