Chapter 52: Antineoplastic Drugs Part 1 – Cancer & Cell-Specific Agents

Malignancies are classified based on their tissue of origin, including carcinomas (epithelial), sarcomas (connective tissue), lymphomas (lymphoid tissue), and leukemias (hematological/circulating tumors). The text explores the etiology of cancer, noting factors such as genetics, environmental and occupational carcinogens, radiation exposure, and oncogenic viruses like HPV and Epstein–Barr virus. Normal and malignant cells progress through five growth phases—G0, G1, S, G2, and M—which dictate the sensitivity of cells to antineoplastic therapy. Chemotherapy drugs are divided into cell cycle–specific (CCS) agents, which target rapidly dividing cells during a particular phase, and cell cycle–nonspecific agents. CCS drug classes discussed include antimetabolites (such as methotrexate and fluorouracil), which interfere with nucleic acid synthesis primarily in the S phase; mitotic inhibitors (vincristine and paclitaxel), which disrupt spindle formation during the M and G2 phases; topoisomerase I inhibitors (irinotecan and topotecan), which cause DNA strand breaks in the S phase; and antineoplastic enzymes (asparaginase and pegaspargase), which uniquely degrade asparagine necessary for leukemic cell survival. Due to the inability of these cytotoxic drugs to differentiate between cancerous cells and highly proliferating normal cells (e.g., bone marrow, GI tract, hair follicles), major adverse effects include myelosuppression (leading to leukopenia, anemia, and thrombocytopenia), alopecia, and GI toxicities like stomatitis, nausea, vomiting (emetic potential), and diarrhea. Nursing management requires meticulous assessment for these toxicities, especially monitoring the nadir (lowest blood count), preventing life-threatening errors (such as intrathecal vincristine administration), and managing specific drug toxicities like irinotecan-induced cholinergic diarrhea or asparaginase-related pancreatitis.