Protein arginine methyltransferases (PRMTs) are a class of enzymes that mediate critical post-translational modifications through arginine methylation as epigenetic regulators. PRMTs have been shown to have a vast array of regulatory effects including in gene expression, signal transduction, and cellular proliferation. Dysregulation of PRMT activity has been seen in the progression of various cancers, including breast, lung, and colorectal cancer. Moreover, PRMT overexpression has been shown to correlate with poor patient prognosis. This review aims to explore the roles of the individual PRMTs in cancer and aims to highlight the latest and newest developments of PRMT inhibitors as emerging therapeutic strategies. Numerous preclinical and clinical studies have identified several novel compounds that effectively target PRMT activity and have shown significant therapeutic results. As such, this review aims to not only highlight the current research findings, but to also emphasize the significant need for future research on PRMTs as novel therapeutic targets in cancer.

Vitamin B12 (cyanocobalamin) deficiency can lead to ineffective erythropoiesis, intramedullary hemolysis, and, in severe cases, neurologic deficits. Some of those findings are also features of thrombotic microangiopathies, specifically thrombotic thrombocytopenic purpura (TTP), and the distinction between both entities could sometimes be challenging. While the treatment of the former consists of enteral or parenteral repletion, the treatment of TTP is more complex and time-sensitive. For that reason, refining diagnostic strategies is crucial to avoid misdiagnosis and unnecessary interventions. Here is an example of a potential life-threatening hemolysis caused by vitamin B12 deficiency with acute onset neurologic symptoms, which resolved with B12 repletion.

Introduction: Head and neck squamous cell carcinomas (HNSCCs) are among the most common cancers worldwide and continue to carry substantial morbidity and mortality despite advances in surgery, radiation therapy (RT), and systemic therapy. Treatment varies according to disease stage, clinical setting, and prior therapy. The immunologically active tumor microenvironment of HNSCC and expression of immune-regulatory pathways have made immunotherapy an important area of therapeutic development. Methods: This is a narrative review of the established and emerging immunotherapeutic strategies for HNSCC, their clinical applications, mechanisms of resistance, and future directions. We used relevant search terms in PubMed to examine the available literature. Discussion and Conclusions: We discuss several immunotherapeutic agents, including PD-1, PD-L1 and CTLA-4 inhibitors, as well as emerging immune checkpoint targets such as LAG-3, TIGIT, TIM-3 and VISTA. We also consider the importance of HPV status in prognosis and treatment response. The role of immunotherapy is considered across disease stages and treatment settings, with particular emphasis on recurrent or metastatic HNSCC and locally advanced HNSCC in the perioperative setting, for which PD-1 inhibitors have demonstrated the clearest clinical benefit and have become an important component of standard therapy. We also review the expanding role of neoadjuvant and adjuvant immunotherapy, as well as combinations with RT, for which efficacy remains under investigation or has been inconsistent across clinical trials. In addition, we examine mechanisms of primary and acquired resistance related to tumor biology and molecular mutations. Finally, we highlight emerging therapeutic approaches, including chimeric antigen receptor T-cell therapy, therapeutic cancer vaccines, and combinations of immunotherapy with proton beam therapy. Together, these developments illustrate the rapidly expanding role of immunotherapy across HNSCC treatment and identify areas in which further investigation may expand therapeutic options and improve outcomes.