Chapter 36: Targeted Cancer Therapy Medications

Unlike traditional cytotoxic chemotherapy, these agents are primarily cytostatic and work through mechanisms such as signal transduction inhibition, blockage of cell membrane receptors, and the induction of apoptosis. The text classifies these therapies into several major categories, beginning with Angiogenesis Inhibitors (or VEGF inhibitors) like bevacizumab and ziv-aflibercept, which suppress the formation of new blood vessels essential for tumor survival. A significant portion of the chapter is dedicated to Epidermal Growth Factor Receptor (EGFR) inhibitors, distinguishing between small-molecule tyrosine kinase inhibitors (TKIs) such as erlotinib, gefitinib, and osimertinib used for non-small cell lung cancer (NSCLC), and monoclonal antibodies like cetuximab and panitumumab that bind extracellularly. The discussion extends to Tyrosine Kinase Inhibitors (TKIs) like imatinib mesylate, which targets the BCR-ABL fusion protein in Philadelphia chromosome-positive chronic myelogenous leukemia (CML), and Multikinase Inhibitors (MKIs) such as sorafenib and sunitinib that block multiple enzyme pathways simultaneously. Furthermore, the chapter details mTOR kinase inhibitors like temsirolimus and proteasome inhibitors such as bortezomib and carfilzomib, explaining their roles in disrupting cell cycle regulation and protein degradation in conditions like multiple myeloma. The section on Monoclonal Antibodies (mAbs) elaborates on agents such as rituximab, alemtuzumab, and trastuzumab (targeting ERBB2/HER2), describing how they recruit the immune system via antibody-dependent cell-mediated cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC). Finally, the summary underscores critical nursing considerations, including the management of severe side effects like QT prolongation, infusion reactions, and dermatologic toxicities, as well as the importance of monitoring for drug-food interactions involving CYP3A4 enzymes and grapefruit juice.