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# Principles of cancer chemotherapy

How cytotoxic drugs exploit cell division, why they are given in combinations and cycles, and why they share toxicities in fast-growing normal tissues.

Updated Nov 2, 2026

Cytotoxic chemotherapy kills or stops the growth of cells that divide quickly. Cancer cells are the target, but bone marrow, gut lining and hair follicles also divide fast, so they are hurt too. Regimens are designed to kill as many tumour cells as possible while giving normal tissues time to recover between cycles.

## Key points

- Cell-cycle-specific drugs act in one phase: antimetabolites in S phase, vinca alkaloids and taxanes in M phase, bleomycin in G2; alkylating agents, platinum compounds and anthracyclines act in any phase.
- Each cycle kills a fraction of the tumour cells, not a fixed number, so several cycles are needed to bring a large tumour down.
- Combinations use drugs with different mechanisms and non-overlapping toxicities, which increases kill and delays resistance.
- Shared toxicities: myelosuppression (neutropenic fever is an emergency), mucositis, nausea and vomiting, hair loss, infertility and tumour lysis syndrome.
- Cytotoxic drugs are high-alert medicines: route, preparation and extravasation errors can be severe (vincristine must be given only into a vein).

## The cell cycle and phase specificity

Tumours with many dividing cells (leukaemias, lymphomas, germ-cell tumours) respond better to phase-specific drugs than slow-growing solid tumours.

- G1 → S (DNA synthesis) → G2 → M (mitosis); resting cells sit in G0 and are relatively resistant
- S phase: methotrexate, fluorouracil and other antimetabolites
- M phase: vincristine and vinblastine (stop microtubule assembly), paclitaxel and docetaxel (freeze microtubules)
- G2: bleomycin; topoisomerase inhibitors (etoposide, irinotecan) act in S and G2
- Any phase: alkylating agents, cisplatin and carboplatin, doxorubicin

## Fractional kill, cycles and combinations

A given dose kills roughly the same proportion of sensitive cells each time, so a tumour of many billions of cells needs repeated cycles. The gap between cycles lets marrow and gut recover. Combination regimens join drugs that act differently and do not share the same dose-limiting toxicity. Chemotherapy is often combined with surgery or radiation: before them to shrink the tumour (neoadjuvant) or after them to destroy remaining cells (adjuvant).

## Shared toxicities and supportive care

- Bone marrow: neutropenia, anaemia and low platelets; colony-stimulating factors (filgrastim) shorten neutropenia
- Fever during neutropenia needs urgent assessment and antibiotics
- Nausea and vomiting: 5-HT3 antagonists, NK1 antagonists and dexamethasone
- Tumour lysis syndrome: hydration, allopurinol or rasburicase
- Drug-specific rescue or protection: calcium folinate after high-dose methotrexate, mesna for the bladder with cyclophosphamide and ifosfamide, dexrazoxane for anthracycline heart toxicity
- Organ toxicities: kidney (cisplatin), heart (doxorubicin), lung (bleomycin), nerves (vincristine, paclitaxel, oxaliplatin)

## Safety in practice

Cytotoxic drugs are prepared in protected areas, double-checked and given by trained staff. Vesicants such as vincristine and doxorubicin can destroy tissue if they leak out of the vein, so the site is watched closely. Most cytotoxics harm the fetus, and contraception is discussed before treatment. Vaccinations are planned around immunosuppression (see immunopharmacology principles).

## Memory aid

«Vincas and taxanes in M, antimetabolites in S»: the letters match the phase.

## Test yourself

Think of the answer, then tap the question to see it.

## Why are hair, gut lining and bone marrow affected by chemotherapy?

They contain normal cells that divide rapidly, which cytotoxic drugs also damage.

## In which phase of the cell cycle do methotrexate and fluorouracil act?

S phase, when DNA is synthesised.

## Why are cytotoxic drugs given in repeated cycles?

Each cycle kills a fraction of the tumour cells, so several cycles are needed, and the gaps allow normal tissues such as the marrow to recover.

## Which two drugs can protect normal tissues from specific cytotoxics?

Any two of: calcium folinate (methotrexate), mesna (cyclophosphamide or ifosfamide bladder toxicity), dexrazoxane (anthracycline cardiotoxicity), amifostine (cisplatin kidney toxicity).

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[More Pharmacology questions →](https://durgical.com/en/practice/?f=pharmacology)

## Example drugs

- [Methotrexate](https://durgical.com/en/pharmacology/methotrexate/)
- [Fluorouracil](https://durgical.com/en/pharmacology/fluorouracil/)
- [Vincristine](https://durgical.com/en/pharmacology/vincristine/)
- [Paclitaxel](https://durgical.com/en/pharmacology/paclitaxel/)
- [Cisplatin](https://durgical.com/en/pharmacology/cisplatin/)
- [Doxorubicin](https://durgical.com/en/pharmacology/doxorubicin/)
- [Bleomycin](https://durgical.com/en/pharmacology/bleomycin/)
- [Etoposide](https://durgical.com/en/pharmacology/etoposide/)
- [Irinotecan](https://durgical.com/en/pharmacology/irinotecan/)
- [Calcium folinate](https://durgical.com/en/pharmacology/calcium-folinate/)
- [Mesna](https://durgical.com/en/pharmacology/mesna/)
- [Dexrazoxane](https://durgical.com/en/pharmacology/dexrazoxane/)
- [Rasburicase](https://durgical.com/en/pharmacology/rasburicase/)
- [Filgrastim](https://durgical.com/en/pharmacology/filgrastim/)
- [Ondansetron](https://durgical.com/en/pharmacology/ondansetron/)

## Connections

## Related classes 9

- [Antimetabolites](https://durgical.com/en/pharmacology/classes/antimetabolites/)
- [Microtubule inhibitors](https://durgical.com/en/pharmacology/classes/microtubule-inhibitors/)
- [Platinum compounds](https://durgical.com/en/pharmacology/classes/platinum-compounds/)
- [Antitumour antibiotics](https://durgical.com/en/pharmacology/classes/antitumour-antibiotics/)
- [Topoisomerase inhibitors](https://durgical.com/en/pharmacology/classes/topoisomerase-inhibitors/)
- [Chemotherapy supportive agents](https://durgical.com/en/pharmacology/classes/chemotherapy-supportive-agents/)
- [Myeloid colony-stimulating factors](https://durgical.com/en/pharmacology/classes/myeloid-colony-stimulating-factors/)
- [5-HT3 receptor antagonists (setrons)](https://durgical.com/en/pharmacology/classes/5-ht3-receptor-antagonists/)
- [NK1 receptor antagonists](https://durgical.com/en/pharmacology/classes/nk1-receptor-antagonists/)

[← All of pharmacology](https://durgical.com/en/pharmacology/)

Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.

Sources: [Chemotherapy to Treat Cancer](https://www.cancer.gov/about-cancer/treatment/types/chemotherapy) (National Cancer Institute (NCI), 2026); [Infection and Neutropenia during Cancer Treatment](https://www.cancer.gov/about-cancer/treatment/side-effects/infection) (National Cancer Institute (NCI), 2026); [Vincristine Injection: MedlinePlus Drug Information](https://medlineplus.gov/druginfo/meds/a682822.html) (MedlinePlus (U.S. National Library of Medicine), 2026).

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Representative model, for educational purposes only.

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Source: https://durgical.com/en/pharmacology/topics/principles-of-cancer-chemotherapy/
License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/pharmacology/topics/principles-of-cancer-chemotherapy/
