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17th March 2024

Prescribing Chemotherapy

Prescribing Chemotherapy

Introduction

Chemotherapy treatments are not only one of the most common anti-cancer therapies but may also be prescribed to manage non-malignant conditions such as rheumatoid arthritis. Chemotherapy involves systemic treatments that interfere with cellular proliferation through various mechanisms, including preventing DNA and RNA replication and inhibiting cell division. Anti-cancer chemotherapy regimens may be given with curative or palliative intent, with curative therapies given before or after surgery, known respectively as neo-adjuvant and adjuvant treatment. Treatments may be administered using various delivery mechanisms including intravenous, intrathecal, intramuscular, subcutaneous, or intracavitary such as intra-peritoneal.

Chemotherapy has potentially short and long-term toxic associations ranging from mucositis, dermatitis, myelosuppression, teratogenic and carcinogenic side effects. Chemotherapy may additionally develop and limit its utility in practice. Tolerability may be improved through dose and timing adjustments coupled with the prescription of additional medications such as anti-emetics and glucocorticoids. A pre-treatment assessment should be undertaken with baseline tests including imaging, lung function tests, electrocardiogram or echocardiograms, and screening for blood borne viruses. Close monitoring and rapid assessment are required to prevent and treat complications. Repeat investigations may be warranted depending on the agents used, for example, serial echocardiograms for those on anthracyclines.

Overview of chemotherapeutic agents

Chemotherapy Common agents Mechanism of action Important adverse effects Notable clinical details
Alkylating agents Cyclophosphamide, ifosfamide Cross-links DNA leading to DNA breakage Haemorrhagic cystitis, myelosuppression, pulmonary fibrosis, cardiac toxicity, GI toxicity, syndrome of inappropriate antidiuretic hormone secretion (SIADH) Cytotoxic-induced haemorrhagic cystitis occurs due to a build-up of acrolein (a toxic metabolite). Treatment is with mesna and hydration
Platinum Analogues Cisplatin, Carboplatin Cross-links DNA Renal toxicity, ototoxicity, GI toxicity, neurotoxicity, hypomagnesaemia, nephrotoxicity, myelosuppression
Anti-metabolites Methotrexate Inhibits dihydrofolate reductase preventing conversion of folic acid to its active form Myelosuppression, hepatic and pulmonary fibrosis, mucositis, teratogenicity Concurrent folic acid supplementation. Avoid concurrent folate antagonist use (trimethoprim)
5-Fluorouracil Binds thymidine synthetase inhibiting DNA synthesis and repair Risk of toxicity in dihydropyrimidine dehydrogenase (DPD) deficient patients, myelosuppression, mucositis, alopecia DPD testing prior to treatment
Thiopurines: Azathioprine, 6- Mercaptopurine Inhibit purine metabolism High risk of thiopurine toxicity in thiopurine methyltransferase (TPMT) deficient patients, myelosuppression TPMT testing prior to treatment
Gemcitabine Inhibit DNA polymerase Myelosuppression
Antibiotics Anthracycline: Doxorubicin, Epirubicin Inhibit topoisomerase II, prevent RNA and DNA synthesis Cardiotoxicity, mucositis, GI toxicity May cause cardiomyopathy and congestive heart failure
Bleomycin Inhibits DNA synthesis by causing DNA breakage Pneumonitis, pulmonary fibrosis Hypersensitivity reactions are common
Mitomycin C Cross-links DNA Myelosuppression
Taxanes Paclitaxel, Docetaxel Interruption of mitotic spindle disassembly Myelosuppression, glove-and-stocking distribution peripheral neuropathy, palmar-plantar syndrome
Vinca Alkaloids Vincristine, Vinorelbine Inhibition of microtubule assembly Myelosuppression, neurotoxicity, GI toxicity Never to be given intrathecally as this is fatal
Topoisomerase inhibitors Topoisomerase I: irinotecan Inhibition of topoisomerase I resulting in DNA damage Myelosuppression, profuse diarrhoea Irinotecan is metabolised by CYP3A4
Topoisomerase II: etoposide Inhibition of topoisomerase II resulting in DNA damage GI toxicity, myelosuppression
Hydroxyurea Prevents DNA synthesis by inhibiting ribonucleotide reductase Myelosuppression

Selective anti-cancer and immunotherapy agents

Selective treatments target precise cellular markers, prevent angiogenesis, modify host immune responses, or disrupt intracellular signalling pathways. This selectivity aims to target malignant cells with lower levels of toxicity when compared to chemotherapy. Examples of selective anti-cancer therapies include monoclonal antibodies and tyrosine kinase inhibitors (TKIs).

Monoclonal antibodies

Cancer immunotherapies include treatments such as monoclonal antibodies, cytokines and cancer vaccines. Immunotherapy aims to modulate host immune responses to recognise and eliminate cancer cells. Common monoclonal antibody treatments include trastuzumab, rituximab, alemtuzumab and checkpoint inhibitors. Trastuzumab recognises HER2, expressed by breast cancer cells, and requires regular cardiac monitoring, including echocardiography, due to potential cardio-toxic side effects such as a reduction in left ventricular ejection fraction. Rituximab binds CD20 expressed by B cells and may be used in the treatment of non-Hodgkin lymphoma and rheumatoid arthritis, whereas alemtuzumab, binding CD52, is used in the treatment of chronic lymphocytic leukaemia. Immune checkpoint inhibitors, whose targets include CTLA-4, PD-1 and PD-L1, stimulate immune system activity and enhance malignant cell clearance. Checkpoint inhibitors, such as pembrolizumab and nivolumab, targeting PD-1, may be used in the treatment of cancers such as melanoma and non-small cell lung cancer (NSCLC). Limitations of monoclonal antibody efficacy include molecular expression by tumour cells and acquired resistance. Prior investigations require identification of specific target molecules, baseline biochemical markers and screening for hepatitis B. Live vaccine administration should be avoided during or shortly after monoclonal antibody or immunotherapy treatment.

Tyrosine kinase inhibitors

TKIs, such as imatinib and erlotinib, disrupt protein kinase signalling pathways thus preventing downstream phosphorylation driving tumorigenesis. TKIs may not only inhibit abnormal BCR-ABL1 protein in chronic myeloid leukaemia but also target growth factor receptors such as EGFR, HER2 and VEGFR and are therefore used in treatments for cancer, including NSCLC, renal, and breast cancer. Mutational analysis should be performed prior to treatment and although generally well tolerated, acquired resistance may limit efficacy.

References

Complete Guide to Clinical Genetics ST3 Application and Recruitment (2027)

Written by Medibuddy. Last updated: October 2026. Clinical Genetics is

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Complete Guide to Clinical Radiology ST3 Application and Recruitment (2027)

Recruitment paused: NHS England is not running Clinical Radiology ST3+ recru

Clinical Radiology ST3

Complete Guide to Paediatric Surgery ST3 Application and Recruitment in United Kingdom (2026)

Written by Medibuddy. Last updated: October 2026. If you’re planning

Paediatric Surgery ST3
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