The rising cost of pharmaceuticals and, in particular, cancer drugs has made headline news in recent years. Several factors contribute to increasing costs and the burden this places on the health care system and patients. Some of these factors include costly cancer pharmaceutical research and development, longer clinical trials required to achieve drug approval, manufacturing costs for complex compounds, and the economic principles surrounding oncology drug pricing. Strategies to control costs have been proposed, and some have already been implemented to mitigate cancer drug costs such as the use of clinical treatment pathways and tools to facilitate cost discussions with patients. In this article, we briefly review some of the potential factors contributing to increasing cancer pharmaceutical costs and interventions to mitigate costs, and touch on the role of health care providers in addressing this important issue.

Chemotherapy-induced nausea and vomiting (CINV) is one of the most common symptoms feared by patients, but may be prevented or lessened with appropriate medications. Several antiemetic options exist to manage CINV. Corticosteroids, serotonin receptor antagonists, and neurokinin receptor antagonists are the classes most commonly used in the prevention of CINV. There are many alternative drug classes utilized for the prevention and management of CINV such as antihistamines, benzodiazepines, anticonvulsants, cannabinoids, and dopamine receptor antagonists. Medications belonging to these classes generally have lower efficacy and are associated with more adverse effects. They are also not as well studied compared to the aforementioned agents. This review will focus on dronabinol, a member of the cannabinoid class, and its role in CINV. Cannabis sativa L. (also known as marijuana) contains naturally occurring delta-9-tetrahydrocannibinol (delta-9-THC). The synthetic version of delta-9-THC is the active ingredient in dronabinol that makes dronabinol an orally active cannabinoid. Evidence for clinical efficacy of dronabinol will be analyzed in this review as monotherapy, in combination with ondansetron, and in combination with prochlorperazine.

Blinatumomab is approved as an option for Ph chromosome-negative relapsed or refractory B-cell precursor ALL and is a needed addition to the limited treatment options for this difficult-to-treat patient population. Two Phase II clinical trials resulted in impressive results when using blinatumomab as a single agent, resulting in the drug's approval.

Purpose This article explores the efficacy, toxicity, place in therapy, and considerations for use of recently approved immune checkpoint inhibitors (ICIs) in the treatment of non–small cell lung cancer (NSCLC). Summary Lung cancer is the leading cause of cancer mortality in the United States and is responsible for more cancer-related deaths than breast, prostate, and colorectal cancer combined. The landscape for lung cancer treatment is evolving with the approval of new and exciting novel therapies. Within the last decade numerous ICIs have been approved for use in the management of the most common subtype of lung cancer, NSCLC. The ICI agents currently approved by the Food and Drug Administration (FDA) for use in NSCLC include ipilimumab, pembrolizumab, nivolumab, durvalumab, and atezolizumab. These agents are approved for specific indications; therefore, they are not interchangeable. This review focuses on the landmark trials that led to each FDA-approved indication, as well as common toxicities seen with use of these agents. It also discusses the use of ICIs in special populations and unique considerations prior to initiation of treatment with these novel therapies in a patient with NSCLC. Conclusion ICIs can provide a breakthrough treatment option for the management of NSCLC and are rapidly being adopted into clinical practice. It is important to be familiar with appropriate selection of an ICI therapy option for each patient based on approved indication, unique considerations, and anticipated toxicities.

In the United States, 1 in 8 women will be diagnosed with invasive breast cancer in her lifetime. Breast cancer death rates are higher for women in the United States than any other cancer, followed by lung cancer ( National Cancer Institute, 2019 ). More than 70% of breast cancers are hormone receptor (HR)-positive and human epidermal growth factor receptor 2 (HER2)-negative, and of those patients, 40% have driver mutations in the gene phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha ( PIK3CA ) resulting in damaged phosphatidylinositol 3-kinase (PI3K) and uncontrolled cell growth (Mollon et al., 2018; Setiawan et al., 2009). These patients are initially treated with endocrine therapy, but resistance remains an issue. Inhibition of PI3K is a promising new approach to overcome resistance to endocrine therapy in breast cancer. Previous trials of PI3K inhibitors (pictilisib [GDC-0941], buparlisib [BMK120], and taselisib [GDC-0032]) in breast cancer have shown little efficacy secondary to toxicities due to their nonselectivity to PI3K subunits. Alpelisib is a selective inhibitor of PI3K for patients with HR-positive, HER2-negative, PIK3CA -mutated breast cancer who have progressed on endocrine therapy. This drug review will discuss the pharmacology of alpelisib, current data supporting its place in therapy, management of adverse events, and the clinical implications for advanced practitioners treating patients with HR-positive, HER2-negative breast cancer.