I will give an overview of the recent work I have done on stochastic modeling of cancer. I will first talk about the concept of multistage carcinogenesis and how we can describe cancer as "bad evolution" within an organism. I will introduce some simple models and explain the phenomenon of "stochastic tunneling". Then I will talk about the role of stem cells in cancer initiation and present some hypotheses about the cellular origins of colon cancer.

Finally, I will talk about growing cellular colonies and models of treatment: how does resistance arise and what can we do about it? Therapies which target specific molecular alterations in cancer cells have shown promising results. Resistance, however, poses a problem, especially in advanced disease. An example is the treatment of chronic myeloid leukemia (CML) blast crisis with Gleevec. I will elucidate the principles which underlie the emergence of drug resistance in cancer. The model (a birth-death process on a combinatorial mutation network) is based on measurable parameters: the turnover rate of tumor cells, and the rate at which resistant mutants are generated. In the context of CML, the prediction is that a combination of three drugs can successfully treat blast crisis.