Abstract
A satisfactory explanation of a complex biological phenomenon like cancer implies different questions that are simultaneously present: some are related with the definition of the system, others with the definition of the relata of the explanation. Such double dimension is always present when considering regulatory patterns in biological systems. Both kinds of questions seem to be answerable in terms of “function”, an incredibly sensible term both in scientific practice and in philosophy, object of incredibly many conceptual inquiries. Statements of function are implicit explanations, but different notions of “function” might answer different kind of questions. Moreover, functional explanations seem to suffer by an intrinsic circularity that equally requires philosophical reflection and whose epistemological nature needs to be clarified. We will capture the notion of function which seems more fruitful to account for cancer research. Conversely, cancer research offers an interesting case study in order to shed light on some philosophical issues related with functional account and theories of function. This epistemological “equipment” will then be put to analyse the apparent conceptual paradoxes of Cancer Stem Cells research, showing that these paradoxes are dispelled by looking at CSCs from within a Dynamic Relational View of Cancer.
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Notes
- 1.
This theory is often, and especially in more recent literature on function, related with Wright’s work (e.g. Wright 1973). However, as Jim Lennox pointed out to me, Larry Wright’s theory of function cannot be reduced to the etiological account. Wright’s discussion of teleological explanations, actually, seems to be particularly promising to further understand the use of functional explanations in science as well.
- 2.
This theory of function is usually related to Cummins (1975). Although other terms are used to define this theory (Systemic or Causal are the most common ones) we will mainly refer to them in their original form or we will use them as equivalent to ‘dispositional’. Referring to this account in dispositional terms makes more evident, in fact, the epistemological approach to the notion of function that characterizes it. On the contrary, for example, the term “Causal Role” is confusing because a causal dimension is assumed by both theories. For a wider discussion on this point and related literature cf. Bertolaso 2011a.
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As with Nagel’s eliminativism, reductionism seems here to be facing a fatal objection, because it ignores the principal difference between a functional effect and an accidental effect, where accidental does not mean simple occasional effect. In both cases the effect can be constant and typical, but it is accidental in relation to functional effects that specify and characterize the phenomenon as a whole.
- 6.
Feinberg provides us with some considerations clarifying the implication of philosophical reductionism: “Epigenetic changes can provide mechanistic unity to understanding cancer” (Feinberg et al. 2006, p. 25, see also the Appendix for more context). The multistep model, that had put the molecular elements into a sequence needed, in fact, to integrate the schema of neoplastic onset, by means of a polyclonal model in which, not only the genetic, but also the epigenetic gene expression regulatory components, in the broad sense of the term, have to be considered. The Epigenetic Model seemed to have given an answer to the problems of cancer latency and heterogeneity that previous models could not explain. Therefore, as per an already mentioned quote, almost a guarantee for the validity of the model and its legitimacy within the reductionist paradigm, the recognition of a causal role in the epigenetic component is founded on the temporal priority of the rise of epigenetic over genetic alterations. How can an argument for causal argumentation of epigenetics changes be supported? The establishment of a causative relationship has been always molecular biology’s goal and passion, but the argument for causality has always been posed in terms of temporal priority. So that a convincing causal argument is made mainly through different arguments, like the evidence that constitutional epigenetic alterations are linked to cancer risk, as it has been demonstrated in Beckwith–Wiedemann syndrome and Wilms’ tumour, etc. Thus, “the epigenetic change precedes cancer and confers risk for cancer, a strong argument for causality” (Feinberg 2007, p. 437).
- 7.
By ‘goal contribution approach’ (GCA) (Mossio et al. 2009) is meant an approach that links the concept of function to the idea of goal-directedness, introducing more specific constraints on what makes causal relations properly functional. To identify the goal states of a system following a naturalized, and non-arbitrary criterion, the GCA has adopted a characterization of goal-directedness where biological systems can be described as having as their essential goal to survive and reproduce. Hence, biological parts are dispositions that contribute to these goals: still within a Dispositional Theory of function. In the case of malignancy the goal might also be defined in terms of survival advantage. However, even assuming a goal of the system, Dispositional Theories – though providing a general characterization of ‘useful’ contributions – are not able to distinguish between proper functions and accidental, or secondary, contributions.
- 8.
Somebody might ask why heterogeneity isn’t explained by multiple mechanisms. A simple answer could be that what mechanisms would eventually explain is: this kind of heterogeneity still depends on the PCMS. Different examples could be shown from the literature (e.g. stochastic models of cancer, the hierarchical model, a population model, etc.).
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Bertolaso, M. (2016). Complementary Issues of a Relational View of Biological Determination. In: Philosophy of Cancer. History, Philosophy and Theory of the Life Sciences, vol 18. Springer, Dordrecht. https://doi.org/10.1007/978-94-024-0865-2_7
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