The effect of selinexor on prostaglandin synthesis in virus-positive Merkel cell carcinoma cell lines.

Merkel cell carcinoma (MCC) is an aggressive neuroendocrine skin cancer with high rates of metastasis and mortality. In vitro studies suggest that selinexor (KPT-330), an inhibitor of exportin 1, may be a targeted therapeutic option for MCC. This selective inhibitor prevents the transport of oncogenic mRNA out of the nucleus.

Buruli ulcer - A neglected tropical disease in the Barwon region of Victoria, Australia: An emerging public health threat with local and national ramifications.

Mycobacterium ulcerans (MU) is known to be endemic in heavily touristed coastal regions of Victoria and is the cause of Buruli ulcer (BU) disease. The incidence, severity and geographic spread of MU infection/BU disease is increasing, including metropolitan Victorian suburbs. While the specifics of disease transmission and effective prevention strategies remain uncertain, severe complications can be mitigated by health systems that provide vigilant population surveillance to underpin early recognition, early specialist involvement and definitive treatment for the individual.

Effect of selinexor on lipogenesis in virus-positive Merkel cell carcinoma cell lines.

Background: Merkel cell carcinoma (MCC) is a highly aggressive neuroendocrine cutaneous carcinoma aetiologically linked to the Merkel cell polyomavirus (MCPyV). Immune checkpoint inhibitors are currently the first-line therapy for metastatic MCC; however, the treatment is effective in only about half of patients, highlighting the need for alternative therapies. Selinexor (KPT-330) is a selective inhibitor of nuclear exportin 1 (XPO1) and has been shown to inhibit MCC cell growth in vitro, but the pathogenesis has not been established.