Oncology · Medicine Class
Various — DNA damage, cell cycle disruption, targeted receptor inhibition, immunologic activation
Antineoplastic agents encompass the broadest and most mechanistically diverse class in pharmacology. Classical cytotoxic chemotherapy kills rapidly dividing cells through DNA alkylation, topoisomerase inhibition, antimetabolite incorporation, or mitotic spindle disruption — mechanisms that are non-selective and affect both malignant and rapidly dividing normal cells (bone marrow, GI mucosa, hair follicles). Targeted therapies exploit specific molecular vulnerabilities in cancer cells: tyrosine kinase inhibitors (TKIs) block activated kinases that drive tumor growth; monoclonal antibodies target surface antigens or growth factor receptors; PARP inhibitors exploit DNA repair defects in BRCA-mutated cancers. Immunotherapy (checkpoint inhibitors — PD-1, PD-L1, CTLA-4 inhibitors) removes the immunologic brakes that tumors exploit to evade T-cell killing, unleashing the immune system against cancer.
Pembrolizumab (Keytruda)
Anti-PD-1 checkpoint inhibitor. Approved for 30+ cancer types. First tumor-agnostic approval (MSI-H). Immune-related adverse events (irAEs) require vigilance.
Nivolumab (Opdivo)
Anti-PD-1. Used in melanoma, NSCLC, renal cell carcinoma, others. Often combined with ipilimumab (CTLA-4 inhibitor) for synergistic immune activation.
Trastuzumab (Herceptin)
Anti-HER2 mAb. Transformed HER2+ breast and gastric cancer outcomes. Black box warning: cardiotoxicity (monitor LVEF) and embryo-fetal toxicity.
Rituximab (Rituxan)
Anti-CD20 mAb. First-line in follicular lymphoma, DLBCL, CLL. Also used in autoimmune diseases. Infusion reactions; reactivation of HBV.
Imatinib (Gleevec)
BCR-ABL TKI. Revolutionary for CML (Ph+ CML) — transformed from fatal to manageable disease. Also used in GIST (c-KIT, PDGFR mutations).
Docetaxel (Taxotere)
Taxane. Stabilizes microtubules, preventing mitotic spindle depolymerization. Used in breast, prostate, NSCLC, gastric. Neutropenia, fluid retention, neuropathy.
Carboplatin
Platinum compound. DNA cross-linking. Used in ovarian, NSCLC, other solid tumors. Thrombocytopenia dose-limiting. Less nephrotoxic than cisplatin.
Capecitabine (Xeloda)
Oral prodrug of 5-FU. Used in breast, colorectal cancer. Hand-foot syndrome characteristic side effect.
Live vaccines — contraindicated during immunosuppressive chemotherapy
Strong CYP3A4 inhibitors/inducers — affect TKI plasma levels (most TKIs are CYP3A4 substrates)
Warfarin — INR markedly altered by many chemotherapy regimens; switch to LMWH preferred
Nephrotoxic drugs (NSAIDs, aminoglycosides) — additive nephrotoxicity with cisplatin
QTc-prolonging agents — many antineoplastics prolong QTc; avoid combinations
Traditional chemotherapy (cytotoxic agents) kills rapidly dividing cells non-selectively — including cancer cells and normal rapidly proliferating cells like bone marrow and GI mucosa. Targeted therapies are designed to inhibit specific molecular targets (mutated kinases, surface receptors, oncoproteins) that are expressed or activated in cancer cells but not essential in most normal cells. Targeted therapies generally have more favorable side effect profiles, but they only work if the tumor expresses the targeted molecule — requiring biomarker testing before use.
Checkpoint inhibitors block proteins (PD-1, PD-L1, CTLA-4) that cancer cells exploit to hide from immune attack. By blocking these 'brakes' on the immune system, checkpoint inhibitors allow T cells to recognize and kill cancer cells. They produce durable responses in some patients — including long-term remissions in metastatic melanoma and lung cancer where previously survival was measured in months. Their unique side effects are immune-related adverse events (irAEs), where the activated immune system attacks normal organs, requiring careful monitoring and sometimes immunosuppression with corticosteroids.