Cancer Treatment Modalities: Local Therapy, Systemic Agents, and Response Assessment
Local therapy
Surgery aims at complete resection (R0 = negative margins, R1 = microscopic, R2 = gross residual) and may be curative, debulking, or palliative. Radiation is delivered as external beam, brachytherapy, or stereotactic ablative therapy; effect depends on total dose, fractionation, volume, and radiosensitizers. Acute toxicities occur during treatment (mucositis, dermatitis, fatigue); late toxicities emerge months to years later (fibrosis, xerostomia, second malignancy).
Systemic therapy
- Cytotoxic chemotherapy is classified by mechanism (alkylators, platinums, antimetabolites, topoisomerase inhibitors, taxanes, vinca alkaloids) and by cell-cycle specificity, which drives scheduling.
- Targeted agents block defined alterations: tyrosine kinase inhibitors, monoclonal antibodies, PARP inhibitors (homologous-recombination deficiency), CDK4/6 inhibitors (HR-positive breast cancer), proteasome inhibitors.
- Immune checkpoint inhibitors release T-cell brakes. Immune-related adverse events (colitis, pneumonitis, thyroiditis, hypophysitis) may appear weeks to months after starting and are managed with corticosteroids and interruption, not continued dosing.
- Endocrine therapy and hematopoietic stem cell transplant apply to specific diseases.
Measuring benefit
RECIST 1.1 sums target-lesion longest diameters: complete response = disappearance; partial response = at least 30% decrease; progressive disease = at least 20% increase with an absolute increase of at least 5 mm, or new lesions; otherwise stable disease.
Worked example
Baseline sum 100 mm, follow-up 68 mm = 32% decrease, so partial response. A rise from 10 mm to 12 mm is 20% but only 2 mm absolute - not progressive disease, because both criteria must be met.
Rule of thumb: phase I = safety and dosing, II = activity, III = comparative effectiveness; marker change alone is not a RECIST response.