Immunotherapy in Pediatric Oncology: An Overview of Therapy Types and Nursing Implications.

BACKGROUND: By using the body's own protective system to fight cancer, immunotherapy is not only effective but also is associated with fewer side effects than chemotherapy. OBJECTIVES: This article provides an overview of four types of immunotherapy (monoclonal antibodies, chimeric antigen receptors, immune checkpoint inhibitors, and cancer vaccines) and discusses the critical role assumed by nurses in the care of patients receiving immunotherapy. METHODS: A review of the literature was undertaken to identify, describe, and compare the types of immunotherapy used and studied for use in pediatric oncology. FINDINGS: Nurses caring for pediatric patients with cancer may have little experience with immunotherapy. However, they should become knowledgeable about it, particularly as it becomes further integrated into pediatric cancer treatments.

Improving the quality of care for the hospitalized tobacco user--one institution's transformational journey.

Hospitalization represents an ideal time to address tobacco cessation. For a variety of reasons, current users do not always receive appropriate support or treatment during the hospitalization. An improvement team was created to improve the care for the hospitalized tobacco user. The team's aim was to develop a standardized process to increase the assessment, documentation, and delivery of cessation counseling, and increase community referrals upon discharge. After implementation of the project, percentages of hospitalized patients who had their tobacco use status documented in the electronic medical record increased to 80-90%. The percentage of patients admitted with heart failure or pneumonia had their rates of tobacco cessation counseling improved to 82-96%. The care of the hospitalized tobacco user can be improved and sustained by utilizing community resources and creating a team of motivated care providers. This improvement work stimulated the creation of a smoke-free institution and other preventive health measures throughout the institution.

Systemic challenge with the TLR3 agonist poly I:C induces amplified IFNalpha/beta and IL-1beta responses in the diseased brain and exacerbates chronic neurodegeneration.

The role of inflammation in the progression of neurodegenerative disease remains unclear. We have shown that systemic bacterial insults accelerate disease progression in animals and in patients with Alzheimer's disease. Disease exacerbation is associated with exaggerated CNS inflammatory responses to systemic inflammation mediated by microglia that become 'primed' by the underlying neurodegeneration. The impact of systemic viral insults on existing neurodegenerative disease has not been investigated. Polyinosinic:polycytidylic acid (poly I:C) is a toll-like receptor-3 (TLR3) agonist and induces type I interferons, thus mimicking inflammatory responses to systemic viral infection. In the current study we hypothesized that systemic challenge with poly I:C, during chronic neurodegenerative disease, would amplify CNS inflammation and exacerbate disease. Using the ME7 model of prion disease and systemic challenge with poly I:C (12 mg/kg i.p.) we have shown an amplified expression of IFN-alpha and beta and of the pro-inflammatory genes IL-1beta and IL-6. Similarly amplified expression of specific IFN-dependent genes confirmed that type I IFNs were secreted and active in the brain and this appeared to have anti-inflammatory consequences. However, prion-diseased animals were susceptible to heightened acute sickness behaviour and acute neurological impairments in response to poly I:C and this treatment also accelerated disease progression in diseased animals without effect in normal animals. Increased apoptosis coupled with double-stranded RNA-dependent protein kinase (PKR) and Fas transcription suggested activation of interferon-dependent, pro-apoptotic pathways in the brain of ME7+poly I:C animals. That systemic poly I:C accelerates neurodegeneration has implications for the control of systemic viral infection during chronic neurodegeneration and indicates that type I interferon responses in the brain merit further study.