1. How do tyrosine kinase inhibitors differ from conventional cytotoxics?
- They target specific signalling proteins that drive particular tumours, giving different toxicities such as rash, diarrhoea and hypertension rather than marrow suppression
- They have no adverse effects
- They act on all dividing cells equally
- They are always given intravenously
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A. They target specific signalling proteins that drive particular tumours, giving different toxicities such as rash, diarrhoea and hypertension rather than marrow suppression
Targeting a driver mutation, as imatinib does for BCR-ABL in chronic myeloid leukaemia, transformed outcomes and shifted the toxicity profile toward class-specific effects reflecting the pathway's normal roles. Most are oral, many are CYP3A4 substrates with important interactions, and resistance through new mutations is the usual mode of failure.