Background: Colorectal cancer (CRC) is one of the most prevalent digestive cancers, ranking the 2nd cause of cancer-related fatality worldwide. The worldwide burden of CRC is predicted to rise by 60% by 2030. Environmental factors drive, first, inflammation and hence, cancer incidence increase. Main: The Notch-signaling system is an evolutionarily conserved cascade, has role in the biological normal developmental processes as well as malignancies. Long non-coding RNAs (LncRNAs) have become major contributors in the advancement of cancer by serving as signal pathways regulators. They can control gene expression through post-translational changes, interactions with micro-RNAs or down-stream effector proteins. Recent emerging evidence has emphasized the role of lncRNAs in controlling Notch-signaling activity, regulating development of several cancers including CRC. Conclusion: Notch-associated lncRNAs might be useful prognostic biomarkers or promising potential therapeutic targets for CRC treatment. Therefore, here-in we will focus on the role of “Notch-associated lncRNAs in CRC” highlighting “the impact of Notch-associated lncRNAs as player for cancer induction and/or progression.” Graphical
Objective. The proapoptotic protein, granzyme B (GZB), was identified as a contributor to the atherosclerotic plaque instability and recently as inflammatory activator. We studied the release kinetics of GZB and other markers of inflammation such as high sensitivity C reactive protein (hsCRP), interleukin 18 (IL-18), and fractalkine (FKN) in the early phase after acute cardiac events in different ACS subgroups. Methods. Thirty-six nondiabetic patients with ACS were compared to 12 control subjects. According to ACS diagnosis, the patients were classified into 22 patients with ST elevation myocardial infarction (STEMI) and 14 patients with non-ST elevation myocardial infarction or unstable angina (NSTEMI/UA). Blood samples were taken on day 1 (day of onset) and day 3 to measure hsCRP, IL-18, FKN, and GZB by ELISA. Results. Patients with ACS showed significantly higher GZB, IL-18, and FKN levels than the controls. STEMI group showed significantly higher GZB levels than NSTEMI/UA group. On day 3, FKN levels displayed a significant decrease, while GZB levels were significantly increased. IL-18 levels were more or less constant. GZB levels were positively correlated with IL-18 (, ) and FKN (, ). Conclusions. Unlike IL-18 and FKN, plasma GZB may be a marker of ACS disease severity.