ABSTRACT Introduction: Salivary gland tumors (SGTs) may represent a considerable diagnostic challenge, primarily because of the complexity of the classification and the rarity of several entities. Since proliferative activity is a reliable method to assess tumor biology. There has been continuous research to find such biological markers. Ki-67 is a widely accepted proliferation marker, with its expression tightly associated with the cell cycle. It is implicated in many of human cancers as a prognostic factor. MCM-3, member of minichromosome maintenance proteins family, is upregulated in proliferating cells. MCM-3 overexpression in almost all human cancers implicates that it might facilitate the tumorigenesis by playing a role in the malignant transformation of cells. Objectives: to evaluate the MCM-3 protein expression in benign and malignant salivary gland tumors and compare the obtained results with the expression of Ki-67 proliferation antigen. Materials and methods: Immunohistochemical analysis of 20 cases of SGTs with 2 sections from each specimen (20 sections for antiKi67antibody and 20 sections for antiMCM3antibody) and 5 control cases. Immunohistochemical staining was performed using a Labeled StreptAvidin Biotin method (LSAB). Results: Normal salivary gland tissue showed negative immunoreactivity for both Ki-67 and MCM-3 in epithelial and myoepithelial cells. All the examined cases showed positive expression for both proliferative markers in benign and malignant SGTs, with different intensities. Conclusions: The proliferative markers Ki-67 and MCM-3 proteins are overexpressed in malignant salivary gland tumors, than benign ones. Both Ki-67 and MCM-3 may be reliably applied as diagnostic markers to distinguish benign from malignant salivary gland tumors. Keywords: Salivary gland tumor, Immunohistochemistry, MCM-3, KI-67.

Circulating microvesicles (cMVs) are the extracellular MVs released from the cells in the blood and on the vascular wall. Our previous study demonstrates that cMVs of diabetic mouse are detrimental to endothelial progenitor cells (EPCs), which are known to be very important for maintaining normal endothelial function and structure. In this study, we compared the levels of circulating EPCs and EPC-derived MVs (EPC-MVs) in diabetic and healthy subjects. Also, the migration ability, apoptosis rate and reactive oxygen species (ROS) production of EPCs cultured from diabetic and healthy subjects were determined. More importantly, we evaluated whether cMVs from healthy subjects (ch-MVs) improves the function of EPCs from diabetic patients (d-EPCs), and whether cMVs from diabetic patients (cd-MVs) impairs the function of EPCs from healthy subjects (h-EPCs). The d-EPCs or h-EPCs were incubated with ch-MVs or cd-MVs for 24 hours. The migration ability of EPCs was analyzed by an assay kit. The apoptotic rate and ROS production were analyzed by labeling with propidium iodide (PI) and dihydroethidium (DHE) respectively, followed with flow cytometeric analysis. Our data showed that (1) there was a decrease in EPCs iv and an elevation in EPC-MVs in diabetic patients when compared to healthy subjects; (2) The migration ability of d-EPCs were decreased, and the apoptosis rate and ROS production were increased in d-EPCs; (3) ch-MVs improve the function of d-EPC through improving its migration ability and decreasing the apoptosis and ROS production; (4) cd-MVs increase h-EPC apoptosis, and increase ROS production. We conclude that cMVs modulate EPC function and this role of cMVs is reversed in diabetes with the mechanism linked to ROS production.