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We recognise six hallmarks of anti-cancer drug resistance. Cancer cells may alter drug targets by mutation or reduced expression; upregulate the expression of drug pumps; increase the activity of expression of drug detoxification mechanisms; reduce their susceptibility to apoptosis; alter their level of proliferation; and increase their ability to repair DNA damage. All of these may be employed at once, but there is considerable heterogeneity between tumours, requiring an individualised approach to cancer treatment