Evaluation of autophagy related ATG4B gene, protein and miR-655-3p expression levels in endometrial cancer and hyperplasia.

Objective: The pathogenesis of endometrial cancer (EC) and hyperplasia is complex and poorly understood. Autophagy has emerged as a crucial aspect of this process.

Methods: This study examines the role of autophagy in the pathogenesis of EC and hyperplasia by investigating the expression of the autophagy-related 4B cysteine peptidase (ATG4B) gene, protein, and miR-665-3p levels in patients compared to a control group.

Differential gene expression patterns in ST-elevation Myocardial Infarction and Non-ST-elevation Myocardial Infarction.

The ST-elevation Myocardial Infarction (STEMI) and Non-ST-elevation Myocardial Infarction (NSTEMI) might occur because of coronary artery stenosis. The gene biomarkers apply to the clinical diagnosis and therapeutic decisions in Myocardial Infarction. The aim of this study was to introduce, enrich and estimate timely the blood gene profiles based on the high-throughput data for the molecular distinction of STEMI and NSTEMI.

The expression changes of PD-L1 and immune response mediators are related to the severity of primary bone tumors.

The expression pattern, diagnostic value, and association of PD-L1, IFN-γ and TGF-β with bone tumor type, severity, and relapse are determined in this study. 300 human samples from patients with osteosarcoma, Ewing sarcoma, and GCT were enrolled. The PD-L1 gene and protein expression were assessed by qRT-PCR and immunohistochemistry, respectively.

Cellular crosstalk in atherosclerotic plaque microenvironment.

Atherosclerosis is an underlying pathology of many vascular diseases as a result of cellular, structural and molecular dysfunctions within the sub-endothelial space. This review deals with the events involved in the formation, growth and remodeling of plaque, including the cell recruitment, cell polarization, and cell fat droplets. It also describes cross talking between endothelial cells, macrophages, and vascular smooth muscle cells, as well as the cellular pathways involved in plaque development in the plaque microenvironment.