Introduction

The random mutation model of drug resistance explored in Chapters 5 and 6 can be used to derive a number of unambiguous predictions about the behaviour of clinical tumours in response to chemotherapy. These are basically the same as the ones that were developed from the consideration of the experimental tumours described in Chapter 5 but with the necessary qualifications. The clinical malignancies are much more heterogeneous and complex than the experimental systems. One important distinction is that it is not possible to stage clinical tumours with anything like the accuracy that can be achieved in the laboratory. The number of actual clonogenic cells in a transplanted tumour can be measured with precision whereas only a very rough approximation can be made for clinical malignancies. The strongest predictions made by the model include:

• there will be an unpredictable variation in response to treatment in what appears to be identical cases of malignancy

• there will be an inverse relationship between tumour mass and likelihood of cure

• combination chemotherapy will be superior to single-agent treatment with respect to the production of cures

• the sequence of drug administration influences outcome.

There are a number of other inferences that can be made from the model. The above predictions, however, can be considered to be strong predictions which easily lead from the model and which can be subjected to experimental and clinical tests.