Anya Plutynski

Cancer is not one, but many diseases, and each is a product of a variety of causes acting at distinct temporal and spatial scales, or ‘‘levels’’ in the biological hierarchy. In part because of this diversity of cancer types and causes, there has been a diversity of models, hypotheses, and explanations of carcinogenesis. However, there is one model of carcinogenesis that seems to have survived the diversification of cancer types: the multi-stage model of carcinogenesis. This paper examines the history of the multistage theory, and uses the theory as a case study in the limits and goals of unification as a theoretical virtue, comparing and contrasting it with ‘‘integrative’’ research.

Debates concerning the character, scope, and warrant of abductive inference have been active since Peirce first proposed that there was a third form of inference, distinct from induction and deduction. Abductive reasoning has been dubbed weak, incoherent, and even nonexistent. Part, at least, of the problem of articulating a clear sense of abductive inference is due to difficulty in interpreting Peirce. Part of the fault must lie with his critics, however. While this article will argue that Peirce indeed left a number of puzzles for interpreters, it will also contend that interpreters should be careful to distinguish discussion of the formal and strictly epistemic question of whether and how abduction is a sound form of inference from discussions of the practical goals of abduction, as Peirce understood them. This article will trace a history of critics and defenders of Peirce’s notion of abduction and discuss how Peirce both fueled the confusion and in fact anticipated and responded to several recurring objections.

In 1966, Richard Levins argued that there are different strategies in model building in population biology. In this paper, I reply to Orzack and Sober’s (1993) critiques of Levins, and argue that his views on modeling strategies apply also in the context of evolutionary genetics. In particular, I argue that there are different ways in which models are used to ask and answer questions about the dynamics of evolutionary change, prospectively and retrospectively, in classical versus molecular evolutionary genetics. Further, I argue that robustness analysis is a tool for, if not confirmation, then something near enough, in this discipline.

This paper uses a number of examples of diverse types and functions of models in evolutionary biology to argue that the demarcation between theory and practice, or "theory model" and "data model," is often difficult to make. It is shown how both mathematical and laboratory models function as plausibility arguments, existence proofs, and refutations in the investigation of questions about the pattern and process of evolutionary history. I consider the consequences of this for the semantic approach to theories and theory confirmation. The paper attempts to reconcile the insights of both critics and advocates of the semantic approach to theories

There are several different ways in which chance affects evolutionary change. That all of these processes are called “random genetic drift” is in part a due to common elements across these different processes, but is also a product of historical borrowing of models and language across different levels of organization in the biological hierarchy. A history of the concept of drift will reveal the variety of contexts in which drift has played an explanatory role in biology, and will shed light on some of the philosophical controversy surrounding whether drift is a cause of evolutionary change.