Results 211 to 220 of about 2,137,840 (268)
Portal Vein Thrombosis Risk in Cirrhotic Patients With Portal Hypertension on Beta-Blockers: A Multi-Institutional Cohort Study. [PDF]
Abosheaishaa H +9 more
europepmc +1 more source
Temozolomide treatment activates GSK3β, driving DNMT1 phosphorylation, destabilization, and CD47 promoter hypomethylation in glioblastoma. This epigenetic shift upregulates CD47, enabling TMZ‐treated GBM cells to evade macrophage phagocytosis, survive chemotherapy, and acquire resistance.
Jie Li +11 more
wiley +1 more source
APDS treatment in Germany: decision criteria, costs and contribution of leniolisib to outcomes. [PDF]
Baumann U +9 more
europepmc +1 more source
AARS1 drives PI3K–AKT–mTOR‐dependent glycolysis in bladder cancer, promoting lactate accumulation, increased lactylation, H3K27la enrichment at the HK2 promoter, and HK2 transcription. HK2 reinforces glycolysis, sustaining a metabolic–epigenetic program associated with tumor progression, recurrence, and metastasis.
Qin Yuan +13 more
wiley +1 more source
Survival Analysis in Orthopaedics: Techniques to Evaluate Long-term Treatment Efficacy and Patient Outcomes. [PDF]
Vatkar AJ, Kale S, Shyam A, Shinde S.
europepmc +1 more source
Integrative multi‐cohort analyses identify 14‐3‐3γ as a biomarker and regulator of cognitive vulnerability. Experimental studies show that 14‐3‐3γ loss is associated with Tau Thr205 phosphorylation, synaptic dysfunction, and cognitive impairment, while genetic overexpression or pharmacological stabilization of 14‐3‐3γ confers protective effects in ...
Shouqiang Zhu +5 more
wiley +1 more source
Bridging tumor growth dynamics and survival in preclinical oncology drug development - a Tumor Growth Inhibition and Time-to-Event (TGI-TTE) modeling framework. [PDF]
Niloy KK +8 more
europepmc +1 more source
Lai et al. find that m6A reader YTHDC1 is specifically overexpressed in triple‐negative breast cancer (TNBC) and orchestrates glucose and glutamine metabolism in an m6A‐dependent manner to confer robust adaptability to lethal metabolic stress. Leveraging YTHDC1 knockdown‐induced metabolic vulnerability, an ATF4 mRNA‐targeted nanotherapy is developed to
Zheng‐Hao Lai +12 more
wiley +1 more source

