Targeted Therapy
Key Points
- Targeted therapies block specific molecular targets (receptors, enzymes, signaling proteins) that drive cancer growth.
- They differ from chemotherapy by selectivity — attacking tumor-specific pathways with less systemic toxicity.
- Common classes: tyrosine kinase inhibitors (TKIs), monoclonal antibodies (mAbs), PARP inhibitors, CDK4/6 inhibitors.
- Resistance development is a major challenge, often requiring biomarker-guided therapy selection.
Mechanism
Targeted agents interrupt cancer-specific signaling cascades (e.g., EGFR, HER2, BCR-ABL, VEGF pathways) that normal cells do not heavily depend on. Biomarker testing (tumor molecular profiling) guides agent selection.
Nursing Assessment
NCLEX Focus
Side effects are target-specific. Know the class and its associated toxicity profile.
- Monitor for class-specific toxicities: skin rash (EGFR inhibitors), hepatotoxicity (TKIs), cardiotoxicity (HER2 agents).
- Assess for drug interactions, particularly cytochrome P450 interactions with TKIs.
- Evaluate patient adherence to oral TKI regimens and barriers to consistent dosing.
Nursing Interventions
- Educate on expected vs. concerning side effects and when to notify provider.
- Support dermatologic management for EGFR-inhibitor rash (moisturizers, sun protection).
- Reinforce oral medication adherence strategies and missed-dose protocols.
- Monitor laboratory parameters specific to agent class (LFTs, CBC, cardiac function).
Related Concepts
- immunotherapy - Immunotherapy and targeted therapy are frequently combined in cancer regimens.
- antineoplastic-agents - Broader oncology pharmacology context.
Self-Check
- How does targeted therapy differ from traditional chemotherapy in mechanism?
- Which toxicity profiles are associated with EGFR-inhibitor and HER2-targeted agents?