Is cancer one disease or many diseases? There are many ways to classify cancers: based on where they originate in the body, whether or not they involve solid tumors, and many other features. Plutynski (2018) challenges the presupposition of this question and argues that there is no single correct answer. She illustrates that the variety of classifications comes from different epistemic aims (such as diagnosis, prognosis, treatment, or understanding) and argues for a pragmatic pluralist stance. Building on Plutynski’s account, I discuss the question of whether cancer is one disease or many diseases as follows: Cancer's heterogeneity can be understood in different ways; for example, it may be a single heterogeneous disease with multiple manifestations or many fundamentally different diseases. In medicine, we differentiate diseases because they matter for diagnosis, prognosis, or treatment. I argue that for identifying cases that clinically matter as different cancer diseases (or a single disease), (1) we should clarify what we mean when we use the ambiguous term ‘cancer’, for example, whether it refers to cancer cells or a state of disease, (2) it should be clear what cancer is as a ‘disease’ and what makes cancer a disease, and (3) we should understand how we can utilize the plurality of classifications in identifying and differentiating cases with clinical importance as different diseases. Drawing on insights from the disease entity and dispositional models of disease (Benjamin Smart, 2025), I propose a hybrid model for understanding cancer that clarifies the contributions of different classification targets in identifying cases of disease.
This paper poses a puzzle about partner choice. On one hand, an actor appears to exert causal control over its partner’s phenotype through partner choice; on the other hand, the partner’s phenotype seems largely determined by its genotype, leaving little room for the actor’s influence. I argue that this puzzle arises from adopting different causal models with different variable choices—an actor-centred model and an index-fixed model. The former is standard in social evolution theory, while the latter is my proposed alternative. I show that the puzzle has a distinctive philosophical character by interpreting it as a variant of Frege’s puzzle, rooted in ambiguity about how to represent “the partner’s phenotype” as a causal variable. I then challenge the actor-centred model on three pragmatic grounds: first, it is difficult to extend beyond a single focal individual; second, it conflates partner choice with partner control; and third, it diverges from modelling practices in economics. I conclude that the index‑fixed model offers a better representation of partner choice, and I urge reconsideration of the actor‑centred perspective in social evolution theory.
Can natural selection explain why an individual has a particular trait, or can it only explain the prevalence of that trait in a population to which that individual belongs? In the late 1980s and 1990s Karen Neander and Elliot Sober debated this topic at length, Neander defending the former view and Sober the latter. The exchange was inconclusive, but much recent work in the philosophy of biology assumes that Sober was right. Here I revisit the Neander/Sober debate and consider its implications for current issues in the philosophy of biology.
The concept of biological function has been a persistent source of debate in the philosophy of biology. This is driven in part by attempts to develop a unified account of function that can be applied across diverse biological disciplines. I suggest that such attempts may motivate the extension of particular accounts of function into unsuitable domains. At the same time, adherence to a single account risks paying inadequate attention to how the concept is currently being deployed within specific fields. I use the function debate within the philosophy of psychiatry to explore how prior explanatory commitments can motivate preferences for particular theories, resulting in poor explanatory fit. Instead, I argue that function can be understood as scientifically polysemous, whereby different subdisciplines may use the concept to refer to different properties or processes that are salient within that domain. I suggest that such variation can be legitimate when anchored to the epistemic and pragmatic goals of the field in question. Finally, I explore how the framework provided by a patchwork concept might help constrain the legitimate use of the function concept across different scientific contexts (Haueis, 2024).
In this talk, I argue that holding conflicting sets of norms does not constitute a pathological breakdown of group agency. Prominent accounts of group agency assume a demanding coherence condition: groups are taken to require a unified point of view, where persistent internal contradiction is treated as a breakdown of agency (List & Pettit 2011; Collins 2019). Yet in ordinary practice, groups are still regarded as agents despite incoherence and ongoing conflict causing tensions for views that emphasize coherence as central to agency attribution. I argue that existing theories overlook a key phenomenon: internal interference. Once interference originating from within the group is taken seriously, these accounts lack the resources to explain how contradictory groups can continue to act as agents and how to distribute responsibility. The argument proceeds in three steps. First, it examines group-level programming, including List and Pettit’s idea of “arranging things non-causally” (2011). Second, drawing on Rachar’s distinction (2024), it analyzes implicit programming as norms that guide behavior without explicit endorsement and may constitute a group’s effective program. Third, it highlights that recent responsibility-focused approaches (de Haan & Collins 2024) neglect internally generated interference. This reveals a structural gap in current accounts.
