Quick revision ↓ Medical Dictionary
Deep Learning — Module 19
Read this section in sequence. It moves from drug targets to therapeutic effects, adverse reactions and safe use.
Cancer treatment principles
Cancer drugs exploit vulnerabilities in proliferating cells or specific tumor pathways. Combination regimens aim to improve tumor control while managing overlapping toxicity and resistance. Cytotoxic drugs often injure marrow, mucosa and hair follicles because these tissues also proliferate. Treatment intent may be curative, adjuvant or palliative, and outcome assessment must match that intent. Tumor type, stage, biomarkers, organ function and patient goals determine therapy; a class list is not a cancer treatment protocol.
Cytotoxic mechanisms and rescue
Alkylating agents damage DNA, antimetabolites disrupt nucleotide pathways, anthracyclines affect topoisomerase and other cellular processes, and microtubule drugs disrupt mitosis. Cyclophosphamide metabolites can injure the bladder; mesna protects against urotoxic metabolites in indicated regimens. Doxorubicin can cause cardiotoxicity; cisplatin is associated with renal and auditory toxicity. Methotrexate inhibits dihydrofolate reductase and high-dose regimens may require folinic-acid rescue and concentration-guided monitoring. Rescue strategies are drug and regimen specific.
Targeted, endocrine and radiation treatment
Imatinib inhibits selected tyrosine kinases and is effective in biomarker-defined diseases. Trastuzumab targets HER2 in appropriate tumors and requires attention to cardiac function. Endocrine therapies exploit hormone dependence, while checkpoint inhibitors release inhibitory immune signals and can cause immune-mediated organ inflammation. Radiation damages cellular DNA locally or through selected systemic radionuclide approaches; fractionation and tissue sensitivity shape effects. Targeted does not mean harmless, and treatment choice follows molecular evidence rather than the organ name alone.
Immunosuppression
Calcineurin inhibitors such as ciclosporin and tacrolimus reduce T-cell activation and can cause nephrotoxicity and important interactions. Mycophenolate inhibits lymphocyte purine synthesis; glucocorticoids suppress multiple inflammatory pathways. Biologics such as TNF inhibitors target specific mediators but increase infection risks and require appropriate screening. Balancing rejection or autoimmune injury against infection and malignancy risk requires longitudinal monitoring. Similar clinical purposes do not make these mechanisms or adverse effects identical.
Vaccines, passive immunity and immunostimulation
Vaccination generates active immunity and memory; immunoglobulin or antiserum provides passive, usually temporary protection. Live vaccines need special assessment in immunocompromised patients and pregnancy. Colony-stimulating factors can support selected blood-cell lineages, while probiotics have strain- and indication-specific evidence and are not universal immune boosters. Vaccine schedules, contraindications and post-exposure regimens follow current local guidance. Anaphylaxis preparedness, cold-chain integrity and accurate documentation are part of safe administration.
High-Yield Revision
- Targeted therapy still has important on-target and off-target toxicity.
- Active immunity develops memory; passive protection is transferred and temporary.
- Immunosuppression requires infection-risk assessment and monitoring.
Common Exam & Concept Pitfalls
- Do not extrapolate one tumor biomarker to every cancer.
- Folinic-acid rescue is not interchangeable with mesna protection.
Sources & Further Reading
Curriculum scope checked 23 September 2026. These original study notes summarize established principles; current institutional guidance and product information govern clinical use. Faculty review is pending.
