Liver masses account for 5 to 6% of pediatric cancer, which includes hepatoblastoma (HBL) along with rare cases of hepatocellular carcinoma (HCC). The most dangerous form of pediatric liver cancer is aggressive HBL, which can be characterized by chemo-resistance and multiple nodules or metastases at diagnosis, all correlating with worse clinical prognosis. Despite intensive studies and a significant improvement in overall outcomes, very little is known about the key molecular pathways which determine the aggressiveness of pediatric liver cancer.

Hypoxic-ischemic encephalopathy (HIE) continues to be an important cause of long-term neurologic disability among newborn infants. The estimated incidence ranges from 2-3/1000 live births in developed countries, to as high as 10-20/1000 in developing countries [1]. Affected infants who survive are at a 25% risk for cerebral palsy, epilepsy, and cognitive deficits and may require lifelong medical care.

The significant metastatic potential of uveal melanoma (UVM) lends to high mortality. Even with successful local tumor treatment, many patients will develop metastatic disease. The present study aims to elucidate the relationship between tumor-infiltrating immune cell (TIIC) diversity and survival to identify potential therapeutic targets and improve UVM prognosis.

Immune checkpoint inhibitors (ICI) have emerged as promising treatment options for many cancers. ICIs exert their therapeutic effects by targeting immune inhibitory molecules on T-cells in adaptive immunity, such as cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), programmed cell death 1 (PD-1) and its ligand programmed cell death ligand 1 (PD-L1). ICIs, however, can result in a wide variety of immune-related adverse events (iRAE), including myocarditis, a rare and potentially deadly complication that necessitates early diagnosis.

Ischemic stroke is the main cause of disability worldwide affecting around 6 million deaths per year. A cascade of events following the ischemic insult induce energy failure, excitotoxicity and release of inflammatory mediators that provoke cell death and brain injury. In this process, astrocytes undergo a change on gene expression that leads to reactive astrocytes.