A study investigating the knowledge and responses of Italian medical students to the COVID-19 pandemic.

Italy was initially one of the worse affected countries by the novel coronavirus (COVID-19). Medical students frequenting hospitals are more susceptible to be infected by the virus but also able to see the effects of the pandemic from the frontline. The aim of this study was to assess the COVID-19 related knowledge, behavioral changes, and perceptions of Italian medical students within the first 90 days after the onset of the outbreak in Italy.

Epigenetic reprogramming and post-transcriptional regulation during the epithelial-mesenchymal transition.

The epithelial-mesenchymal transition (EMT) is a developmental process that is important for organ development, metastasis, cancer stemness, and organ fibrosis. The EMT process is regulated by different signaling pathways as well as by various epigenetic and post-transcriptional mechanisms. Here, we review recent progress describing the role of different chromatin modifiers in various signaling events leading to EMT, including hypoxia, transforming growth factor (TGF)-β, Notch, and Wnt.

Linkage between Twist1 and Bmi1: molecular mechanism of cancer metastasis/stemness and clinical implications.

Cancer metastasis is the major cause of cancer-related death despite significant improvements in multimodal cancer therapy. Epithelial-mesenchymal transition (EMT), a major mechanism of cancer metastasis, is a process that generates cells with stem cell-like properties (cancer stemness). Cancer stemness is a concept that describes a minor population of cells (cancer stem cells) residing within a tumour that are able to self-renew and are resistant to conventional therapy.

Induction of HSPA4 and HSPA14 by NBS1 overexpression contributes to NBS1-induced in vitro metastatic and transformation activity.

Background: Nijmegen breakage syndrome (NBS) is a chromosomal-instability syndrome associated with cancer predisposition, radiosensitivity, microcephaly, and growth retardation. The NBS gene product, NBS1 (p95) or nibrin, is a part of the MRN complex, a central player associated with double-strand break (DSB) repair. We previously demonstrated that NBS1 overexpression contributes to transformation through the activation of PI 3-kinase/Akt.