Principles of cytotoxic chemotherapy: cell kinetics, dosing, combination and resistance
Gompertzian tumour growth, the log-kill hypothesis, cell-cycle specificity, the rules for combining drugs, dosing by body surface area and by carboplatin AUC (Calvert formula), pharmacogenomic dose adjustment (DPYD, UGT1A1, TPMT), and the mechanisms of drug resistance, including P-glycoprotein.
Tier 2Medical sciences concept
Written with AI assistance and fact-checked against the sources below. For exam study, not clinical decisions. How notes are made
At a glance
- Cytotoxics kill dividing cells. Their selectivity for cancer depends on tumours having a higher growth fraction or defective DNA repair and checkpoints than normal tissue, so the therapeutic index is narrow.
- Log-kill: each dose kills a constant fraction of cells. Cure needs repeated cycles long after the tumour is clinically undetectable.
- Gompertzian growth: small tumours grow fastest and respond best, which justifies adjuvant treatment.
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Sources
- eviQ cancer treatments onlineAU/NZCancer Institute NSW, 2025
- MSAC application 1760: DPYD genotyping to predict fluoropyrimidine-induced toxicityAU/NZMedical Services Advisory Committee, Australian Government, 2024
- Clinical Pharmacogenetics Implementation Consortium (CPIC) guideline for dihydropyrimidine dehydrogenase genotype and fluoropyrimidine dosing: 2017 updateClinical Pharmacology and Therapeutics (Amstutz et al., 2018;103:210-6), 2017
- Appropriate systemic therapy dosing for obese adult patients with cancer: ASCO guideline updateJournal of Clinical Oncology (Griggs et al., 2021;39:2037-48), 2021
- Carboplatin dosage: prospective evaluation of a simple formula based on renal functionJournal of Clinical Oncology (Calvert et al., 1989;7:1748-56), 1989
- DeVita, Hellman, and Rosenberg's Cancer: Principles and Practice of Oncology (12th ed.)Wolters Kluwer (2023), 2023
- Last updated
- 14 November 2026
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