SARS-CoV-2 is a worldwide pandemic, that has led to the morbidity and mortality of millions of people. This virus rapidly proliferates and destroys lung epithelial cells directly, which is worsened by a subsequent cytokine storm. This cytokine storm diffusely damages the alveolar barriers and leads to fibrin and fluid exudation, hyaline membrane formation, and infiltration of inflammatory cells into the lung causing acute respiratory distress syndrome (ARDS). To date, there exists no medication to treat SARS-CoV-2 infection and novel new therapeutics are still being explored to prevent or limit the damage to the lung. Sphingosine 1-phosphate (S1P) is an effective bioactive lipid mediator and its related signaling pathways are vital for endothelial cell integrity. Stabilizing the pulmonary endothelial barrier and decreasing the inflammatory infiltrate by S1P analogs such as Fingolimod (FTY720-P) would be a new therapeutic approach for the hindrance of pulmonary exudation and subsequent ARDS.

Lung cancer is the leading cause of cancer deaths worldwide, accounting for an estimated 1.8 million deaths. Lung cancer is also the most common primary cancer leading to soft tissue (ST) metastasis. Renal disease may occur as a direct or indirect consequence of the cancer itself (e.g., postrenal obstruction, compression, or infiltration), its treatment (e.g., radiotherapy or chemotherapy), or its related complications (e.g., opportunistic infection). Existing evidence shows that the most frequent primary solid tumor responsible for renal metastasis is pulmonary carcinoma, followed by gastric, breast, soft tissue, and thyroid carcinomas. Chronic kidney disease is a potential risk factor in the survival of patients with lung cancer. In this review, we will discuss causes of kidney injury in relation to lung cancer, potential mechanisms of kidney injury, and treatment options.

Pancreatic cancer is the fourth or fifth leading cause of cancer death in the Western world. Human pancreatic cancers frequently overexpress human epidermal growth factor receptors including Met, also known as hepatocyte growth factor receptor. Over stimulation of c-Met via its natural ligand, hepatocyte growth factor (HGF), has been associated with cell scattering, angiogenesis, enhanced cell motility, invasion and eventually metastasis. The overexpression of c-Met was confirmed by western blot and RT-PCR in a panel of human pancreatic cancer cell lines. The results from this expression analysis suggested there is an over activation of the c-Met signaling pathway, which may contribute to pancreatic cancer growth and metastasis. This hypothesis was tested using a cell-based invasion assay through which the invasive effects of c-Met signaling in pancreatic tumorigenesis was evaluated. Preliminary results indicate a two-fold increase of invasion in those CF-Pac1 cells treated with HGF. In addition to providing information regarding the role that c-Met and HGF play in tumorigenesis, this work further validates c-Met as a therapeutic target for the treatment of pancreatic cancer and other tumor types.