Results 221 to 230 of about 13,122,822 (311)
Assessment of h-index and associated demographic and academic parameters for academic hematologists in Canada. [PDF]
Ordaz DJG +8 more
europepmc +1 more source
The k-index is introduced to replace the h-index to evaluate better the scientific excellence of individuals. [PDF]
Kaptay G.
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
The H-index is an unreliable research metric for evaluating the publication impact of experimental scientists. [PDF]
Akhtar MK.
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
Beyond the h-index: Unveiling nuances and demanding rigor in academic metrics. [PDF]
Saleem SM, Jan SS.
europepmc +1 more source
Identifying essential proteins in dynamic protein networks based on an improved h-index algorithm. [PDF]
Dai C, He J, Hu K, Ding Y.
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

