The working hypothesis in cancer research is that cells within a tumor have descended from a single initiated aberrant cell. In contrast to this clonality hypothesis, data have emerged which support the polyclonality of certain intestinal tumors. I will discuss statistical and biological aspects of polyclonality from a recent study of mouse aggregation chimeras. Three important issues are: (1) Random collision: Is it possible that observed polyclonality can be explained by the chance proximity of initiated clones? A hypothesis test is derived using some classical results from stochastic geometry. (2) What is the spatial extent of interaction among initiated clones? Techniques from Bayesian image analysis are used to combine image data on the chimeric patch structure of the intestinal wall with tumor count data. (3) What fraction of tumors are polyclonal? The lower bound proposed by Novelli and colleagues is shown to be flawed owing to a misinterpretation of conditional probability. This is a joint project with A. Thliveris, R. Halberg, L. Clipson, R. Sullivan and W.F. Dove from the McArdle Laboratory, and S. Stanhope from Statistics.
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